Jennifer Vines raises the question of other potential sources of HIV
. During our follow-up, 569 participants
received blood transfusions, were hospitalized, or received injections. We observed 15 infections among those who had such a nosocomial risk factor during the period when HIV
infection occurred. We observed 50 infections among those without such a risk factor. In a multivariate analysis of risk factors of HIV infection during the follow-up, the presence of a nosocomial risk factor was not significantly associated with HIV infection (rate ratio RR 1.7;
p 0.092). Among those with a nosocomial risk factor, the protective effect of the intervention (intention-to-treat analysis) is about 58. Among those without a nosocomial risk factor, the protective effect of the intervention is about 62. In a multivariate analysis, when taking into account the nosocomial risk factors, the
association between group of randomization and HIV infection was unchanged (protection of 60 versus 60). The fact that patients with a nosocomial risk factor were not significantly more at risk of HIV infection, and were protected by male circumcision in a similar way to those without a nosocomial risk factor, strongly supports the view that the majority of HIV infections observed in our study were due to sexual transmission.
John Potterat and colleagues make a number of points to which we must respond
. The association between clinic attendance for a health problem related to genitals and HIV infection is most likely due to genital herpes, which is common in South Africa and strongly associated with HIV. We believe that those who became HIV positive also became infected with HSV-2 just before, at the same time, or just after the acute primary HIV infection. Primary genital herpes infection concomitant with HIV infection can lead to clinic attendance because of herpes genital lesions, and can explain the observed association.
In this population of young men, as shown in Table 4 of our Research Article
, we did not observe any significant association between reported sexual behaviour characteristics and HIV infection when controlling for other factors, including the randomisation group. However, in univariate analysis, there is an association between HIV infection and number of sexual contacts (RR 2.0;
p 0.035) and risk of infection (RR 1.7;
p 0.045). This last variable includes lack of condom use. We believe that because of the small number of infections, and the importance of male circumcision on the transmission of HIV, the factors associated with sexual behaviour do not appear in the multivariate analysis. In addition, we think that the HIV status of female partners of these young men is a key factor. In Table 4, it is clear that HIV infection increases with the age of the participants, which is a proxy for the risk of having a partner who is infected with HIV for two reasons: (1) because the age of female partners increase with age of their male partners and (2) because, in young women, HIV status is strongly associated with age.
We did ask the sex of all reported sexual partners. We found that 0.07 of these reported partners were men. Three participants reported sexual partnerships with men. None became infected during the follow-up.
At recruitment, HIV prevalence was 0.7 (two out of 278) among those who reported never having any sexual contact, and 4.8 (144 out of 2,994) among those who reported having sexual contact (
p < 0.001).
HIV incidence was about two out of 100 per year in the control group during the follow-up. Knowing that HIV incidence increases with age, and assuming that the incidence is negligible before 17, we can estimate the HIV incidence between the age of 17 (median age of first sexual experience) and the age of 21 (age at recruitment) by about half the incidence of the control group during the follow-up, leading to an estimated HIV inc