OBJECTIVE:

Sequential acquisition of viral variants, or HIV-1 superinfection, has been proposed to explain the high fractions of recombinant viruses observed in some geographical regions, but only a few cases of superinfection in humans have been reported. Animal models suggest that susceptibility to superinfection may be restricted to a short period of time after initial infection, possibly due to maturation of broad antiviral immune responses.

METHODS:

A mathematical model involving a system of differential equations was developed to identify transmission and superinfection patterns that would lead to the observed global patterns of viral diversity.

RESULTS:

Requirements for a high prevalence of infections involving recombinant viruses include high viral infectivity, the presence of highly sexually active core groups, and introduction of divergent viruses early in the epidemic spread of HIV-1. Restricted superinfection could explain the persistent predominance of single virus subtypes in regions with well-established HIV-1 epidemics. The rate of recombination within individuals was not strongly related to recombinant fractions in populations.

CONCLUSIONS:

HIV-1 superinfection restricted to early HIV-1 infection could account for the high fraction of recombinant virus infections observed in populations. The relationship between recombination in cellular infections and recombinant fractions in populations is complex and depends on epidemiological factors and biological factors that can be modeled.