Inhibition of Coxsackievirus B4 Replication in Stably Transfected Cells Expressing Human MxA Protein
Autor: | Wassim Chehadeh, Pierre Wattré, Jeanne Harvey, Otto Haller, Vincent Chieux, Didier Hober |
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Rok vydání: | 2001 |
Předmět: |
Myxovirus Resistance Proteins
viruses Coxsackievirus Infections Fluorescent Antibody Technique In situ hybridization Coxsackievirus Immunofluorescence Semliki Forest virus Transfection Virus Replication Antiviral Agents Capsid GTP-Binding Proteins Virology Chlorocebus aethiops medicine Animals Vero Cells In Situ Hybridization medicine.diagnostic_test biology Reverse Transcriptase Polymerase Chain Reaction RNA Proteins RNA virus biology.organism_classification Molecular biology Enterovirus B Human Vero cell RNA Viral |
Zdroj: | Virology. 283(1):84-92 |
ISSN: | 0042-6822 |
DOI: | 10.1006/viro.2001.0877 |
Popis: | Coxsackieviruses B (CVB) (B1–B6), positive-strand RNA viruses, cause a variety of diseases. CVB4 may have a causal role in insulin-dependent diabetes mellitus. IFN-α inhibits CVB replication; however, the mechanism is not well known. The interferon-α-inducible human MxA protein exerts an antiviral activity against negative-strand RNA viruses and against Semliki Forest virus, a positive-strand RNA virus. To test the antiviral spectrum of MxA against CVB4, we took advantage of stably transfected Vero cells expressing MxA (Vero/MxA) in 98% of cells. Compared with control cells, in Vero/MxA cells, CVB4 yields were dramatically reduced and expression of the VP1 CVB protein analyzed by immunofluorescence was highly restricted. Furthermore, the accumulation of positive- and negative-strand CVB4 RNA was prevented as shown by in situ hybridization and RT-PCR. These results indicate that the antiviral activity of MxA extends to CVB4 and that its replication cycle is inhibited at an early step in Vero/MxA cells. |
Databáze: | OpenAIRE |
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