Involvement of temperature sensitive syncytium inducing VSV or defective retroviruses in the development of spongiform encephalopathies.
Various enveloped viruses can induce syncytia in competent cells. Some temperature-sensitive mutants can express the trans-membrane viral G antigen under non-permissive conditions. The G antigen can then migrate at long distances, engulfing thousands of cells without producing any virus. When a temperature-sensitive vesicular stomatitis virus (VSV) infects a sensitive host, and under the condition that the G antigen is expressed, spongiosis can be induced in the central nervous system in the absence of detectable virus multiplication. We postulate that such a mechanism might be observed with various enveloped viruses, as recently illustrated with knock-out mice experimentally infected with defective murine leukemia virus (MULV).
Chany
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Laboratory of Cellular Physiology, University Pierre and Marie Curie, Paris, France.
D000818:Animals; D001921:Brain / Q000473:pathology* / Q000821:virology; D003673:Defective Viruses / Q000502:physiology*; D015726:Giant Cells; D006801:Humans; D051379:Mice; D008954:Models, Biological; D017096:Prion Diseases / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D012190:Retroviridae / Q000502:physiology*; D014721:Vesicular stomatitis Indiana virus / Q000502:physiology*