Specialist Registrar in Public Health Medicine
Dept. of Public Health Sciences, University of Edinburgh, Medical School, Teviot Place, EH8 9AG
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I would like to add another critical comment on Fassin & Schneider's otherwise excellent article this week:
As a native Zambian, with first hand clinical experience of AIDS in Southern Africa since 1986 (and in South Africa itself since 1992), I find much to agree with in their analysis of the political and social causes of the HIV epidemic in the RSA. However, what they fail entirely to mention is the role of biological factors, e.g. the nature of HIV-1C, the virus that predominates in this region. In this way, they may have fallen into the same trap as Mr Mbeki...
Yes, undeniably, inequality, mobility and violence have fuelled the flames of HIV transmission there, as throughout the world. South African society does indeed have all three factors in abundance. However, it is not unique, as the authors seem to imply. These pressures affect people all over the world, yet no other region has been quite as badly affected as Southern Africa. So what can we learn from the RSA experience?
Firstly, there are two HIV epidemics in South Africa: The first, among predominantly gay, white men started in the early 1980's and was with the same HIV-1B virus that paved the way in North America, Western Europe and Australasia. It was not until 1987 that the first case of AIDS was diagnosed in a black person there, despite all the inequality, mobility and violence associated with this group. However, within a decade, South Africa had more people with HIV than any other country in the world. Why such a delay and why the sharp rise thereafter? Perhaps the answer lies with the second HIV epidemic, that of HIV-1C, which found its niche among predominantly heterosexual, black Africans...
HIV-1C spread initially from its source of origin to the west of Lake Victoria, both north to Ethiopia and south through Malawi to the countries of the south. (A & D spread east and west.) Although its prevalence was small in 1990, compared with the others, HIV-1C has since shot up exponentially, colonising the Caribbean, India, China and is now the UK. In Africa, it is now moving back up the way into Tanzania (where is has been shown to be 6.7x as transmissible perinatally as HIV-1D), and having a ball in DR Congo, where the Zimbabwean army have no doubt played a part in its spread. Approximately two-thirds of all new infections world- wide are now thought to be HIV-1C. So why is it so successful?
HIV-1C appears to have been selected for vaginal transmission (either sexually or vertically), rather than via rectal or injection routes, like HIV-1B. By at least five different mechanisms it is more aggressive: It specifically targets Langerhans cells in vaginal and penile epithelium; it has a simplified co-receptor mechanism for entering T-cells (i.e. requiring one molecular handshake, instead of two); when inside, it is more readily activated by elevated cytokines such as TNF-alpha, (produced e.g. in response to other STI's and malaria); it produces higher viral loads, so it is more infective; and it mutates and forms recombinants more easily than other HIV-1 viruses. Even its transmission across the placenta is higher (mechanism unknown), so more babies are born infected, with or without peripartum nevirapine prophylaxis...
HIV-1C is probably more aggressive by design - it had to be to survive in the relatively low contact rate niche for which it evolved. Only once it reaches a critical level in the general population is it able to take off, hence the late start in South Africa, Botswana, Namibia etc. Perhaps this is the main reason for the scale of the epidemic in the south!
Ethiopia, was for many years the second highest epicentre for HIV and yet this is not a country with a classical, urban migration pattern. On the other hand, Nigeria, a magnet for migrant workers throughout West Africa, and which therefore one might think should have an epidemic of similar scale to to RSA, has been more fortunate.
Madagascar, which has a good deal of internal migration and inequality-related sexual risk going on - evidenced by its very high rates of other STI's (e.g. syphilis 36%), teenage pregnancy and Western sex tourism, has a very low HIV rate - officially 0.15% in 1999. Even if this was a ten-fold underestimate, it was still 100 times lower than KwaZulu-Natal, just across the water! Yes, there is certainly less sexual violence in Madagascar and almost universal male circumcision, but is that enough to explain the difference...?
I can see why Thabo Mbeki, in a country with two HIV epidemics, one small affecting mainly rich whites and one huge, affecting often poor blacks, would think first of possible confounders such as poverty. His background is in economics, not epidemiology.
He was perhaps unwise to question the links so publicly, so soon into his presidency. It has certainly cost him and the ANC dearly. I would even go so far as to say his reluctance to grasp the nettle of AIDS and to embrace HAART has also undoubtedly contributed to several thousands of people unnecessarily suffering and dying.
However, he is also human and we all make mistakes. There are millions of people who deny the reality of HIV/AIDS daily, either by taking risks with their own lives, or ignoring the plight of neighbours and family already affected. ...perhaps because it's too big or too awful, or they feel so powerless to do anything about it.
However, I believe the Western media has also played a role in this catastrophe. Since the Durban AIDS Conference in 2000, there has not been an HIV event, when some high-minded reporter does not thrust an aggressive microphone at Thabo Mbeki with a reminder of the subject. I myself was once invited onto a radio station on the occasion of the president visiting Scotland to unveil a plaque in honour of his father, Govan Mbeki, an often overlooked hero in the struggle against apartheid. All the interviewer wanted from me was to dig the dirt on Thabo Mbeki and his dissenter stance. No wonder he now instinctly switches off at the sound of the word, 'Aids'!
Perhaps this is not the most contructive way to engage with someone we need to play a pivotal role in leading the region through the current crisis...
PS I haven't used the terms 'subtype' or 'clade', although the former is still the accepted term in the HIV world. HIV-1 subtypes, such as B and C, have remained recognisably stable for over 25 years now, despite their huge turnover and mutation rates. They each have their own specific characters in terms of usual mode of transmission, infectivity and rate of disease progression, at both the individual as well as the population levels. They can, and probably most usefully should, therefore be taxonomically regarded as distinct viruses.
Perhaps if this were more widely recognised, it might help to dispel some of the myths and factoids about African sexuality and social behaviour?
[PPS References available by request]
Competing interests: None declared