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Crimean‐Congo hemorrhagic fever virus delays activation of the innate immune response
Author(s) -
Andersson Ida,
Karlberg Helen,
MousaviJazi Mehrdad,
MartínezSobrido Luis,
Weber Friedemann,
Mirazimi Ali
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.21222
Subject(s) - innate immune system , virology , interferon , biology , virus , immune system , viral replication , bunyaviridae , virulence , secretion , immunology , microbiology and biotechnology , gene , biochemistry
Abstract As a first line of defence against virus infection, mammalian cells elicit an innate immune response, characterized by secretion of type I interferons and the up‐regulation of interferon stimulated genes. Many viruses down‐regulate the innate immune responses in order to enhance their virulence. Crimean‐Congo hemorrhagic fever virus (CCHFV), a Nairovirus of the family Bunyaviridae is the causative agent of severe hemorrhagic fever in humans with high mortality. Knowledge regarding the innate immune response against CCHFV is most limited. Interestingly, in this study it is shown that replicating CCHFV delays substantially the IFN response, possibly by interfering with the activation pathway of IRF‐3. In addition, it is demonstrated that CCHFV replication is almost insensitive to subsequent treatment with interferon‐α. Once the virus is replicating, virus replication is more or less insensitive to the antiviral effects induced by the interferon. By using an interferon bioassay, it is shown that infected cells secrete interferon relatively late after infection, that is, 48 hr post‐infection. In summary, the results suggest the presence of a virulence factor encoded by CCHFV that delays the host defence in order to allow rapid viral spread in the host. J. Med. Virol. 80:1397–1404, 2008. © 2008 Wiley‐Liss, Inc.