Summary auto-generated
Researchers identified a cytopathogenic variant of influenza C virus (C/AA-cyt) that causes significant cell death in MDCK cell cultures, a property unusual for influenza C viruses which typically undergo non-destructive infection. The variant was derived through serial passage in embryonated eggs and exhibited enhanced infectivity compared to wild-type virus. To characterize the mechanism of cell death, the authors performed multiple assays including viral neutralization studies, DNA fragmentation analysis, and apoptosis quantification. Results demonstrated that infected cells maintained plasma membrane integrity while exhibiting characteristic apoptotic features including cell rounding, shrinkage, nuclear DNA fragmentation in a typical 200 bp ladder pattern, and elevated mono- and oligonucleosome levels. Cell death was dependent on active virus replication and was suppressed at non-permissive temperatures. These findings establish that influenza C viruses, like influenza A and B viruses, are capable of inducing programmed cell death (apoptosis) in cell culture, challenging the traditional understanding of influenza C as causing primarily persistent, non-lytic infections.
Key findings
- A highly cytopathogenic influenza C virus variant (C/AA-cyt) induces extensive cell death in MDCK cells through apoptosis rather than necrosis
- Cell death is dependent on active viral replication and suppressed at non-permissive temperatures
- Infected cells show characteristic apoptotic features including maintained membrane integrity, DNA laddering, and oligonucleosome release
- This demonstrates that influenza C viruses can induce programmed cell death, similar to influenza A and B viruses
- The cytopathogenic phenotype may be associated with increased pathogenic potential in human infections
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Abstract
An influenza C virus variant, C/AA-cyt, was identified as the agent responsible for highly effective induction of cytopathogenicity in MDCK cells. The cytopathogenic effect was manifested by cell rounding, cell shrinkage and foci of cell destruction leading finally to disruption of the monolayer in a virus dose-dependent manner. Virus-induced cytopathogenicity was suppressed by temperatures nonpermissive for virus replication. Maintenance of plasma membrane integrity post- infection, in connection with induction of a DNA fragmentation ladder, revealed the characteristic picture of apoptosis. In support of this, quantitative analysis demonstrated high levels of apoptosis-like oligonucleosomal DNA. The results indicate that influenza C viruses can induce programmed cell death, as formerly reported for influenza type A and B viruses.