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Influenza C virus persistence depends on exceptional steps in viral RNA synthesis and transport
A Zach1, M Marschall, H Meier-Ewert
1Abteilung für Virologie, Technischen Universität München, Germany.
Abstract:
The cell line MDCK-pi, which is persistently infected with a variant of influenza C/AnnArbor/1/50 virus (C/AA-pi), was studied as a long-term persistence model by means of a strand-specific in situ hybridization assay. As a typical feature of the persistence, we identified a continuous synthesis of antigenomic positive-strand RNA encoded by segment 7 (NS) during virus production. In contrast, infection with the parental wild-type virus led to a rapid reduction of antigenomic RNA as observed in the late period of replication particularly for RNA segment 7. Furthermore, the replication cycle of the persistent variant did not show the switch from early to late replication events followed by clearance of intracellular virus, but was regulated in terms of productive and nonproductive phases. Nonproductive phases were reversible and characterized by a low level of virus-specific RNA signals. In the productive phase, a difference in cytoplasmic RNA transport was detected for the two viruses: a marked cytoplasmic accumulation of negative- and positive-strand wild-type virus RNAs stood in contrast to a RNA localization in different cellular compartments for the persistent virus. Also, Vero cells infected with the C/AA-pi variant were restricted to a transient, non-persistent replication cycle and produced a wild-type-like course of virus-specific RNA transport. These data indicate that influenza C virus persistence depends on a distinctly modified and cell type-specific regulation of virus-specific RNA synthesis and transport.
Insights
Influenza C virus persistence involves continuous antigenomic RNA synthesis and altered RNA transport in infected cells. This differs from wild-type virus replication, which shows RNA reduction and clearance.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Influenza C virus can establish persistent infections.
- Understanding the mechanisms of viral persistence is crucial for developing effective treatments.
- The role of viral RNA synthesis and transport in influenza C virus persistence remains unclear.
Purpose of the Study:
- To investigate the mechanisms underlying long-term persistence of influenza C virus in a cell culture model.
- To compare the RNA synthesis and transport of a persistent influenza C virus variant with its wild-type counterpart.
- To determine the cell type-specific regulation of influenza C virus replication.
Main Methods:
- Utilized the MDCK-pi cell line persistently infected with influenza C/AnnArbor/1/50 virus (C/AA-pi).
- Employed strand-specific in situ hybridization assays to analyze viral RNA synthesis and localization.
- Infected Vero cells with the C/AA-pi variant to assess cell type-specific effects.
Main Results:
- Persistent C/AA-pi infection showed continuous synthesis of antigenomic positive-strand RNA (segment 7).
- Wild-type influenza C virus infection led to rapid reduction of antigenomic RNA, particularly segment 7.
- The persistent variant exhibited regulated productive/nonproductive phases and distinct cytoplasmic RNA transport compared to wild-type virus.
- Vero cells infected with C/AA-pi showed transient, non-persistent replication with wild-type-like RNA transport.
Conclusions:
- Influenza C virus persistence is dependent on modified regulation of viral RNA synthesis.
- Altered virus-specific RNA transport in different cellular compartments is a key feature of persistence.
- The regulation of RNA synthesis and transport is cell type-specific for influenza C virus persistence.