The interface between the innate interferon response and expression of host retroviral restriction factors.
Inhibition of the expression and replication of human retroviruses by different families of host restriction factors has emerged as an important component of antiviral innate immunity. The term "intrinsic immunity" is used to define this specific arm of innate immunity and suggests that host restriction factors are constitutively present within infected cells. The essential role of the interferon (IFN) signaling pathways in eliciting host restriction factor gene transcription - triggered a consequence of pattern recognition receptor signaling - may be an under-recognized aspect of intrinsic immunity. This review discusses the relevance of innate IFN signaling in the induction of retroviral restriction factors, the mechanisms of action of these factors, as well as the counter-regulation of IFN response that results from the plethora of retrovirus-restriction factor interactions.
Douville
Renée N
RN
Molecular Oncology Group, Lady Davis Institute for Medical Research, Jewish General Hospital, 3999 Côte Ste-Catherine, Dept. of Microbiology and Medicine, McGill University, Montreal, Quebec, Canada H3T 1E2.
Hiscott
John
J
D000818:Animals; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D012190:Retroviridae / Q000276:immunology* / Q000378:metabolism; D012192:Retroviridae Infections / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology*
D007372:Interferons