Influenza A virus coinfection dynamics are shaped by distinct virus-virus interactions within and between cells.

Autor: Delima GK; Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America., Ganti K; Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America., Holmes KE; Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America., Shartouny JR; Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America., Lowen AC; Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, United States of America.; Emory Center of Excellence for Influenza Research and Response (Emory-CEIRR), Atlanta, Georgia, United States of America.
Jazyk: angličtina
Zdroj: PLoS pathogens [PLoS Pathog] 2023 Mar 02; Vol. 19 (3), pp. e1010978. Date of Electronic Publication: 2023 Mar 02 (Print Publication: 2023).
DOI: 10.1371/journal.ppat.1010978
Abstrakt: When multiple viral populations propagate within the same host environment, they often shape each other's dynamics. These interactions can be positive or negative and can occur at multiple scales, from coinfection of a cell to co-circulation at a global population level. For influenza A viruses (IAVs), the delivery of multiple viral genomes to a cell substantially increases burst size. However, despite its relevance for IAV evolution through reassortment, the implications of this positive density dependence for coinfection between distinct IAVs has not been explored. Furthermore, the extent to which these interactions within the cell shape viral dynamics at the level of the host remains unclear. Here we show that, within cells, diverse coinfecting IAVs strongly augment the replication of a focal strain, irrespective of their homology to the focal strain. Coinfecting viruses with a low intrinsic reliance on multiple infection offer the greatest benefit. Nevertheless, virus-virus interactions at the level of the whole host are antagonistic. This antagonism is recapitulated in cell culture when the coinfecting virus is introduced several hours prior to the focal strain or under conditions conducive to multiple rounds of viral replication. Together, these data suggest that beneficial virus-virus interactions within cells are counterbalanced by competition for susceptible cells during viral propagation through a tissue. The integration of virus-virus interactions across scales is critical in defining the outcomes of viral coinfection.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2023 Delima 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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