Lobigs, MarioMullbacher, ArnoLee, Eva2015-12-132015-12-130818-9641http://hdl.handle.net/1885/85772An appealing hypothesis for the biological role of flavivirus-induced, interferon-independent, upregulation of MHC class I on the surface of infected cells is that of viral immune evasion from NK cell recognition. Here we show that a mechanism for efficient flavivirus morphogenesis interferes with the MHC class I pathway, using a flavivirus budding mutant and recombinant expression of wild-type and mutant forms of the flavivirus structural proteins. We propose that the phenomenon of flavivirus-mediated MHC class I upregulation is a by-product of a unique assembly strategy evolved by flaviviruses and therefore did not evolve primarily as an immune escape mechanism for virus growth in the vertebrate host.Keywords: major histocompatibility antigen class 1; protein precursor; virus protein; antigen expression; budding; Flavivirus; human; immune system; molecular biology; nonhuman; protein expression; review; upregulation; virogenesis; virus assembly; virus morphogene Budding; Flavivirus; Immune escape; MHC class I; Virus assembly200410.1046/j.0818-9641.2004.01218.x2015-12-12