Human Immunodeficiency Virus Type 2 (HIV-2) likely emerged in humans around 1930-40 and is less widespread than the predominant HIV-1, remaining mostly within West Africa. Male circumcision is known to be associated with reduced HIV-1 prevalence because the foreskin is highly vulnerable to infection. However, the association between male circumcision and HIV-2 prevalence had not been examined until now.
João Dinis de Sousa from the University of Leuven, Belgium, and his colleagues investigated this association, and he answered additional questions about their study below.
What prompted you to study science as a career?
JS: At 19 years old, I built a telescope to observe the moon and the planets. At the same time, I read several science books, mostly centered in physics and cosmology. My interest in biology came later. I had the good fortune of reading Richard Dawkins’ “The Selfish Gene” in my early thirties, and I was fascinated at once. It prompted me to read his other books, and other books on evolutionary biology and sociobiology. In the early 1990s, I became a member of the Portuguese Ethological Society and the international Human Behavior and Evolution Society, and attended several conferences about sociobiology. I had no academic affiliation and had no plan — I was studying that field out of sheer fascination.
What drew you to HIV origins and early epidemiology in Africa?
JS: My previous interest in evolutionary biology led me to exploring the origins of HIV. I noticed there was a gap in the research about HIV origin and emergence. Previous researchers had assumed that HIV jumped from simians to humans through bushmeat-related activities, and then it adapted and spread. However, this did not explain why the virus emerged so late in our species, since humans have hunted simians for tens of thousands of years. I thought I needed to focus on Central and West Africa in the early 20th century to investigate which factors could have contributed to HIV emergence in humans at that time.
The literature on HIV transmission mentions that the sexually transmitted diseases (STDs) that cause genital ulcers (such as syphilis) increase HIV transmission probability a lot. Additionally, sources about medicine in Africa during colonial times indicated that these genital ulcer-causing STDs became strongly epidemic in early 20th century as these areas became enmeshed with the colonial networks, with the concomitant disruption of traditional ways and onset of commercial sex work. Thus, I focused my attention, not only on ulcer-causing STDs, but also on commercial sex work, differential male circumcision, and indeed on any factors that could contribute to HIV propagation.
Why was this study conducted in West Africa? How might your results differ in other parts of the world?
JS: This study was centered on HIV-2 early epidemiology, and that virus originated in West Africa. The virus crossed from sooty mangabey monkeys to humans there, most likely in the Ivory Coast, and started to spread in this country and others of the same region. Up until the late 1980s, the virus was mostly confined there and so, since we correlated patterns of male circumcision (MC) with HIV-2 prevalence rates measured in the late 1980s, it is legitimate to study that correlation in those West African countries. It is not useful to extend the study of HIV-2 to other parts of the world because the prevalence rates of HIV-2 is tiny in most countries and might be more affected by patterns of international travel.
Were there any limitations to your study?
JS: One limitation is that our measures of HIV-2 prevalence in the cities included in the study were based on published serological studies that were performed in the 1980s — when the serological assays had less sensitivity and specificity than modern assays. But these are the best data we have, and similar data was used in other studies to test the correlation for HIV-1. In addition, while we demonstrate a correlation with MC, we cannot guarantee that MC was the only source of the differential spread of HIV-2. There could have been founder events earlier in some cities than in others, potentially contributing to explain the differential prevalence rates. However, as we write in our paper, even in that case, a low MC rate would increase the odds of an early founder event, since the virus would more likely form new foci in cities with higher transmission potential.
Did your findings surprise you? Why?
JS: It did not surprise me because the correlation between MC and HIV was already demonstrated for HIV-1, and this led to several published studies, including studies showing an ecological association and estimating MC based on an ethnographic approach, as in this study. It is logical to expect HIV-2 to show the same association because both viruses spread in Africa mostly by heterosexual relations, and the biology of sexual transmission is similar (although HIV-2 is less transmissible than HIV-1). Basically the human prepuce [foreskin] has more HIV target cells and forms micro-abrasions easily, thus leading to a higher risk of HIV acquisition by the uncircumcised male.
What are the next steps for your research?
JS: I am presently developing a project involving epidemiological computer simulations of early HIV-1 spread. These simulations will replicate the conditions prevailing in an early 20th-century colonial city, and will model the spread of syphilis and other STDs too. This work will have, like the previous ones, the precious collaboration of Anne-Mieke Vandamme and Viktor Müller. Our aim is to determine which factors were more likely to contribute to early spread.
Image Credits: Fig. 1 from Sousa et al (2016); headshot from João Dinis de Sousa
Citation: Sousa JD, Temudo MP, Hewlett BS, Camacho RJ, Müller V, Vandamme A-M (2016) Male Circumcision and the Epidemic Emergence of HIV-2 in West Africa. PLoS ONE 11(12): e0166805. doi:10.1371/journal.pone.0166805