Abstract

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.

Highlights

  • Herpes Simplex Virus Evasion of Early Host Antiviral ResponsesHerpes simplex viruses (HSVs) 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

  • Herpes simplex viruses (HSVs) type 1 (HSV-1 or human herpesvirus 1, HHV-1) and type 2 (HSV-2 or human herpesvirus 2, HHV-2), are members of the Herpesviridae family and Alphaherpesvirinae subfamily, similar to varicella zoster virus (VZV) (Davison, 2010; Sharma et al, 2016)

  • A relatively low proportion of the infected individuals show clinical manifestations, the high percentage of the world population infected with these viruses yields an enormous number of individuals that effectively suffer from HSV-related illnesses

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Summary

Herpes Simplex Virus Evasion of Early Host Antiviral Responses

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. 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. 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

INTRODUCTION
Early Immune Evasion by HSVs
Replication Cycle of HSVs
HSVs INTERFERE WITH THE HOST INTERFERON RESPONSE
CONCLUDING REMARKS
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