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What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

Right, HUVECs in six-well plates were transfected with control plasmids vector , pCMV-NEAT1-1, or pCMV-NEAT1-2 3 g . Twenty-four hours after transfection, the cells were infected with HTNV at an MOI of 1. At Continued on next page NEAT1 Promotes Innate Antiviral Responses Journal of Virology maintaining IFN-␤ promoters, we found NEAT1-2 silencing or overexpression could inhibit or increase the promoter activity of the IFN-␤ gene after HTNV infection, respectively, whereas silencing NEAT1-2 or ectopically expressing NEAT1-2 without HTNV infection could not inhibit or enhance IFN-␤ expression Fig.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

RIG-I and DDX60 had synergic effects on IFN production. Taken together, our findings demonstrate that NEAT1 modulates the innate immune response against HTNV infection, providing another layer of information about the role of lncRNAs in controlling viral infections. IMPORTANCE Hantaviruses have attracted worldwide attention as archetypal emerging pathogens.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

At Continued on next page NEAT1 Promotes Innate Antiviral Responses Journal of Virology maintaining IFN-␤ promoters, we found NEAT1-2 silencing or overexpression could inhibit or increase the promoter activity of the IFN-␤ gene after HTNV infection, respectively, whereas silencing NEAT1-2 or ectopically expressing NEAT1-2 without HTNV infection could not inhibit or enhance IFN-␤ expression Fig. 3F . These results showed that NEAT1-2 regulated HTNV-induced IFN-␤ expression.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

1E and F and generated hantavirus progeny Fig. 1G . Similar to the data obtained from HUVECs, NEAT1 was indeed upregulated by HTNV at a multiplicity of infection MOI of 1 beginning at 24 hpi in HUVECs and A549, HEK293, and HeLa cells, and the increasing tendency occurred in a time-dependent manner Fig. 1H .

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

Of note, we applied multiple cell lines to explore the role of NEAT1 during HTNV infection. HTNV primarily targets vascular endothelial cells in vivo and contributes to the increased vascular permeability and coagulation disorders in HFRS; hence, HUVECs are the most common in vitro cell model to study host innate immunity against HTNV infection or viral pathogenesis . .

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

However, the involvement of host lncRNAs in hantaviral control remains uncharacterized. In this study, we identified the lncRNA NEAT1 as a vital antiviral modulator. NEAT1 was dramatically upregulated after Hantaan virus HTNV infection, whereas its downregulation in vitro or in vivo delayed host innate immune responses and aggravated HTNV replication.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

Taken together, our findings provide novel insights into the lncRNA-mediated regulatory mechanism of host innate defense against HTNV infection. To explore the potential role of long noncoding RNAs in host innate immune responses, DGE analysis of HUVECs for whole-genome profiling was performed at 24 h post-HTNV infection. As shown in Fig.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

NEAT1 was dramatically upregulated after Hantaan virus HTNV infection, whereas its downregulation in vitro or in vivo delayed host innate immune responses and aggravated HTNV replication. Ectopic expression of NEAT1 enhanced beta interferon IFN-β production and suppressed HTNV infection. Further investigation suggested that NEAT1 served as positive feedback for RIG-I signaling.

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

The innate immune system, characterized by interferon IFN responses and immunocyte activation, provides the initial defense against viral invasions. Cellular pathogen recognition receptors PRRs , including Toll-like receptors TLRs and RIG-I like receptors RLRs , can detect distinct pathogen-associated molecular patterns PAMPs and trigger the expression of IFNs and cytokines. RIG-I has been shown to recognize hantaviral invasion, but its regulatory process remains unclear .

What plays a role in innate immunity to Hantavirus infection?

Among these noncoding RNAs ncRNAs , long noncoding RNAs lncRNAs emerged as important regulators of gene expression and are closely related to the activation of the host innate immune system. TLR2 controls lncRNA-COX2 expression in a MyD88-and NF-B-dependent manner, whereas lncRNA-COX either promotes interleukin 6 IL-6 secretion or represses ISG15 and CCL5 expression . .

1D . To further investigate whether NEAT1 expression was altered in other cell lines, HEK293, HeLa, and A549 cells were used. All these cells could be infected by HTNV Fig. 1E and F and generated hantavirus progeny Fig. 1G .

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects. To verify the antiviral role of RIG-I and DDX60, we designed a series of siRNAs targeting RIG-I and DDX60, and we selected the si-RIG-I-2 and siRNA-DDX60-1 with the highest knockdown efficiency by qRT-PCR in HUVECs data not shown . Simultaneously knocking down RIG-I and DDX60 significantly promoted HTNV NP expression Fig.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

DDX60 was recently reported as an important activator of RIG-I, but the antiviral effects of DDX60 remain a subject of debate . , Here, we found that multiple Toll-like receptors like TLR1, TLR2, TLR3, and TLR4, as well as MDA5, were increased after HTNV infection, but none of them were influenced by silencing NEAT1-2 Fig. 4A .

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

Ectopic expression of either RIG-I or DDX60 inhibited viral replication, whereas overexpression of both resulted in superior antiviral effects Fig. 4H , indicating that efficient anti-HTNV responses might depend on the interactive effects of DDX60 and RIG-I. More importantly, RIG-I or/and DDX60 overexpression enhanced HTNV-induced IFN-␤ expression, and they had synergistic effects on IFN-␤ production Fig.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

Simultaneously knocking down RIG-I and DDX60 significantly promoted HTNV NP expression Fig. 4E , and knockdown of both of them could greatly affect IFN-␤ expression Fig. 4F and G . Ectopic expression of either RIG-I or DDX60 inhibited viral replication, whereas overexpression of both resulted in superior antiviral effects Fig.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

TLR3, TLR4, and RIG-I have been shown to recognize HTNV infection . . DDX60 was recently reported as an important activator of RIG-I, but the antiviral effects of DDX60 remain a subject of debate .

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

. Here, considering the interaction of RIG-I and DDX60 and the effect of DDX60 on IFN-␤ production, we hypothesize that DDX60 might mediate RIG-I signaling activation upon HTNV infection, which requires further investigation. Of note, we applied multiple cell lines to explore the role of NEAT1 during HTNV infection.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

DDX60 recognizes viral RNA and activates endogenous RIG-I, thereby promoting the RIG-I signaling-related IFN response. However, the antiviral effects of DDX60 seem to vary among viruses . . We found that NEAT1-regulated DDX60 was involved in IFN production in response to HTNV infection.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

RIG-I and DDX60 had synergic effects on IFN production. Taken together, our findings demonstrate that NEAT1 modulates the innate immune response against HTNV infection, providing another layer of information about the role of lncRNAs in controlling viral infections. IMPORTANCE Hantaviruses have attracted worldwide attention as archetypal emerging pathogens.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

This finding excludes the possibility that NEAT1-2 directly promoted IFN-␤ and that IFN-␤ promoted the expression of PRRs such as RIG-I. Thereafter, NEAT1 was found to modulate HTNV-induced RIG-I and DDX60 expression. Recent findings have shown that RIG-I signaling is essential for an efficient polyfunctional T cell response during IAV infection . .

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

We found that NEAT1-regulated DDX60 was involved in IFN production in response to HTNV infection. In HTNV-infected cells, double-stranded RNA dsRNA could not be detected, and it is unclear how host PRRs, especially RIG-I, recognize HTNV invasion . .

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

Together these results demonstrated that NEAT1-2 especially enhanced the host antihantaviral innate immune responses by regulating IFN-␤ signaling. RIG-I and DDX60 regulated by NEAT1-2 facilitate HTNV-induced IFN-␤ production. PRRs maintain a vital role in the promotion of IFN responses, and we conjectured that NEAT1 might amplify IFN responses by modulating these molecules.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

Further investigation suggested that NEAT1 served as positive feedback for RIG-I signaling. HTNV infection activated NEAT1 transcription through the RIG-I–IRF7 pathway, whereas NEAT1 removed the transcriptional inhibitory effects of the splicing factor proline- and glutamine-rich protein SFPQ by relocating SFPQ to paraspeckles, thus promoting the expression of RIG-I and DDX60. RIG-I and DDX60 had synergic effects on IFN production.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

Further investigation showed that NEAT1 promoted RIG-I and DDX60 expression by relocating SFPQ and removing the transcriptional inhibitory effects of SFPQ, which are critical for IFN responses against HTNV infection. We also found that RIG-I signaling, rather than TLR3 and TLR4, accounted for the elevation of HTNV-induced NEAT1. Taken together, our findings provide novel insights into the lncRNA-mediated regulatory mechanism of host innate defense against HTNV infection.

What evidence suggests that RIG-I and DDX60 collaborate to exert antiviral effects?

4C . These data indicated that NEAT1-2 could positively modulate RIG-I and DDX60 expression, while the role of RIG-I and DDX60 upon HTNV infection is obscure. We then found that RIG-I and DDX60 colocalized after HTNV infection Fig. 4D , implying that RIG-I and DDX60 might collaborate with each other to exert antiviral effects.

4A . The upregulated RIG-I and DDX60 were blocked in the cells with low NEAT1-2 expression after HTNV infection Fig. 4A . HUVECs with declining NEAT1-2 expression showed gradually decreasing expression of RIG-I and DDX60 Fig. 4B , and increasing NEAT1-2 transcription was found to activate RIG-I and DDX60 production accordingly Fig. 4C .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Values are means Ϯ SD n ϭ 3; *, P Ͻ 0.01; **, P Ͻ 0.001; ***, P Ͻ 0.0001; Student's t test, compared with the NC group . NS, nonsignificant. B HUVECs in six-well plates were transfected with NC sequences the amount of Si-NEAT1-2 is considered 0 g or increasing amounts of si-NEAT1 0.1, 0.5, 1, and 3 g .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

n ϭ 4; *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the vector group . H HUVECs were treated as described for panel F, right. The expression of HTNV S segment was measured by qRT-PCR.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

B The effects of NEAT1 on HTNV virulence in mice were determined by body weight loss from 0 to 10 dpi left panel, n ϭ 10 in each group . The IFN-␤ in sera of different groups was measured by ELISA at 3dpi right panel, n ϭ 8 in each group . Values are means Ϯ SD *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the NCϩHTNV group .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Values are means Ϯ SD n ϭ 3; *, P Ͻ 0.01; **, P Ͻ 0.001; ***, P Ͻ 0.0001; Student's t test, compared with the vector group . G HUVECs in six-well plates were transfected with control plasmids vector, the amount of pCMV-NEAT1-1 plus pCMV-NEAT1-2 is considered 0 g or increasing amounts of pCMV-NEAT1-1 plus pCMV-NEAT1-2 0.05 ϩ 0.05 g, 0.25 ϩ 0.25 g, 0.5 ϩ 0.5 g, 1.5 ϩ 1.5 g, respectively . Twenty-four hours after transfection, the cells were infected with HTNV at an MOI of 1 for 48 h. The expression of HTNV NP was measured by Western blotting.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Values are means Ϯ SD n ϭ 3; *, P Ͻ 0.01; Student's t test, compared with the vector group . might be involved in SFPQ. Interestingly, the protein level of SFPQ, as well as another paraspeckle-forming constituent, NONO, remained unchanged after HTNV infection Fig.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

D HUVECs were treated as described for panel A, right, but at an MOI of 0.1. The expression of HTNV S segment was measured by qRT-PCR. Values are means Ϯ SD n ϭ 3; *, P Ͻ 0.01; Student's t test, compared with the NC group .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

5D . The enhanced interaction of SFPQ and NONO indicated excess formation of paraspeckles in the nucleus Fig. 5E and relocalization of SFPQ. SFPQ knockdown could inhibit HTNV replication Fig. 5F and G , which might have been related to the increase in RIG-I Fig. 5H and DDX60 Fig. 5I .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

To avoid the possible noise signal from high-throughput sequencing, the genes with average TPM of less than 1 in these three states were excluded. In this study, an absolute fold change of no less than 1.5 and a false discovery rate FDR of less than 0.001 were used to define the differentially expressed genes. Genes were selected as differentially expressed using a P value threshold of 0.01.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

2B . Intriguingly, depletion of NEAT1-2 alone could mimic the antiviral effects of simultaneous NEAT1-1 and NEAT1-2 silencing Fig. 2C , indicating that NEAT1-2 was critical for the antiviral responses. Consistent with those data, the expressions of HTNV mRNA of S segment Fig. 2D and HTNV titers Fig. 2E were increased after NEAT1 silencing.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

The expression of HTNV S segment was measured by qRT-PCR. Values are means Ϯ SD n ϭ 3; *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the vector group . I HUVECs were treated as described for panel F, right.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Values are means Ϯ SD *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the NCϩHTNV group . C Mice were sacrificed at 3 dpi, and livers, spleens, and kidneys were collected for ELISA detection of HTNV NP titers upper panels, n ϭ 8 in each group and qRT-PCR to assess HTNV S segment levels bottom panels, n ϭ 8 in each group at 3 dpi. Values are means Ϯ SD *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the NCϩHTNV group .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Finally, the samples were observed using a BX60 fluorescence microscope Olympus . Cells were washed twice with ice-cold DPBS and lysed with 1ϫ SDS protein loading buffer 50 mM Tris, 2% SDS, 10% glycerol, 2% 2-mercaptoethanol, and 0.1% bromophenol blue . The samples were then boiled at 95°C for 10 min.

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

1D . To further investigate whether NEAT1 expression was altered in other cell lines, HEK293, HeLa, and A549 cells were used. All these cells could be infected by HTNV Fig. 1E and F and generated hantavirus progeny Fig. 1G .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

Values are means Ϯ SD *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the NCϩHTNV group . D NEAT1 effects on HTNV infection kinetics at 3 dpi were determined by testing the HTNV titers in livers, spleens, and kidneys. Values are means Ϯ SD n ϭ 8; *, P Ͻ 0.01; **, P Ͻ 0.001; Student's t test, compared with the NCϩHTNV group .

What was the major contribution of this study?

In conclusion, this is the first study to describe the role of NEAT1 in HTNV infection. HTNV infection induced NEAT1 expression through the RIG-I-IRF7 pathway, while NEAT1 displayed positive feedback for RIG-I signaling. NEAT1 relocated SFPQ from the potential promoter region of several antiviral genes to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ.

As a consequence, the intensity represented the quantity of NP production but could not directly indicate the virulence, which was better shown by plaque-forming assays. The RNAi studies in vivo are encouraging Fig. 8 , but the NC used by our group was not mutated si-NEAT1-2 i.e., same sense strand, but with a point mutation in the targeting strand .

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98-2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43-4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19. Text: non-survivors p=0.21 with regard to mortality from COVID-19. Similarly, Zhang et al.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

We identified five studies that reported data on the smoking status of patients infected with COVID-19. Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases 12 . However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98-2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43-4.04 .

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study. Finally, Liu et al. 13 found among their population of 78 patients with COVID-19 that the adverse outcome group had a significantly higher proportion of patients with a history of smoking 27.3% than the group that showed improvement or stabilization 3.0% , with this difference statistically significant at the p=0.018 level.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Huang et al. 11 studied the epidemiological characteristics of COVID-19 among 41 patients. In this study, none of those who needed to be admitted to an ICU n=13 was a current smoker.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

In their multivariate logistic regression analysis, the history of smoking was a risk factor of disease progression OR=14.28; 95% CI: 1.58–25.00; p= 0.018 . We identified five studies that reported data on the smoking status of patients infected with COVID-19. Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases..

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Huang et al.. studied the epidemiological characteristics of COVID-19 among 41 patients. In this study, none of those who needed to be admitted to an ICU n=13 was a current smoker. In contrast, three patients from the non-ICU group were current smokers, with no statistically significant difference between the two groups of patients p=0.31 , albeit the small sample size of the study.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

13 found among their population of 78 patients with COVID-19 that the adverse outcome group had a significantly higher proportion of patients with a history of smoking 27.3% than the group that showed improvement or stabilization 3.0% , with this difference statistically significant at the p=0.018 level. In their multivariate logistic regression analysis, the history of smoking was a risk factor of disease progression OR=14.28; 95% CI: 1.58-25.00; p= 0.018 . We identified five studies that reported data on the smoking status of patients infected with COVID-19.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study. Finally, Liu et al.. found among their population of 78 patients with COVID-19 that the adverse outcome group had a significantly higher proportion of patients with a history of smoking 27.3% than the group that showed improvement or stabilization 3.0% , with this difference statistically significant at the p=0.018 level. In their multivariate logistic regression analysis, the history of smoking was a risk factor of disease progression OR=14.28; 95% CI: 1.58–25.00; p= 0.018 .

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

In this study, none of those who needed to be admitted to an ICU n=13 was a current smoker. In contrast, three patients from the non-ICU group were current smokers, with no statistically significant difference between the two groups of patients p=0.31 , albeit the small sample size of the study. The largest study population of 1099 patients with COVID-19 was provided by Guan et al.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

The results showed that among severe patients n=58 , 3.4% were current smokers and 6.9% were former smokers, in contrast to non-severe patients n=82 among which 0% were current smokers and 3.7% were former smokers , leading to an OR of 2.23; 95% CI: 0.65-7.63; p=0.2 . Huang et al. 11 studied the epidemiological characteristics of COVID-19 among 41 patients.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Among the 191 patients, there were 54 deaths, while 137 survived. Among those that died, 9% were current smokers compared to 4% among those that survived, with no statistically significant difference between the smoking rates of survivors and non-survivors p=0.21 with regard to mortality from COVID-19. Similarly, Zhang et al.. presented clinical characteristics of 140 patients with COVID-19.

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Similarly, Zhang et al. 10 presented clinical characteristics of 140 patients with COVID-19. The results showed that among severe patients n=58 , 3.4% were current smokers and 6.9% were former smokers, in contrast to non-severe patients n=82 among which 0% were current smokers and 3.7% were former smokers , leading to an OR of 2.23; 95% CI: 0.65-7.63; p=0.2 .

How does being a smoker impact COVID-19 patient outcomes?

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

In contrast, three patients from the non-ICU group were current smokers, with no statistically significant difference between the two groups of patients p=0.31 , albeit the small sample size of the study. The largest study population of 1099 patients with COVID-19 was provided by Guan et al.. from multiple regions of mainland China. Descriptive results on the smoking status of patients were provided for the 1099 patients, of which 173 had severe symptoms, and 926 had non-severe symptoms.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Smoking, to date, has been assumed to be possibly associated with adverse disease prognosis, as extensive evidence has highlighted the negative impact of tobacco use on lung health and its causal association with a plethora of respiratory diseases.. Smoking is also detrimental to the immune system and its responsiveness to infections, making smokers more vulnerable to infectious diseases.. Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 .

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98-2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43-4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

We identified five studies that reported data on the smoking status of patients infected with COVID-19. Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases 12 . However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98-2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43-4.04 .

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases.. However, from their published data we can calculate that the smokers were 1.4 times more likely RR=1.4, 95% CI: 0.98–2.00 to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers RR=2.4, 95% CI: 1.43–4.04 . In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Additionally, in the group of patients that either needed mechanical ventilation, admission to an ICU or died, 25.5% were current smokers and 7.6% were former smokers. In contrast, in the group of patients that did not have these adverse outcomes, only 11.8% were current smokers and 1.6% were former smokers. No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Additionally, in the group of patients that either needed mechanical ventilation, admission to an ICU or died, 25.5% were current smokers and 7.6% were former smokers. In contrast, in the group of patients that did not have these adverse outcomes, only 11.8% were current smokers and 1.6% were former smokers. No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

In their multivariate logistic regression analysis, the history of smoking was a risk factor of disease progression OR=14.28; 95% CI: 1.58–25.00; p= 0.018 . We identified five studies that reported data on the smoking status of patients infected with COVID-19. Notably, in the largest study that assessed severity, there were higher percentages of current and former smokers among patients that needed ICU support, mechanical ventilation or who had died, and a higher percentage of smokers among the severe cases..

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Huang et al. 11 studied the epidemiological characteristics of COVID-19 among 41 patients. In this study, none of those who needed to be admitted to an ICU n=13 was a current smoker.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

and Italy ... However, as the pandemic is still unfortunately under progression, there are limited data with regard to the clinical characteristics of the patients as well as to their prognostic factors.. Smoking, to date, has been assumed to be possibly associated with adverse disease prognosis, as extensive evidence has highlighted the negative impact of tobacco use on lung health and its causal association with a plethora of respiratory diseases..

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

In conclusion, although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19. Text: non-survivors p=0.21 with regard to mortality from COVID-19. Similarly, Zhang et al.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

Huang et al.. studied the epidemiological characteristics of COVID-19 among 41 patients. In this study, none of those who needed to be admitted to an ICU n=13 was a current smoker. In contrast, three patients from the non-ICU group were current smokers, with no statistically significant difference between the two groups of patients p=0.31 , albeit the small sample size of the study.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study. Finally, Liu et al. 13 found among their population of 78 patients with COVID-19 that the adverse outcome group had a significantly higher proportion of patients with a history of smoking 27.3% than the group that showed improvement or stabilization 3.0% , with this difference statistically significant at the p=0.018 level.

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

No statistical analysis for evaluating the association between the severity of the disease outcome and smoking status was conducted in that study. Finally, Liu et al.. found among their population of 78 patients with COVID-19 that the adverse outcome group had a significantly higher proportion of patients with a history of smoking 27.3% than the group that showed improvement or stabilization 3.0% , with this difference statistically significant at the p=0.018 level. In their multivariate logistic regression analysis, the history of smoking was a risk factor of disease progression OR=14.28; 95% CI: 1.58–25.00; p= 0.018 .

Are smokers more likely to contract influenza?

Previous studies have shown that smokers are twice more likely than non-smokers to contract influenza and have more severe symptoms, while smokers were also noted to have higher mortality in the previous MERS-CoV outbreak 7,8 . Given the gap in the evidence, we conducted a systematic review of studies on COVID-19 that included information on patients’ smoking status to evaluate the association between smoking and COVID-19 outcomes including the severity of the disease, the need for mechanical ventilation, the need for intensive care unit ICU hospitalization and death. The literature search was conducted on 17 March 2020, using two databases PubMed, ScienceDirect , with the search terms: ‘smoking’ OR ‘tobacco’ OR ‘risk factors’ OR ‘smoker*’ AND ‘COVID-19’ OR ‘COVID 19’ OR ‘novel coronavirus’ OR ‘sars cov-2’ OR ‘sars cov 2’ and included studies published in 2019 and 2020.

The results showed that among severe patients n=58 , 3.4% were current smokers and 6.9% were former smokers, in contrast to non-severe patients n=82 among which 0% were current smokers and 3.7% were former smokers , leading to an OR of 2.23; 95% CI: 0.65-7.63; p=0.2 . Huang et al. 11 studied the epidemiological characteristics of COVID-19 among 41 patients.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Understanding the natural history of ebolaviruses is a health priority, and investigating these alternative hypotheses could complete the current effort focused on the role of bats. Text: Ebolaviruses EBVs , according to Kuhn et al. classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans .

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

As warned above, the EBOV multi-host maintenance system could include a complex network of interacting bat species Figure 1A2 and to proceed by elimination of alternative hypotheses may be a way to zoom-in on the maintenance community. The hypothesis of human playing a role in ebolavirus maintenance has not been addressed here, even if persistence of EBOV in previously infected humans has been recently proven . This scenario would be more indicating of a change in the evolutionary trajectory of the pathogen as moving from Step 4 to 5 in Figure 1 of Wolfe et al.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

This scenario would be more indicating of a change in the evolutionary trajectory of the pathogen as moving from Step 4 to 5 in Figure 1 of Wolfe et al. than of the natural maintenance of ebolaviruses that is considered here. In order for these protocols to be efficient and well designed, insights from behavioural ecology, plant phenology, and molecular biology amongst other disciplines will be necessary.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Currently this is logically the most investigated hypothesis given the available data, and represents the maintenance mechanism for another filovirus, the Marburg virus, as currently understood. A2 Several bat species are needed to create a maintenance community for Zaire ebolavirus EBOV ; each bat species cannot complete EBOV maintenance alone, as it requires interactions with the other species. B Alternate non-bat maintenance host hypothesis: if it exists, it is known that it can transmit ebolaviruses to some bat species.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

How does one puzzle out? Since recent studies have revealed that several bat species have been exposed to ebolaviruses, the common denominator to these hypotheses is that within the epidemiological cycle, some bats species must be exposed to the viruses and infected by these potential alternative hosts. Under this constraint, and given the peculiar ecology of bats roosting behaviour, habitat utilisation, and flight mode , we review the hosts and transmission pathways that can lead to bat exposure and infection to ebolaviruses.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Given the number of species already involved/exposed to EBOV, the ecology of EBOV and its maintenance system can be expected to be complex, ecosystem dependent , and dynamic, due to global changes . The Ebola maintenance system, once isolated in the forests, is now interacting with humans and their modified environments and will adapt to it. Aiming at this moving target will require out-of-the-box thinking and interdisciplinary collaboration.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge. Circles plain or dotted indicate a maintenance function play by the host s ; arrows represent infectious transmission pathways between hosts. Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge. Circles plain or dotted indicate a maintenance function play by the host s ; arrows represent infectious transmission pathways between hosts. Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

The maintenance mechanisms of ebolaviruses in African forest ecosystems are still unknown, but indirect evidences point at the involvement of some bat species. Despite intense research, the main bat-maintenance hypothesis has not been confirmed yet. The alternative hypotheses of a non-bat maintenance host or a maintenance community including, or not, several bat and other species, deserves more investigation.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

C The maintenance community hypothesis, in which several hosts are needed to maintain ebolaviruses ellipses represent different scenarios of community maintenance . This could be one or more alternative hosts involving possibly bat species. By definition, if such an alternative host exists, there are infectious transmission pathways from this host towards bats that are reviewed here red arrows .

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, . Recently, a new ebolavirus species with an unknown pathogenic risk has also been isolated from two insectivorous bat species roosting inside a house . Moreover, Swanepoel et al.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

It would be tedious to quantitatively estimate probabilities in the case of ebolavirus maintenance given the current lack of information, but trying to define the components of this probability could help. Hence, instead of proving that bats are the maintenance host for EBOV, what if we consider that "bats are not the only maintenance host for EBOV"? Here, we consider the scenario presented in Figure 1B ,C, namely, that bats are not the maintenance host for EBOV or that bat species are involved with alternative host s in the EBOV maintenance community.

What is the structure of the Ebolavirus?

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host. A1 Main maintenance hypothesis: there is one bat species maintaining each ebolavirus alone. Currently this is logically the most investigated hypothesis given the available data, and represents the maintenance mechanism for another filovirus, the Marburg virus, as currently understood.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans . The different ebolaviruses have caused localised but dramatic human outbreaks, mainly in Central Africa, in the last 40 years. The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens .

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

The maintenance of EBV in equatorial forests is yet to be understood. Some mammal species played a major role in triggering human outbreaks: apes such as chimpanzees Pan troglodytes troglodytes and P. t. verus and western lowland gorillas Gorilla gorilla gorilla were at the origin of several human outbreaks , but have been found to be highly susceptible to EBV with potential drastic impact for their populations . EBOV PCR positive duiker carcasses Cephalophus sp.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

Understanding the natural history of ebolaviruses is a health priority, and investigating these alternative hypotheses could complete the current effort focused on the role of bats. Text: Ebolaviruses EBVs , according to Kuhn et al. classification are single-strand RNA filoviruses that can induce a high mortality in some hosts, including apes and humans .

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

This scenario would be more indicating of a change in the evolutionary trajectory of the pathogen as moving from Step 4 to 5 in Figure 1 of Wolfe et al. than of the natural maintenance of ebolaviruses that is considered here. In order for these protocols to be efficient and well designed, insights from behavioural ecology, plant phenology, and molecular biology amongst other disciplines will be necessary.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

As warned above, the EBOV multi-host maintenance system could include a complex network of interacting bat species Figure 1A2 and to proceed by elimination of alternative hypotheses may be a way to zoom-in on the maintenance community. The hypothesis of human playing a role in ebolavirus maintenance has not been addressed here, even if persistence of EBOV in previously infected humans has been recently proven . This scenario would be more indicating of a change in the evolutionary trajectory of the pathogen as moving from Step 4 to 5 in Figure 1 of Wolfe et al.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, . Recently, a new ebolavirus species with an unknown pathogenic risk has also been isolated from two insectivorous bat species roosting inside a house . Moreover, Swanepoel et al.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

The maintenance mechanisms of ebolaviruses in African forest ecosystems are still unknown, but indirect evidences point at the involvement of some bat species. Despite intense research, the main bat-maintenance hypothesis has not been confirmed yet. The alternative hypotheses of a non-bat maintenance host or a maintenance community including, or not, several bat and other species, deserves more investigation.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

Given the number of species already involved/exposed to EBOV, the ecology of EBOV and its maintenance system can be expected to be complex, ecosystem dependent , and dynamic, due to global changes . The Ebola maintenance system, once isolated in the forests, is now interacting with humans and their modified environments and will adapt to it. Aiming at this moving target will require out-of-the-box thinking and interdisciplinary collaboration.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

This does not mean that they can automatically inform on "what maintains ebolaviruses". When looking for the maintenance host, investigations should also target the same and other alternative hosts during inter-outbreak periods with ecologically driven hypotheses. This is what is currently done for bats following the main maintenance hypothesis e.g., , but not often for alternative hosts.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

Currently this is logically the most investigated hypothesis given the available data, and represents the maintenance mechanism for another filovirus, the Marburg virus, as currently understood. A2 Several bat species are needed to create a maintenance community for Zaire ebolavirus EBOV ; each bat species cannot complete EBOV maintenance alone, as it requires interactions with the other species. B Alternate non-bat maintenance host hypothesis: if it exists, it is known that it can transmit ebolaviruses to some bat species.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

How does one puzzle out? Since recent studies have revealed that several bat species have been exposed to ebolaviruses, the common denominator to these hypotheses is that within the epidemiological cycle, some bats species must be exposed to the viruses and infected by these potential alternative hosts. Under this constraint, and given the peculiar ecology of bats roosting behaviour, habitat utilisation, and flight mode , we review the hosts and transmission pathways that can lead to bat exposure and infection to ebolaviruses.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

The EBOV susceptibility and exposure tested by virology, serology and/or PCR of many other potential forest hosts, including invertebrates, birds, bats, monkeys, rodents, and other small mammals, have been tested in the field or experimentally with an interestingly large amount of negative results e.g., 12, . A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge.

When was the West African Ebolavirus outbreak?

The recent West African outbreak in 2013-2016 gave an outline of the pandemic potential of these pathogens . Disentangling the complexity of maintenance hosts or communities in multi-host systems at the wildlife/livestock/human interface is a difficult task . The maintenance of EBV in equatorial forests is yet to be understood.

Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host. A1 Main maintenance hypothesis: there is one bat Figure 1 . Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge.

What animals are considered to be maintenance hosts to the Ebolavirus?

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host. A1 Main maintenance hypothesis: there is one bat Figure 1 . Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge.

What animals are considered to be maintenance hosts to the Ebolavirus?

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host. A1 Main maintenance hypothesis: there is one bat species maintaining each ebolavirus alone. Currently this is logically the most investigated hypothesis given the available data, and represents the maintenance mechanism for another filovirus, the Marburg virus, as currently understood.

What animals are considered to be maintenance hosts to the Ebolavirus?

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

The EBOV susceptibility and exposure tested by virology, serology and/or PCR of many other potential forest hosts, including invertebrates, birds, bats, monkeys, rodents, and other small mammals, have been tested in the field or experimentally with an interestingly large amount of negative results e.g., 12, . A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge.

What animals are considered to be maintenance hosts to the Ebolavirus?

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

Currently this is logically the most investigated hypothesis given the available data, and represents the maintenance mechanism for another filovirus, the Marburg virus, as currently understood. A2 Several bat species are needed to create a maintenance community for Zaire ebolavirus EBOV ; each bat species cannot complete EBOV maintenance alone, as it requires interactions with the other species. B Alternate non-bat maintenance host hypothesis: if it exists, it is known that it can transmit ebolaviruses to some bat species.

What animals are considered to be maintenance hosts to the Ebolavirus?

A few monkey and bat individuals serologically positive to EBV antigen represent the only exceptions . Today, African bats are considered by many as the best candidates for acting as maintenance hosts for EBOV. Partial vRNA was sequenced from living specimens of three different bat species in Central Africa , and antibodies against ebolavirus antigen have been detected in 9 bat species 8 frugivorous and 1 insectivorous 3, 23, .

Potential maintenance mechanisms of ebolaviruses in wildlife, according to current knowledge. Circles plain or dotted indicate a maintenance function play by the host s ; arrows represent infectious transmission pathways between hosts. Humans, non-human primates, and duikers are examples of known non-maintenance hosts, exposed occasionally to ebolavirus directly or indirectly through the main maintenance host.