  The coexistence of different viral strains (quasispecies) within the same
host are nowadays observed for a growing number of viruses, most notably HIV,
Marburg and Ebola, but the conditions for the formation and survival of new
strains have not yet been understood. We present a model of HIV quasispecies
competition, that describes the conditions of viral quasispecies coexistence
under different immune system conditions. Our model incorporates both T and B
cells responses, and we show that the role of B cells is important and additive
to that of T cells. Simulations of coinfection (simultaneous infection) and
superinfection (delayed secondary infection) scenarios in the early stages
(days) and in the late stages of the infection (years) are in agreement with
emerging molecular biology findings. The immune response induces a competition
among similar phenotypes, leading to differentiation (quasi-speciation), escape
dynamics and complex oscillations of viral strain abundance. We found that the
quasispecies dynamics after superinfection or coinfection has time scales of
several months and becomes even slower when the immune system response is weak.
Our model represents a general framework to study the speed and distribution of
HIV quasispecies during disease progression, vaccination and therapy.
