Encyclopedia of Evolution.pdf - Online Reading Center

AIDS, evolution of
and mangabeys. The original suspects from the 1980s, African
green monkeys, are hosts to SIV that are not closely related
to any strains of HIV. The method by which the virus entered
human populations has not been determined but did not necessarily
involve sexual contact. SIV could have infected the
first human host by blood contact by a hunter with an infected
animal he had killed.
Evolutionary scientists have even been able to estimate
a time of origin for HIV. Evolutionary biologist Bette Korber
and colleagues limited their study to group M viruses. They
estimated the degree of nucleotide difference between a strain
of HIV and the common ancestor of all group M viruses. For
each year between about 1983 and 1998, each of the strains
became more and more different from the common ancestor.
The researchers calculated a statistical line through these data,
then extrapolated the line all the way back to a time when there
would have been zero difference between the strains and their
common ancestor. The line crossed zero for the year 1931.
Especially with extrapolation, error ranges become very large,
so the estimated age of group M viruses is between 1918 and
1941. It appears that HIV has been present in human populations
for only about 70 years, while SIV has been in other primate
populations for many millennia. Parasites often have their
most severe effects upon first infecting a host species; thereafter,
coevolution may result in less severe disease, both because of
more resistant hosts and also because of milder parasites.
Evolutionary Diversity of HIV and of Human Hosts
There are several strains of HIV. One reason for this is, as
noted above, HIV-1 and HIV-2, as well as different strains of
HIV-1, had distinct evolutionary origins. A second reason is
that natural selection among HIV variants occurs differently
in each victim’s body. Thus the genetic strain that a person
passes on to the next host is not necessarily the same strain
with which he or she was originally infected. Some strains
of HIV reproduce more slowly than others. A strain of HIV
from Australia, the Sydney Bloodbank Cohort, recognizes a
slightly different class of white blood cells, which reproduce
themselves more slowly, causing the virus to propagate more
slowly. A slower virus would be at a disadvantage in the presence
of viruses that spread more rapidly, but some individuals
were infected only with the slow form of the virus. These
individuals have few symptoms, even after two decades.
There are also differences among individual humans in
their ability to resist HIV. Apparently some individuals, who
have not developed AIDS even after exposure to HIV, have a
slightly different set of surface proteins on their white blood
cells. HIV cannot bind to these mutant proteins and therefore
cannot get into the white blood cells. Interestingly, 9
percent of Europeans (more than 14 percent from Scandinavian
areas) have the mutant protein form that conferred resistance
to HIV infection, while less than 1 percent of Asians
and Africans have this mutant protein. Nobody knows why
this geographical pattern exists. Two explanations have been
suggested. The first proposal is that the mutant protein was
produced by natural selection, because the mutant proteins
also conferred resistance to other kinds of infection that
had struck the populations in earlier centuries. Resistance to
bubonic plague has been suggested, since plague also spreads
in conjunction with white blood cells, and because the
Black Death struck especially hard in 1347–50 in the areas
of Europe that today have the most people that resist HIV
infection. The second proposal was that the mutant protein
was produced by genetic drift (see founder effect), because
just by accident the Vikings had these mutant proteins, and
they spread them whenever they went on raids. Genetic drift
does not explain why the highest allele frequency for the
mutant protein is found among Ashkenazi Jews. Estimates
from population genetics equations suggest that the mutation
apparently occurred about 700 years ago. This would be
right at the time of the Black Death, but a little later than the
heyday of Viking expansion.
Evolutionary Changes in HIV after It Infects an Individual
Evolutionary changes occur in populations of the viruses
within an individual victim. In a typical victim, for example,
a very small amount of AZT is all that is necessary to inactivate
a large proportion of the viruses during early infection.
By the second year of infection, much larger doses are needed
to achieve the same effect. This occurs because the percentage
of viruses that can resist AZT increase in the population of
viruses. The figure on page 13 relates dosage of AZT to effectiveness;
the horizontal axis is in powers of 10, which means
that almost 10,000 times as much AZT was needed to kill
about half the viruses in the second year of infection as in the
second month in this particular person.
The most likely reason for the evolution of AZT-resistant
viruses within an individual is that random mutations in
the viral genes resulted in reverse transcriptase molecules that
would not recognize AZT as a nucleotide. While a mutant
reverse transcriptase molecule would normally be detrimental
to a virus, in the presence of AZT this mutant enzyme, though
somewhat defective, is at least able to operate. Therefore,
mutant viruses thrive in the presence, but not in the absence, of
AZT. This pattern, in which resistant organisms thrive in the
presence of the chemical agent used against them but are otherwise
inferior to the susceptible organisms, is general among the
many cases of the evolution of resistance to antibiotics, pesticides,
and herbicides (see resistance, evolution of).
Resistance is less likely to evolve if several different
chemical agents are used together. This is the reason that
many different antibiotics, pesticides, and herbicides are in
use and more are being developed. Populations of HIV can
evolve resistance to any of the chemical treatments against
it (reverse transcriptase inhibitors such as AZT; chemicals
that inhibit proteases; chemicals that block the entry of HIV
into white blood cells; chemicals that block the integration
of viral DNA into host chromosomes) but a combination
or “cocktail” of different chemicals has proven effective at
stopping the spread of HIV within a victim. It is much less
likely that any virus will happen to possess mutations that
render it resistant to all four means of chemical control than
that it will possess a mutation against any one of them. In
fact, mathematical calculations show that a cocktail of three
chemicals is much more than three times as effective as each
chemical individually.