Current Thinking on Genital Herpes

Annika M. Hofstetter; Susan L. Rosenthal; Lawrence R. Stanberry

Disclosures

Curr Opin Infect Dis. 2014;27(1):75-83. 

In This Article

Herpes Simplex Virus Reinfection

Exogenous reinfection with a different HSV type or strain at the same or new anatomical site has been reported.[65–71] Epidemiological studies clearly demonstrate that HSV-1 seropositive individuals are more likely to develop asymptomatic HSV-2 infection than their HSV-1 seronegative counterparts, that is prior HSV-1 infection affords protection against HSV-2 disease,[72–76] It may also alter recurrence patterns of the original HSV infection.[65] However, the extent that prior HSV infection protects against reinfection of a secondary HSV type or strain is uncertain. Some studies have observed decreased HSV-2 acquisition among HSV-1 seropositive vs. seronegative individuals, suggesting that at least partial protection against reinfection may be conferred by prior HSV-1 infection (Table 1).[63,76–79] Unpublished results from a large vaccine trial[75] found that only 5.9% of HSV-1 seropositive individuals, yet 14.2% of HSV-1 seronegative individuals became HSV-2 infected during the study. This difference was significant for all individuals and for women (P < 0.001), but not for men (P = 0.120). These results suggest that women maybe more likely to derive some protection against genital herpes by prior HSV-1 infection. Conversely, two studies failed to show that prior HSV-1 infection impacted the rate of subsequent HSV-2 infection, and a large cross-sectional study found higher HSV-2 seroprevalence among those with vs. without HSV-1 antibody, suggesting a lack of protective immunity.[72,73,78] Another study found no protective effect of HSV-1 immunity on HSV-2 seroconversion, yet revealed a higher rate of HSV-1 acquisition among HSV-2 seronegative vs. seropositive pregnant women; 75% of those with symptomatic HSV-1 seroconversion exhibited genital lesions.[79] These conflicting data could reflect site-specific immunity, that is antecedent oro-labial HSV-1 infection may offer less protection than antecedent genital HSV-1 infection against subsequent genital HSV-2 infection. Given that asymptomatic genital HSV-2 infections are known to occur, it is biologically plausible that individuals may experience asymptomatic genital HSV-1 infections, affording greater protection against genital reinfection with HSV-2 than is provided by oro-labial HSV-1 infection. Further elucidation of the complex host immune response to HSV, including type and site-specific differences, is needed.

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