There is speculation in the scientific community that the smallpox virus selectively pressured a gene (encoding receptor CCR5) to evolve and mutate, thus creating resistance to HIV-1 infection. HIV-1 requires two cellular proteins, the receptor CD4, and a co-receptor, either CXCR4 or CCR5, in order to enter lymphocytes. People who have a mutation in the gene encoding CCR5, known as delta 32, are resistant to HIV-1 infection.
Ten percent of humans possess the CCR5 delta 32 deletion, yet HIV-1 only recently began to infect humans, when it crossed from chimpanzees in 1930. Therefore, it cannot be HIV itself that selected for the gene mutation. What then, could account for the selection pressure?
Professor Racaniello of Columbia University posits that the evolution of the CCR5 delta 32 deletion is actually due to the smallpox virus, which has been plaguing the world since before 1000 AD. Myxoma virus (a poxvirus) is highly fatal in rabbits; however, cells that cannot be infected by this virus can be made susceptible to infection by expression of genes encoding various chemokine receptors, including CCR5. Effectively, this shows that CCR5 is an entry receptor for myxoma virus, and Racaniello suspects that it may be for the related smallpox virus as well. If so, Racaniello believes that smallpox is the most likely cause of the selective pressure responsible for fixation of the CCR5 delta 32 HIV-1 resistance allele.
See http://www.virology.ws/2009/02/20/hiv-1/ for more info.