Variable reactivation of HSV-1 and HSV-2 from neurons within the trigeminal or sacral ganglia may be given by differences in gene expression profiles by neurons that innervate these tissues ( Kaneko et al., 2008 Flegel et al., 2015 Lopes et al., 2017).Ī clinically relevant concern associated with HSV-2 genital infection is that it is associated with a three-fold increase in the likelihood of acquiring the human immunodeficiency virus type 1 (HIV-1), due to synergistic aspects related to the co-infection with both viruses ( Wasserheit, 1992 Freeman et al., 2006 Barnabas et al., 2011). A similar phenomenon may occur in the orofacial area, with most viral reactivations being attributed to HSV-1. However, HSV-2 reactivates more frequently from the genital tissue than HSV-1 and hence, despite the finding that the latter is commonly detected during primary infection, HSV-2 is more often isolated from this site than HSV-1 at any time during infection ( Lafferty et al., 1987 Kaneko et al., 2008). On the other hand, HSV-2 is mainly associated with genital lesions and neonatal encephalitis ( Gupta et al., 2007 Berger and Houff, 2008 Looker et al., 2008 Suazo et al., 2015b), despite the fact that HSV-1 is nowadays more frequently related to primary genital infection worldwide ( Buxbaum et al., 2003 Coyle et al., 2003 Xu et al., 2006 Pereira et al., 2012). HSV-1 is mainly associated with orofacial lesions, yet it is also the leading cause of infectious blindness in developed countries and the number one cause of viral encephalitis in adults ( Kaye and Choudhary, 2006 Horowitz et al., 2010 Farooq and Shukla, 2012 Bernstein et al., 2013). Although 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. Additionally, during recurrent viral reactivations, most individuals are asymptomatic, with 5–15% of those infected displaying clinical symptoms related to HSV infections ( Benedetti et al., 1994 Wald et al., 2000 Sudenga et al., 2012 Suazo et al., 2015b). HSV-1 and HSV-2 are associated with diverse clinical manifestations, yet disease widely varies from one individual to another, with nearly 40% of those that are infected displaying symptoms during primary infection ( Langenberg et al., 1999 Bernstein et al., 2013). HSVs are present among humans at a high prevalence ( Looker et al., 2008 CDC, 2010 Yawn and Gilden, 2013 Dickson et al., 2014 Suazo et al., 2015b), with two thirds of the global population infected with HSV-1 ( Looker et al., 2015a), and ~11% of the world population infected with HSV-2 ( Looker et al., 2015b).
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 comprehensive understanding of how HSVs evade host early antiviral responses could contribute to the development of novel therapies and vaccines to counteract these viruses. 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. 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. 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. Therefore, diseases caused by HSVs represent significant public health burdens.
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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. 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.