Evidence that a mechanism for efficient flavivirus budding upregulates MHC class I.
An 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.
Lobigs
Mario
M
Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia. Mario.Lobigs@anu.edu.au
Müllbacher
Arno
A
Lee
Eva
E
D004721:Endoplasmic Reticulum / Q000276:immunology; D005416:Flavivirus / Q000276:immunology* / Q000502:physiology; D018177:Flavivirus Infections / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D011498:Protein Precursors / Q000276:immunology; D015854:Up-Regulation / Q000276:immunology; D014764:Viral Proteins / Q000276:immunology; D019065:Virus Assembly / Q000502:physiology
D015395:Histocompatibility Antigens Class I; D011498:Protein Precursors; D014764:Viral Proteins