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In this issue of the Journal, Hobbs et al. [1] present evidence that the severity of herpes simplex virus (HSV) type 1 (HSV-1) infection may be associated with a genotype on human chromosome 21. Their report explicitly addresses a question that is frequently presented to general clinicians and those specializing in infectious diseases and sexually transmitted infections: why ismyherpes so bad? Implicit subtexts concern the “normalcy” of the immune system, as well as the possibility of an intervention predicated on the mechanisms behind variations in severity. Although no definitive answers are provided by the current study, these questions are well worth asking and have been approached from several angles in recent years.

With exceptions, such as rabies, infections display great variation in disease severity. For chronic infections, such as those caused by herpesviruses, both the primary and recurrent episodes may range in severity from clinically quite significant, leading to doctor visits and time lost from work, to clinically silent, occurring without signs or symptoms [2]. This spectrum is particularly apparent among persons considered to be immunocompetent. Findings of type-specific HSV serological assays have been correlated with clinical histories to demonstrate that most HSV-1 and HSV type 2 (HSV-2) infections are, at least superficially, asymptomatic [3–5]. Hobbs and colleagues explore the recurrent phase of HSV-1 infection and compare the genomic structure of HSV-1—infected persons who do or do not have clinical histories of recurrent herpes simplex labialis (HSL). This is the first study using a family-pedigree approach that investigates the milder end of the HSV severity spectrum, thereby addressing the general hypothesis that host variation underlies the phenotype of HSV infection.

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