Though 75% to 90% of HSV-2 infected persons may be unaware of their condition, they may still be capable of transmitting the infection. A recent study investigates the patterns of viral shedding and presumed infectivity in “asymptomatic” HSV-2 (i.e. HSV-2 in persons unaware of their condition prs to diagnosis) as against “symptomatic” infection. The occasion seems to have been offered by a group of 88 asymptomatic persons whose status emerged during a previous trial. These, along with a group of 410 symptomatic persons, were instructed to inspect the genital region for lesions daily and obtain swabs.
What do we learn? Overall, viral shedding in the asymptomatic participants took place in 10.2% of days, as opposed to 20.1% (risk ratio for asymptomatic group on adjusted multivariate model = 0.57). Shedding occurred sub-clinically both in asymptomatic and in symptomatic, though less than in asymptomatic participants (8.5% vv. 12.9%, RR = 0.66); and it also occurred in the presence of lesions in asymptomatic as well as symptomatic (3.8% vv. 13.8%, RR = 0.28), since lesions were detected by 19 of the 88 asymptomatic participants in the course of the follow-up. Presence of lesions impacted on infectivity through increased duration of episodes of viral shedding. Asymptomatic differed from symptomatic infection in the frequency of these episodes of greater duration. For those in the asymptomatic group who reported lesions, shedding rate was 18.7 % as against 7.6% for those in the asymptomatic group who reported no lesions.
What are the implications of this study? The authors claim to be addressing a management problem posed by the situation of “asymptomatic patients with an HSV-2 seropositive test result”. Given the mildness of the condition, we might ask whether this “management problem” is created by the HSV-2 infection or the seropositive test result! So it is disconcerting to find a Swedish health researcher on Herpes using findings from this study (and her own) in order to urge us not to “wait for sores to appear or other visual symptoms” but to “go get checked out” (http://www.medicalnewstoday.com/articles/222161.php). Is this really a sensible reaction to the findings of this trial?

Elizabeth Tronstein et al., “Genital Shedding of Herpes Simplex Virus Among Symptomatic and Asymptomatic Persons With HSV-2 Infection”, Journal of the American Medical Association 2011;305(14)

http://jama.ama-assn.org/content/305/14.toc

Still on the topic of HSV-2 … A clinically effective vaccine has yet to be achieved, though efforts are being made to develop one. A replication-defective HSV-2 mutant virus – the US strain HSV-2 dl5-29 – has been shown to induce immunity against the US strains HSV-2 G and 333 in mice and guinea pigs. The potential benefits of an effective vaccine could be enormous in sub-Saharan Africa, where epidemiological studies have shown that genital herpes leads to a multi-fold increase in the risk of HIV transmission.
In line with these ambitions, a recent study has sought to improve our knowledge of the genetic and epitope diversity of HSV-2, and its effect on vaccine efficacy, by testing HSV-2 vaccine candidates against HSV-2 strains derived from African, as well as, US isolates. A first stage involved the testing of HSV-2 dl5-29 against both a panel of three US strains (G, 89-390, 186) and a panel of African strains (SD15, SD66, SD90). HSV-2 dl5-29 proved effective against both US and African strains, though in the latter case equivalent protection required higher doses. A second stage involved assessment of the ability of two replication-defective mutant viruses to protect against the same panels of US and African derived viruses – 5BlacZ, deriving from a US strain, and SD90-8LacZ, deriving from an African one. The US derived 5BlacZ tended to be more protective against US strains, and the African derived SD90-LacZ against African strains; at the same time, neither vaccine was as protective against the African strains as 5BlacZ was against the US ones, despite levels of humoral and cellular immune response that were equivalent in the US and African case.
The authors draw two conclusions: first, that immune protection appears to be partially specific for the viruses from the US versus Africa; second, that the African HSV-2 viruses seem more virulent. They call for further research in this area on account of its potential impact on the reduction of HIV transmission risk.

Timothy E. Dudek, “Evidence for Differences in Immunologic and Pathogenesis Properties of Herpes Simplex Virus 2 Strains From the United States and South Africa”, Journal of Infectious Diseases 2011:203 (15th May)

http://jid.oxfordjournals.org/content/current