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Persistent Infection byHelicobacter pyloriDown‐Modulates Virus‐Specific CD8+Cytotoxic T Cell Response and Prolongs Viral Infection
Author(s) -
Mutsunori Shirai,
Tatsumi Arichi,
Teruko Nakazawa,
Jay A. Berzofsky
Publication year - 1998
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/513827
Subject(s) - ctl* , cytotoxic t cell , virology , vaccinia , biology , virus , helicobacter pylori , cd8 , immunology , cytokine , microbiology and biotechnology , immune system , recombinant dna , in vitro , biochemistry , gene , genetics
To determine whether Helicobacter pylori infection affects clearance of a concomitant viral infection and cytotoxic T lymphocyte (CTL) and cytokine response to that infection, H. pylori-infected BALB/c mice were challenged with a recombinant vaccinia virus expressing human immunodeficiency virus type 1 gp160. Two H. pylori strains, a colonizing clinical isolate (KS612) and an established standard noncolonizing strain (NCTC11637), were compared. Clearance of recombinant vaccinia virus was reduced in KS612-infected mice compared with NCTC11637-infected and control mice. As a potential mechanism, in contrast to control or NCTC11637-infected mice, the H. pylori clinical isolate KS612 diminished gp160-specific and vaccinia virus-specific CTL activity, even in the presence of exogenous interleukin-2. Furthermore, KS612-infected mice had reduced Th1 cytokine responses to gp120 in vitro compared with control or NCTC11637-infected mice. These results have implications for possible effects of prevalent H. pylori infection on other human diseases.

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