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Virology
. 2026 Feb 23:618:110847.
doi: 10.1016/j.virol.2026.110847. Online ahead of print.
Sequential infection with rhinovirus followed by Influenza Virus led to an increased antiviral response in A549 cells
Nallely López-López 1 , Manuel Mejía-Torres 1 , Mildred A Diaz-Caldera 1 , Azalia M Martinez-Castilla 1 , Jorge A Gonzalez-Chapa 1 , Armando S Flores-Torres 1 , Mario C Salinas-Carmona 1 , Viviana L Mata-Tijerina 2 , Adrian G Rosas-Taraco 3
Affiliations
Alveolar epithelial cells play an important role in innate immunity against respiratory viral infection. While most respiratory infections are caused by single pathogens, co-infections and/or sequential infections can occur, substantially modifying clinical outcomes in a process that is not completely understood. To address this phenomenon, we tested the hypothesis that epithelial respiratory cells have differential responses according to the configuration of sequential viral infection. In our protocol, we infected A549 cells with human rhinovirus followed by influenza A virus (HRV→IAV) and vice versa (IAV→HRV). We then measured the synthesis of antiviral genes, released cytokines, microRNAs (miRs), and viral entry receptors. Our results showed that only HRV→IAV infection potentiated the transcription of the antiviral genes RIG-I and IRF7 and increased the synthesis of miRs -26b, -146a, and -326. In addition, sequential infections decreased the synthesis of the inflammatory chemokine IL-8 without changing the expression of viral entry receptors. In conclusion, our findings suggest that in A549 cells, the response to in vitro sequential infections varies according to the configuration of the viruses involved, likely modifying the activation of leukocyte-mediated immune responses.
Keywords: A549 cells; Human rhinovirus; Influenza a virus; MicroRNAs; Respiratory epithelial cells; Sequential viral infection.
. 2026 Feb 23:618:110847.
doi: 10.1016/j.virol.2026.110847. Online ahead of print.
Sequential infection with rhinovirus followed by Influenza Virus led to an increased antiviral response in A549 cells
Nallely López-López 1 , Manuel Mejía-Torres 1 , Mildred A Diaz-Caldera 1 , Azalia M Martinez-Castilla 1 , Jorge A Gonzalez-Chapa 1 , Armando S Flores-Torres 1 , Mario C Salinas-Carmona 1 , Viviana L Mata-Tijerina 2 , Adrian G Rosas-Taraco 3
Affiliations
- PMID: 41740429
- DOI: 10.1016/j.virol.2026.110847
Alveolar epithelial cells play an important role in innate immunity against respiratory viral infection. While most respiratory infections are caused by single pathogens, co-infections and/or sequential infections can occur, substantially modifying clinical outcomes in a process that is not completely understood. To address this phenomenon, we tested the hypothesis that epithelial respiratory cells have differential responses according to the configuration of sequential viral infection. In our protocol, we infected A549 cells with human rhinovirus followed by influenza A virus (HRV→IAV) and vice versa (IAV→HRV). We then measured the synthesis of antiviral genes, released cytokines, microRNAs (miRs), and viral entry receptors. Our results showed that only HRV→IAV infection potentiated the transcription of the antiviral genes RIG-I and IRF7 and increased the synthesis of miRs -26b, -146a, and -326. In addition, sequential infections decreased the synthesis of the inflammatory chemokine IL-8 without changing the expression of viral entry receptors. In conclusion, our findings suggest that in A549 cells, the response to in vitro sequential infections varies according to the configuration of the viruses involved, likely modifying the activation of leukocyte-mediated immune responses.
Keywords: A549 cells; Human rhinovirus; Influenza a virus; MicroRNAs; Respiratory epithelial cells; Sequential viral infection.