Transmission Rates and the Evolution of HIV Virulence

Abstract

Recent publications dealing with sexually transmitted HIV consider how the average number of sexual partners, as well as the rate of partner exchange, can determine the evolution of increased mutation rates, genetic (and antigenic) diversity, and consequently, increased virulence of the virus (Ewald 1991(Ewald , 1994. It is intuitive that in a population of relatively monogamous individuals HIV would benefit from remaining latent. If such outside sexual activity takes too long to occur, only the pathogen variants that have some way to extend their potential infectiousness would be transmitted venereally.When sexual activity increases so that people are involved with different partners more frequently, the factors contributing to virulence shift. A particular strain, or variant, of a sexually transmitted virus, like HIV, that actively reproduces in an infected person could soon infect several new hosts, whereas a strain that is latent for several years would propagate less extensively, if at all. Therefore, increased number of sexual partners and/or rates of partner exchange would favor HIV variants that replicate rapidly. Here fast replicating, highly cythopatic strains that are not recognized by the immune system have a disproportionately larger effect (Nowak et al. 1990). This evolutionary process leads eventually to the development of AIDS after a variable incubation period. So, the pressures favoring the evolution of fast viral reproduction when sexual contact is high and of delayed viral reproduction when sexual contact is low provide the basis for a prediction: HIV virulence should be correlated with rates of sexual contact (Ewald 1994).Actually, literature concerning the capacity of HIV variants to induce AIDS (and eventually kill their hosts) with different rates show that AIDS progression is associated with the history of sexual intercourse (Perkins et al. 1987;Ward et al. 1989;van Griensven et al. 1990;Blower and Boe 1993; Ewald 1994).Obviously, the rationale exposed above is also valid for parenteral transmission of HIY. As the number of people sharing injecting equipment, as well as the rate of exchanges increase, the fast replicator strains of HIV are favored. This is an example of how a host behavior can act as a selective pressure for increased virulence of some parasites.Here I provide a mathematical treatment to Ewald's (1994) verbal arguments for the evolution of virulence of HIY. It assumes that an evolutionary mechanism-on a very fast time scale-is responsible for viral pathogenesis (Nowak et al. 1990).In the first analysis, I propose an adaptation of Levin and Pimentel's (1981) model for the study of the evolution of virulence of HIY. More recently, Nowak and May (1994) analyzed the same model for the study of superinfection and the evolution of parasite virulence. In the second analysis, this model is rewritten in terms of Volterra-Lotka interspecific competition equations, as done by Massad et al. (1993) for the study of the evolution of resistance against antibiotics. Both analyses yiel...

The influence of social behaviour on competition between virulent pathogen strains

“…When the impact of human behaviour is discussed in such models, it is discussed in terms of hypothesized effects of human behaviour on the value of the fixed parameter representing virulence. A Human Immunodeficiency Virus (HIV) virulence model by Massad (1996) shows that reducing the number of sexual partners could possibly drive HIV to be a more benign pathogen. However, the model assumes that the number of sexual partners can simply be moved up or down as a model parameter, whereas in reality the number of sexual partners in a population is the outcome of a dynamic socioepidemiological process that merits its own mechanistic modelling, and itself responds to pathogen virulence.…”

Coevolutionary cycling of host sociality and pathogen virulence in contact networks

“…For instance, theoretical studies suggest that the average number of sexual or needle-sharing partners and the rate of sexual or needle partner switching can determine the evolution of mutation rate, genetic and antigenic diversity, and virulence in HIV (Ewald, 1994;Ewald et al, 1994;Massad, 1996). Further, experiments have shown that pathogens may evolve different degrees of infectivity (i.e., probability of successfully infecting a susceptible host upon contact) and/or virulence (i.e., how quickly the pathogen kills its host) in response to changes in the way hosts move and contact each other (Boots and Mealor, 2007;Kerr et al, 2006).…”

“…A more virulent pathogen kills its host sooner, reducing the period during which it can jump to a new host. However, some of the traits that lead to higher virulence are also thought to provide separate benefits such as enhanced transmission rates and/or superior intra-host competitive ability Massad, 1996;Nowak and May, 1994). Such pathogen traits may simultaneously come with advantages (higher rate of movement to new hosts) and disadvantages (shorter period infecting any one living host).…”

“…Many theoretical models have focused on the evolution of pathogen virulence (Boots et al, 2004;Sasaki, 1999, 2003;Day 2002;Gandon et al, 2002;Nowak and May, 1994;Massad, 1996;van Baalen, 1998van Baalen, , 2002see Galvani, 2003 for a review). Very few, however, have explored how host sociality and pathogen virulence coevolve.…”

Modeling the Dynamics of Viral Evolution Considering Competition Within Individual Hosts and at Population Level: The Effects of Treatment

“…From a theoretical point of view, viral evolution and competition have been addressed by several authors (e.g., Day, 2001;Lipsitch and Nowak, 1995;Lipsitch et al, 1996;Manrubia and Lázaro, 2006;Massad, 1997;Perelson and Nelson, 1999). Other relevant references will be mentioned as we go along in the paper.…”