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Antibody‐mediated enhancement of the rate, magnitude, and responsiveness of vesicular stomatitis virus induced alpha interferon production
Author(s) -
Green D.S.,
Lum T.,
Mullins B.T.,
Green J.A.
Publication year - 2008
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.21232
Subject(s) - vesicular stomatitis virus , virology , vesicular stomatitis , vesicular stomatitis indiana virus , antibody , virus , interferon , biology , oncolytic virus , titer , in vitro , rhabdoviridae , immunology , biochemistry
A majority of adults without evidence of exposure to vesicular stomatitis virus (VSV) have serum IgG antibodies that interact with pro‐inflammatory TLR7 in the presence of VSV, and enhance several aspects of VSV‐induced IFN‐α production. Enhancing IgG antibody enables human PBMC to make IFN‐α more rapidly and in higher titers in response to a broad range of VSV‐concentrations that include those too low to independently stimulate IFN‐α production. These antibody‐mediated functions compensate for the inherent delay in virus‐induced IFN‐α production in vitro, and have the potential to improve the in vivo IFN‐α response and effectively terminate infection before the occurence of clinically apparent disease. The frequent presence of enhancing antibody in persons without predictable VSV exposure has implications for naturally occurring infections with this and other viruses, and for the use of viruses as vaccine vectors and oncolytic agents. J. Med. Virol. 80:1675–1683, 2008. © 2008 Wiley‐Liss, Inc.