Interferon-independent increases in class I major histocompatibility complex antigen expression follow flavivirus infection.

Abstract

Infection of tertiary-passaged mouse embryo fibroblasts by four flaviviruses, West Nile (WNV), Kunjin, Murray Valley encephalitis and Japanese B encephalitis, resulted in a six- to 10-fold increase in the expression of individual H-2K and H-2D class I major histocompatibility complex (MHC) antigens 16 to 48 h after infection. The mechanism(s) by which flaviviruses increased antigen expression has not been fully elucidated, but appears to be mediated partly independently of interferon-beta (IFN-beta) secretion, as anti-IFN-alpha beta antibodies partially inhibited the WNV-induced increase but totally prevented increases caused by the addition of (i) pure IFN-beta, (ii) IFN-beta-containing supernatants from WNV-infected mouse embryo fibroblasts (MEF), or (iii) polyinosinic-polycytidylic acid. Actinomycin D treatment of MEF, which inhibited mRNA synthesis by greater than 90% as determined by [3H]uridine uptake, totally inhibited the increased MHC expression caused by WNV infection. Thus, the increase in class I MHC antigen expression following infection is dependent upon cellular RNA synthesis.

• Authors: N J King, A M Kesson
• Journal: The Journal of general virology (J Gen Virol) Vol. 69 ( Pt 10) Pg. 2535-43 (Oct 1988) ISSN: 0022-1317 [Print] England
• PMID: 2844965 (Publication Type: Journal Article)

Chemical References

• H-2 Antigens
• Interferon Type I
• RNA, Messenger
• Poly I-C

Topics

• Animals
• Cells, Cultured
• Female
• Flavivirus (immunology)
• H-2 Antigens (biosynthesis)
• Interferon Type I (physiology)
• Mice
• Mice, Inbred Strains
• Poly I-C (pharmacology)
• RNA, Messenger (biosynthesis, physiology)
• Virus Cultivation
• West Nile virus (immunology)