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Induction of apoptosis limits cytomegalovirus cross‐species infection
Author(s) -
Jurak Igor,
Brune Wolfram
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601133
Subject(s) - biology , apoptosis , human cytomegalovirus , cytomegalovirus , viral replication , virology , innate immune system , gene , immune system , mechanism (biology) , virus , immunology , genetics , herpesviridae , viral disease , philosophy , epistemology
Cross‐species infections are responsible for the majority of emerging and re‐emerging viral diseases. However, little is known about the mechanisms that restrict viruses to a certain host species, and the factors viruses need to cross the species barrier and replicate in a different host. Cytomegaloviruses (CMVs) are representatives of the beta‐herpesviruses that are highly species specific. They replicate only in cells of their own or a closely related species. In this study, the molecular mechanism underlying the cytomegalovirus species specificity was investigated. We show that infection of human cells with the murine cytomegalovirus (MCMV) triggers the intrinsic apoptosis pathway involving caspase‐9 activation. MCMV can break the species barrier and replicate in human cells if apoptosis is blocked by Bcl‐2 or a functionally analogous protein. A single gene of the human cytomegalovirus encoding a mitochondrial inhibitor of apoptosis is sufficient to allow MCMV replication in human cells. Moreover, the same principle facilitates replication of the rat cytomegalovirus in human cells. Thus, induction of apoptosis serves as an innate immune defense to inhibit cross‐species infections of rodent CMVs.