The Host Response to Influenza A Virus Interferes with SARS-CoV-2 Replication during Coinfection

Oishi, Kohei; Horiuchi, Shu; Minkoff, Judith M; tenOever, Benjamin R.

doi:10.1128/jvi.00765-22

Cited by 40 publications

(58 citation statements)

References 45 publications

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“…Comparably, similar SARS2 vRNA loads within respiratory tissues between 6--8-weeks old GSHs infected with SARS2 and co-infected with FLUAV (PR8) H1N1 were observed at 4 dpc [8]. While we observed a reduction of vRNA in the NT at 6 dpc, a recent report showed that prior FLUAV infection 14 days before SARS2 infection resulted in reduced SARS2 replication in the lung of male 6-8 weeks old GSH [36]. High SARS2 viral loads in respiratory samples, including NT, trachea, and lungs, at early time points, were also observed…”

Section: Discussionsupporting

confidence: 81%

“…These results suggest that previous innate immune response stimulation from FLUAV pre-exposure may influence the duration of opportunistic pathogen enrichment such as Haemophilus post-SARS2 infection. It has also been previously demonstrated that 6–8 week old GSH sustained heightened gene expression of interferon-stimulating genes 7 and 14 days post FLUAV infection [ 36 ]. The innate immune response, including macrophages and neutrophils, is important for viral clearance but also plays a role in regulating commensal microbes [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

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Pathobiology and dysbiosis of the respiratory and intestinal microbiota in 14 months old Golden Syrian hamsters infected with SARS-CoV-2

Seibert

Cáceres²,

Carnaccini³

et al. 2022

PLoS Pathog

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The pandemic of severe acute respiratory syndrome coronavirus 2 (SARS2) affected the geriatric population. Among research models, Golden Syrian hamsters (GSH) are one of the most representative to study SARS2 pathogenesis and host responses. However, animal studies that recapitulate the effects of SARS2 in the human geriatric population are lacking. To address this gap, we inoculated 14 months old GSH with a prototypic ancestral strain of SARS2 and studied the effects on virus pathogenesis, virus shedding, and respiratory and gastrointestinal microbiome changes. SARS2 infection led to high vRNA loads in the nasal turbinates (NT), lungs, and trachea as well as higher pulmonary lesions scores later in infection. Dysbiosis throughout SARS2 disease progression was observed in the pulmonary microbial dynamics with the enrichment of opportunistic pathogens (Haemophilus, Fusobacterium, Streptococcus, Campylobacter, and Johnsonella) and microbes associated with inflammation (Prevotella). Changes in the gut microbial community also reflected an increase in multiple genera previously associated with intestinal inflammation and disease (Helicobacter, Mucispirillum, Streptococcus, unclassified Erysipelotrichaceae, and Spirochaetaceae). Influenza A virus (FLUAV) pre-exposure resulted in slightly more pronounced pathology in the NT and lungs early on (3 dpc), and more notable changes in lungs compared to the gut microbiome dynamics. Similarities among aged GSH and the microbiome in critically ill COVID-19 patients, particularly in the lower respiratory tract, suggest that GSHs are a representative model to investigate microbial changes during SARS2 infection. The relationship between the residential microbiome and other confounding factors, such as SARS2 infection, in a widely used animal model, contributes to a better understanding of the complexities associated with the host responses during viral infections.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Pathobiology and dysbiosis of the respiratory and intestinal microbiota in 14 months old Golden Syrian hamsters infected with SARS-CoV-2

Seibert

Cáceres²,

Carnaccini³

et al. 2022

PLoS Pathog

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“…Further research will have to show the relevance of our findings in the context of SARS-CoV-2/ influenza virus co-infection. Data on the severity of SARS-CoV-2/ influenza A virus co-infections are inconsistent in cell culture and animal models [Andrés et al, 2022; Kim EH et al, 2022; Kim HK et al, 2022; Oishi et al, 2022] and in humans [Cuadrado-Payán et al, 2020; Yue et al, 2020; Alosaimi et al, 2021; Stowe et al, 2021; Xiang et al, 2021; Krumbein et al, 2022; Swets et al, 2022]. This may not be a surprise, given the differences in interferon signalling between different SARS-CoV-2 variants that we present here and that were described in previous studies [Alfi et al, 2022; Bojkova et al, 2022; Bojkova et al, 2022a; Guo et al, 2022; Thorne et al, 2022].…”

Section: Discussionmentioning

confidence: 99%

Omicron-induced interferon signalling prevents influenza A virus infection

Bojkova

Bechtel

Rothenburger

et al. 2022

Preprint

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Recent findings in permanent cell lines suggested that SARS-CoV-2 Omicron BA.1 induces a stronger interferon response than Delta. Here, we show that BA.1 and BA.5 but not Delta induce an antiviral state in air-liquid interface (ALI) cultures of primary human bronchial epithelial (HBE) cells and primary human monocytes. Both Omicron subvariants caused the production of biologically active type I (alpha/beta) and III (lambda) interferons and protected cells from super-infection with influenza A viruses. Notably, abortive Omicron infection of monocytes was sufficient to protect monocytes from influenza A virus infection. Interestingly, while influenza-like illnesses surged during the Delta wave in England, their spread rapidly declined upon the emergence of Omicron. Mechanistically, Omicron-induced interferon signalling was mediated via double-stranded RNA recognition by MDA5, as MDA5 knock-out prevented it. The JAK/ STAT inhibitor baricitinib inhibited the Omicron-mediated antiviral response, suggesting it is caused by MDA5-mediated interferon production, which activates interferon receptors that then trigger JAK/ STAT signalling. In conclusion, our study 1) demonstrates that only Omicron but not Delta induces a substantial interferon response in physiologically relevant models, 2) shows that Omicron infection protects cells from influenza A virus super-infection, and 3) indicates that BA.1 and BA.5 induce comparable antiviral states.

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“…This phenomenon has also been observed in mouse models of SARS-CoV, MERS-CoV, and IAV infection [17] . On the other hand, early IFN/ISG responses elicited by co-infection with rhinovirus or IAV can substantially block SARS-CoV-2 replication 13 , 18 , indicating that delaying IFN responses represents a major strategy of immune evasion by SARS-CoV-2.…”

Section: Ifn Dysregulation and Its Role In Covid-19 Pathogenesismentioning

confidence: 99%

Insights into pandemic respiratory viruses: manipulation of the antiviral interferon response by SARS-CoV-2 and influenza A virus

Liu

Gack

2022

Current Opinion in Immunology

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The Host Response to Influenza A Virus Interferes with SARS-CoV-2 Replication during Coinfection

Cited by 40 publications

References 45 publications

Pathobiology and dysbiosis of the respiratory and intestinal microbiota in 14 months old Golden Syrian hamsters infected with SARS-CoV-2

Pathobiology and dysbiosis of the respiratory and intestinal microbiota in 14 months old Golden Syrian hamsters infected with SARS-CoV-2

Omicron-induced interferon signalling prevents influenza A virus infection

Insights into pandemic respiratory viruses: manipulation of the antiviral interferon response by SARS-CoV-2 and influenza A virus

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