Abstract
Mathematical models and experiments have shown the importance of CD8 responses in control
of HIV infection. In this paper we review the theoretical and empirical evidence and how the
two compliment each other as they shed more light on the progression of HIV infection. This
paper also highlights the controversies pertaining the subject. We present some models that
investigate the role of a CTL response and a CTL memory in control of HIV. These models
show that a strong CTL response can control the viral load, however, in some cases the virus
has been known to persist regardless of the immune response. We extend the basic immune
response model to account for the escape of HIV from CTL responses via epitope mutations.
We find that a broad and long lived CTL response efficiently controls the virus even in the event
of mutations. On the other hand, a gradual switch from a slow replicating HIV strain to a faster
replication kinetics, has also been suggested as amechanism fordisease progression. To explore
the factors influencing this switch, we extend the CTL memory model to include macrophage
cells, non-lytic CD8 responses and the evolution of HIV from a slow replicating strain(R5)
towards a faster replicating strain (X4). We find that macrophages act as a reservoir for the virus
hence promote viral persistence. However in the course of the infection, the success of a switch
from the R5 strain to the X4 strain dependson the cytopathicity of the individual strains. The
cytopathicity, evolution rate, infection rate and the strength of the immune response determine
the time lapse before a switch occurs. We conlude that these factors determine the length of the
asymptomatic period of HIV infection.