期刊
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2019.00127
关键词
interferon (IFN); inflammasome; toll-like receptors (TLRs); natural killer cells (NK cells); dendritic cells (DCs); cytosolic nucleic acid receptors; innate immunity; apoptosis
资金
- FONDECYT (Fondo Nacional de Desarrollo Cientifico y Tecnologico) [1190864]
- Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) [1190830]
- FONDEF [ID17I10143]
- Millennium Institute on Immunology and Immunotherapy (MIII) [P09/016-F]
Herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) have co-evolved with humans for thousands of years and are present at a high prevalence in the population worldwide. HSV infections are responsible for several illnesses including skin and mucosal lesions, blindness and even life-threatening encephalitis in both, immunocompetent and immunocompromised individuals of all ages. Therefore, diseases caused by HSVs represent significant public health burdens. Similar to other herpesviruses, HSV-1 and HSV-2 produce lifelong infections in the host by establishing latency in neurons and sporadically reactivating from these cells, eliciting recurrences that are accompanied by viral shedding in both, symptomatic and asymptomatic individuals. The ability of HSVs to persist and recur in otherwise healthy individuals is likely given by the numerous virulence factors that these viruses have evolved to evade host antiviral responses. Here, we review and discuss molecular mechanisms used by HSVs to evade early innate antiviral responses, which are the first lines of defense against these viruses. A comprehensive understanding of how HSVs evade host early antiviral responses could contribute to the development of novel therapies and vaccines to counteract these viruses.
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