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Transfection of single‐stranded hepatitis A virus RNA activates MHC class I pathway
Author(s) -
SUZUKI K.,
YANAGI M.,
MORIAOKI A.,
MORIYAMA E.,
ISHII K. J.,
KOHN L. D.
Publication year - 2002
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.2002.01767.x
Subject(s) - rna , biology , major histocompatibility complex , virology , mhc class i , transfection , virus , antigen processing , transporter associated with antigen processing , viral replication , immune system , hepatitis c virus , gene , microbiology and biotechnology , immunology , genetics
SUMMARY Although infection of single‐stranded RNA viruses can enhance expression of major histocompatibility complex (MHC) class I genes, the mechanism underlying this process remains unclear. Recent studies have indicated that exposure of non‐immune cells to double‐stranded deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) of viral origin can directly increase the expression of MHC class I and related molecules without immune cell interaction. In this report, we show that transfection of single‐stranded hepatitis A virus RNA into cultured hepatocytes results in the induction of genes for MHC class I, LMP2 and transporter for antigen processing (TAP1), in addition to the generation of viral proteins. We suggest that this stimulatory effect is due to the double‐stranded RNA formed during replication of single‐stranded viral RNA, and involves both double‐stranded, RNA‐dependent protein kinase PKR and the secretion of IFNβ.

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