Abstract
Blattner RJ. J Pediatr 1961;59:784-6 In the section of The Journal “Comments on Current Literature,” Blattner gives a glimpse of the “state-of-the-thinking” on pathogenesis of herpes simplex virus (HSV) infections. Investigators and “thinkers” at the time had so much of it right (ie, most primary HSV infections are subclinical, yet whether clinical or subclinical, infection leads to establishment of latency and cycles of reactivation in most people). Presence of antibody does not prevent superficial recurrences (reactivations), which sometimes take on “zosteriform” characteristics by following nerve distribution. Investigators and clinicians even recognized (and made experimental models in animals to prove) some triggers of reactivation. One thing that they didn’t have quite right was the risk factors for occurrence of HSV encephalitis beyond the neonatal period. They thought that encephalitis would occur only with primary HSV infection and likely was associated with particularly neurotropic strains of HSV, neither of which is true. We now know that the host, rather than the virus, probably has the relevant influence on events. Abel et al have studied extensively and presented evidence that HSV encephalitis beyond the neonatal period, seemingly a rare but sporadic event, is not “bad luck” or “bad bug,” but is attributable at least in part to one or more organism-specific host innate immune defects.1Abel L. Plancoulaine S. Jouanguy E. et al.Age-dependent Mendelian predisposition to herpes simplex virus type 1 encephalitis in childhood.J Pediatr. 2010; 157: 623-629Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar
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