English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

Interferon-independent Increases in Class I Major Histocompatibility Complex Antigen Expression Follow Flavivirus Infection