1. Inhibition of coxsackievirus B4 replication in stably transfected cells expressing human MxA protein.
- Author
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Chieux V, Chehadeh W, Harvey J, Haller O, Wattré P, and Hober D
- Subjects
- Animals, Antiviral Agents genetics, Antiviral Agents metabolism, Capsid metabolism, Chlorocebus aethiops, Fluorescent Antibody Technique, In Situ Hybridization, Myxovirus Resistance Proteins, Proteins genetics, Proteins metabolism, RNA, Viral metabolism, Reverse Transcriptase Polymerase Chain Reaction, Transfection, Vero Cells, Antiviral Agents pharmacology, Coxsackievirus Infections virology, Enterovirus B, Human physiology, GTP-Binding Proteins, Proteins physiology, Virus Replication
- Abstract
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-alpha inhibits CVB replication; however, the mechanism is not well known. The interferon-alpha-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., (Copyright 2001 Academic Press.)
- Published
- 2001
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