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Potential involvement of IL‐8 in the pathogenesis of human cytomegalovirus infection
Author(s) -
Murayama Tsugiya,
Mukaida Naofumi,
Khabar Khalid S. A.,
Matsushima Kouji
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.64.1.62
Subject(s) - biology , human cytomegalovirus , virology , virus , viral replication , cytomegalovirus , interferon , cell culture , fibroblast , pathogenesis , transcription (linguistics) , immunology , herpesviridae , viral disease , genetics , linguistics , philosophy
The observations that several types of viruses induced interleukin (IL)‐8 production prompted us to investigate the interrelationship between IL‐8 and cytomegalovirus (CMV) infection. CMV infection caused IL‐8 production in a human monocytic cell line, THP‐1, in dose‐ and time‐dependent manners. Moreover, CMV induced IL‐8 gene expression by concurrently activating transcription factors, NF‐κB and AP‐1. Furthermore, CMV infection of human fibroblast cell lines increased gene expression of a specific receptor for IL‐8, CXCR1. IL‐8 in turn enhanced CMV replication in a human embryonic fibroblast, MRC‐5, in dose‐ and time‐dependent manners. Augmented replication eventually culminated in the increased production of infectious CMV virions. Moreover, IL‐8 can attenuate the antiviral activity of interferon (IFN), particularly that of α‐type against picornaviruses such as encephalomyocarditis virus and poliovirus. The inhibitory effects were associated with reduced 2′,5′‐A oligoadenylate synthetase activity. These results would imply that CMV can induce IL‐8, which can augment CMV replication directly and indirectly by counteracting antiviral activity of IFN. J. Leukoc. Biol . 64: 62–67; 1998.