Abstract
Lymphocytic choriomeningitis (LCM) virus infection of the mouse is the best-studied model of persistent viral infection. In cell culture, persistent LCM virus infections are associated with the production of large quantities of defective interfering (DI) LCM virus. These defective interfering particles cannot replicate by themselves yet can interfere with the replication of the standard virus and prevent the cytolytic effect caused by the standard virus. It is important to determine the mechanism of interference and to establish whether the DI virus plays a role in vivo. Biological and biochemical properties of the standard and DI virus particles and also virus enzymes are compared. Antigenic analyses reveal that cells releasing only DI virus particles have less cell surface expression of viral antigens than cells releasing the standard virus. In the animal model, the DI virus is shown to have a protective effect against the pathogenesis of the LCM virus disease both in the mouse and in the rat.
MeSH Terms
Animals
Antigens, Viral/analysis
Lymphocytic choriomeningitis virus/immunology,metabolism
Mice
RNA, Viral/metabolism
RNA-Dependent RNA Polymerase/metabolism
RNA-Directed DNA Polymerase/metabolism
Viral Interference
Viral Proteins/biosynthesis
Chemicals
Antigens, Viral
RNA, Viral
Viral Proteins
RNA-Dependent RNA Polymerase
RNA-Directed DNA Polymerase
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Welsh R M
Burner P A
Holland J J
Oldstone M B
Thompson H A
Villarreal L P
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