tetano
Editor, Senior Moderator
J Infect Dis
. 2022 Dec 23;jiac494.
doi: 10.1093/infdis/jiac494. Online ahead of print.
Influenza A and respiratory syncytial virus trigger a cellular response that blocks severe acute respiratory syndrome virus 2 infection in the respiratory tract
Kieran Dee[SUP] 1 [/SUP], Verena Schultz[SUP] 1 [/SUP], Joanne Haney[SUP] 1 [/SUP], Laura A Bissett[SUP] 1 [/SUP], Callum Magill[SUP] 1 [/SUP], Pablo R Murcia[SUP] 1 [/SUP]
Affiliations
Abstract
Background: Multiple viruses cocirculate and contribute to the burden of respiratory disease. Virus-virus interactions can decrease susceptibility to infection and this interference can have an epidemiological impact. As humans are normally exposed to a community of cocirculating respiratory viruses, experimental coinfection studies are necessary to understand the disease mechanisms of multi-pathogen systems. We aimed to characterize interactions within the respiratory tract between severe acute respiratory syndrome virus 2 (SARS-CoV-2) and two major respiratory viruses: influenza A virus (IAV), and respiratory syncytial virus (RSV).
Methods: We performed single infections and coinfections with SARS-CoV-2 combined with IAV or RSV in cultures of human bronchial epithelial cells. We combined microscopy with quantification of viral replication in the presence or absence of an innate immune inhibitor to determine changes in virus-induced pathology, virus spread, and virus replication.
Results: SARS-CoV-2 replication is inhibited by both IAV and RSV. This inhibition is dependent on a functional antiviral response and the level of inhibition is proportional to the timing of secondary viral infection.
Conclusions: Infections by other respiratory viruses might provide transient resistance to SARS-CoV-2. It would therefore be expected that the incidence of COVID-19 may decrease during periods of high circulation of IAV and RSV.Virus-virus interactions impact the infection dynamics of respiratory viruses at multiple levels, from cells to populations. Using three-dimensional cultures of airway epithelium, we showed that SARS-CoV-2 replication is impaired in coinfections with either influenza A or respiratory syncytial virus.
Keywords: Severe acute respiratory syndrome virus 2; human airway epithelium; influenza A virus; respiratory syncytial virus; virus coinfection.
. 2022 Dec 23;jiac494.
doi: 10.1093/infdis/jiac494. Online ahead of print.
Influenza A and respiratory syncytial virus trigger a cellular response that blocks severe acute respiratory syndrome virus 2 infection in the respiratory tract
Kieran Dee[SUP] 1 [/SUP], Verena Schultz[SUP] 1 [/SUP], Joanne Haney[SUP] 1 [/SUP], Laura A Bissett[SUP] 1 [/SUP], Callum Magill[SUP] 1 [/SUP], Pablo R Murcia[SUP] 1 [/SUP]
Affiliations
- PMID: 36550077
- DOI: 10.1093/infdis/jiac494
Abstract
Background: Multiple viruses cocirculate and contribute to the burden of respiratory disease. Virus-virus interactions can decrease susceptibility to infection and this interference can have an epidemiological impact. As humans are normally exposed to a community of cocirculating respiratory viruses, experimental coinfection studies are necessary to understand the disease mechanisms of multi-pathogen systems. We aimed to characterize interactions within the respiratory tract between severe acute respiratory syndrome virus 2 (SARS-CoV-2) and two major respiratory viruses: influenza A virus (IAV), and respiratory syncytial virus (RSV).
Methods: We performed single infections and coinfections with SARS-CoV-2 combined with IAV or RSV in cultures of human bronchial epithelial cells. We combined microscopy with quantification of viral replication in the presence or absence of an innate immune inhibitor to determine changes in virus-induced pathology, virus spread, and virus replication.
Results: SARS-CoV-2 replication is inhibited by both IAV and RSV. This inhibition is dependent on a functional antiviral response and the level of inhibition is proportional to the timing of secondary viral infection.
Conclusions: Infections by other respiratory viruses might provide transient resistance to SARS-CoV-2. It would therefore be expected that the incidence of COVID-19 may decrease during periods of high circulation of IAV and RSV.Virus-virus interactions impact the infection dynamics of respiratory viruses at multiple levels, from cells to populations. Using three-dimensional cultures of airway epithelium, we showed that SARS-CoV-2 replication is impaired in coinfections with either influenza A or respiratory syncytial virus.
Keywords: Severe acute respiratory syndrome virus 2; human airway epithelium; influenza A virus; respiratory syncytial virus; virus coinfection.