Evolution in ecological time

Scientists now agree that evolution can frequently occur over timescales that matter to ecologists, such as a few decades or less. There are few more graphic examples of rapid evolution than of the emergence of new human diseases. In the case of human immunodeficiency virus (HIV), the disease it causes (acquired immune deficiency syndrome or AIDS) was first recognized in 1981. The virus responsible (Figure 8.4) was characterized in 1983 as a retrovirus with similarities to primate lentiviruses, also known as simian immunodeficiency viruses (SIVs). SIVs are widespread among African apes and monkeys, and phylogenetic comparisons of HIV and SIV sequences suggest, with a large margin for error, a likely origin of the current epidemic in the middle decades of the twentieth century (Hahn et al. 2000). Most interestingly, SIVs are not known to cause disease in their hosts, whereas HIVs are, as far as is currently known, 100% fatal. It seems therefore that HIVs have evolved to become more virulent over the timescale of only decades. That, however, is nothing compared to what goes on within a single host.

Hiv Electron Microscope

Fig. 8.4 Particles of HIV infecting a human tissue-culture cell. The HIV particles are about 100 nm across.

Photo courtesy of the Ripple Electron Microscope Facility, Dartmouth College, New Hampshire.

Fig. 8.4 Particles of HIV infecting a human tissue-culture cell. The HIV particles are about 100 nm across.

Photo courtesy of the Ripple Electron Microscope Facility, Dartmouth College, New Hampshire.

When transmitted to an uninfected human, the virus undergoes rapid replication in the so-called 'primary infection' stage. Replication occurs largely in white blood cells, though other tissues can be used. The immune system of the host then rapidly responds and reduces virus to very low levels. At this stage the host can be recognized as sero-positive. During the next, latent, stage of infection, diversity of the virus slowly increases. New strains of the virus arise because of the low fidelity of the enzyme reverse-transcriptase, which converts the RNA virus genome into DNA that can integrate with the host genome. The rate of substitution in the virus genome is roughly one million times that of human genes. Typically 1010 virus particles can be produced per victim per day. After a variable number of years of viral replication and gradually increasing viral diversity, depletion of T-lymphocytes is such that the virus replicates rapidly, and the virus load becomes dominated by fast-replicating strains (Nowak et al. 1991). AIDS symptoms occur, and the victim dies of some secondary infection that would not normally be fatal.

We have observations suggesting evolution on two scales: an increase in the virulence of HIVs relative to SIVs and a within-host evolution towards increasing virulence towards the latter stages of infection. Has natural selection been responsible for these trends? It is likely in both cases. For example, resistance to individual antiviral drugs, such as AZT, occurs typically in six months, and similar mutations characterize the resistant strains. This strongly suggests selective evolution of the virus. What about the increase in HIV virulence relative to SIV virulence? Both viruses have high replication rates, mutation rates, and viral loads. These then do not, on their own, seem to engender high virulence. However, the virus envelope protein of SIVs is very conserved, but rapidly evolves in HIVs. In addition SIVs only stimulate a weak immune response from their hosts, while HIVs stimulate a strong immune response.

This suggests that SIVs experience stabilizing selection, while HIVs are positively selected by the immune response. When a strong immune response occurs, genetic variation is created by strains attempting to evade it, that eventually leads to virulence and AIDS. For SIVs a weaker immune response creates reduced selection on the virus, creating less viral competition and less virulence. In summary, the difference in virulence between HIV and SIV seems to have been driven by the extent of arms race between virus and immune response (Holmes 2001). Under this scenario pressures that select for virulence of HIV relative to SIV are the same as those that select for virulence during HIV infections.

There seems little doubt therefore, that HIV can and has rapidly evolved virulence. It seems obvious, especially in the context of a disease like AIDS, that there will be population consequences of short-term evolution. How in general can we predict such consequences? A taste for this comes from recent work on the evolution of exploited fish stocks. Unlike in HIV, a convincing case for short-term evolution in fish stocks has taken time to accumulate. In contrast to HIV, however, we are much better equipped to predict the population consequences because of the presence of high quality data on relevant parameters.

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