All other things
being equal, people of African background – which includes both Africans living
in Europe and African-Americans in the USA - progress more slowly to AIDS
than people of other racial backgrounds.
from two studies presented at the recent Conference on Retroviruses and
Opportunistic Infections in Montreal,
may seem contrary to experience. But the findings are robust: in both Europe
and the USA
people of African descent with HIV had slower CD4 declines and progressed more
slowly to AIDS compared with people of European descent, and the figures were
highly statistically significant. If they subsequently had higher mortality,
this was to do with unequal access to good treatment; but the studies showed
that they started with an advantage when it came to fighting CD4 declines.
would need to be confirmed by other surveys, and causation is not clear. But
the European researchers suggest that it might be down to having an immune
system already primed to deal with more diseases than Europeans. As in the
‘hygiene hypothesis’ explaining why allergic conditions such as asthma have
increased in rich countries, Europeans may be paradoxically too disease-free to
cope well when HIV comes along.
The US study found
a specific and unexpected association with hepatitis B infection: people who
had caught hepatitis B and had resolved it were more likely to develop AIDS
slowly. The US
researchers suggest that genes that are known to be associated with slow HIV
progression may help people fight off hepatitis B once infected. Hepatitis B
infection, like HIV, is more common in Africans and African-Americans than in
In the European
study,1 the CD4 decline in patients of African and European descent
in the Swiss HIV Cohort2 were compared. For the current study 463
European and 123 African patients were chosen and matched by age. Unusually for
a cohort study, the majority were women. The African patients had, on average,
been infected for a shorter time (seven versus eleven years) and had a lower
CD4 count at the time of cohort recruitment - 494 in Africans and 577 in
were observed for four years before they started HIV therapy and the Europeans
five years. During that time the Africans averaged half the HIV viral load
(5300 versus 10,250 in Europeans). They also had nearly half the rate of CD4
decline of the Europeans: the average annual CD4 decline was 28.2 cells/mm3
in Africans and 52.5 cells/mm3 in Europeans. These differences were
highly statistically significant: there was less than a one-in-a-thousand
chance that the findings were a random effect.
analysed results according to HIV subtype, because in some other studies viral
subtype has been associated with faster progression. The subtypes analysed were
A (most common in East Africa), B (predominant in Europe and North America), C
(mainly from southern Africa) and AG (west
Africa). The average viral load was at least 10,000 in every subtype analysed
in Europeans and below 10,000 in every subtype in Africans, and Africans had
slower CD4 declines in every subtype except type A.
calling their findings “remarkable”, surmise that one reason for slower
progression in Africans might be “evolutionary adaptation to higher overall
levels of antigenic exposure in Africa”. In
other words, Africans may be more likely to have genes that developed in
response to other tropical infections, and which confer a degree of resistance
study3 presented tended to support this theory by finding that
African-Americans had slower HIV progression than other ethnicities and also
tended to have specific genes associated with slower progression. It also
uncovered an unexpected and very strong association with hepatitis B infection.
AIDS Cohort Study (MACS)4 studied 234 people not taking HIV
treatment, comparing 55 ‘long-term non-progressors’ (LTNPs) with 179 ‘expected progressors’
(EPs). The definition used for LTNPs was that none of these people had
progressed to an AIDS-defining illness 15 years after infection, while EPs had
all progressed to AIDS by their twelfth year of infection. The LTNPs were
observed for as long as 22 years after infection, by which time just two people
had developed AIDS. In the EPs the shortest time to an AIDS diagnosis was three
years and the median time about 6.5 years.
A number of
factors were associated with being an LTNP. The first was age at infection: 60%
of LTNPs were aged 25 to 35 at infection compared with 45% of EPs; in contrast
13% of EPs were over 45 at infection compared with 2% of LTNPs (just one
The second was
African ethnicity. Nearly a quarter (22%) of LTNPs were African-American
compared with just 4% of EPs. This was highly statistically significant.
This was a
striking enough finding, but more striking was the association with hepatitis
B. Nearly three-quarters (73%) of LTNPs, versus 42% of EPs, had had hepatitis B
and had ‘resolved’ it, i.e. had cleared the virus and developed protective
antibodies to it. In contrast, 22% of LTNPs and 56% of EPs had either never
been infected with hepatitis B or had been vaccinated against it. The same
associations were not seen with hepatitis C nor with HHV-8, the virus that
causes Kaposi’s sarcoma.
also found three specific immune-system genes to be associated with slow
progression and note that they “have also been associated with recovery from
hepatitis B infection”, though why slow progression should be associated with
higher rates of hepatitis B infection in the first place is unclear. It could
be because white people are more likely to have the hepatitis B vaccine, or because
the same genes that confer resistance to HIV progression might also confer
vulnerability to hepatitis B.
these two surveys produce results contrary to what many people might have
expected. If Africans were given equal access to optimal HIV therapy and
good-quality healthcare, they might well do better than Europeans.