Viral interference between severe acute respiratory syndrome coronavirus 2 and influenza A viruses.

Autor: Gilbert-Girard S; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada., Piret J; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada., Carbonneau J; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada., Hénaut M; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada., Goyette N; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada., Boivin G; Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada.
Jazyk: angličtina
Zdroj: PLoS pathogens [PLoS Pathog] 2024 Jul 22; Vol. 20 (7), pp. e1012017. Date of Electronic Publication: 2024 Jul 22 (Print Publication: 2024).
DOI: 10.1371/journal.ppat.1012017
Abstrakt: Some respiratory viruses can cause a viral interference through the activation of the interferon (IFN) pathway that reduces the replication of another virus. Epidemiological studies of coinfections between SARS-CoV-2 and other respiratory viruses have been hampered by non-pharmacological measures applied to mitigate the spread of SARS-CoV-2 during the COVID-19 pandemic. With the ease of these interventions, SARS-CoV-2 and influenza A viruses can now co-circulate. It is thus of prime importance to characterize their interactions. In this work, we investigated viral interference effects between an Omicron variant and a contemporary influenza A/H3N2 strain, in comparison with an ancestral SARS-CoV-2 strain and the 2009 pandemic influenza A/H1N1 virus. We infected nasal human airway epitheliums with SARS-CoV-2 and influenza, either simultaneously or 24 h apart. Viral load was measured by RT-qPCR and IFN-α/β/λ1/λ2 proteins were quantified by immunoassay. Expression of four interferon-stimulated genes (ISGs; OAS1/IFITM3/ISG15/MxA) was also measured by RT-droplet digital PCR. Additionally, susceptibility of each virus to IFN-α/β/λ2 recombinant proteins was determined. Our results showed that influenza A, and especially A/H3N2, interfered with both SARS-CoV-2 viruses, but that SARS-CoV-2 did not significantly interfere with A/H3N2 or A/H1N1. Consistently with these results, influenza, and particularly the A/H3N2 strain, caused a higher production of IFN proteins and expression of ISGs than SARS-CoV-2. SARS-CoV-2 induced a marginal IFN production and reduced the IFN response during coinfections with influenza. All viruses were susceptible to exogenous IFNs, with the ancestral SARS-CoV-2 and Omicron being less susceptible to type I and type III IFNs, respectively. Thus, influenza A causes a viral interference towards SARS-CoV-2 most likely through an IFN response. The opposite is not necessarily true, and a concurrent infection with both viruses leads to a lower IFN response. Taken together, these results help us to understand how SARS-CoV-2 interacts with another major respiratory pathogen.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Gilbert-Girard et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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