Interferon-independent increases in class I major histocompatibility complex antigen expression follow flavivirus infection.
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.
King
N J
NJ
Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra, A.C.T.
Kesson
A M
AM
D000818:Animals; D002478:Cells, Cultured; D005260:Female; D005416:Flavivirus / Q000276:immunology*; D006183:H-2 Antigens / Q000096:biosynthesis*; D007370:Interferon Type I / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D011070:Poly I-C / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000502:physiology; D014776:Virus Cultivation; D014902:West Nile virus / Q000276:immunology
D006183:H-2 Antigens; D007370:Interferon Type I; D012333:RNA, Messenger; D011070:Poly I-C