  When highly active antiretroviral therapy is administered for long periods of
time to HIV-1 infected patients, most patients achieve viral loads that are
``undetectable'' by standard assay (i.e., HIV-1 RNA $ < 50$ copies/ml). Yet
despite exhibiting sustained viral loads below the level of detection, a number
of these patients experience unexplained episodes of transient viremia or viral
"blips". We propose here that transient activation of the immune system by
opportunistic infection may explain these episodes of viremia. Indeed, immune
activation by opportunistic infection may spur HIV replication, replenish viral
reservoirs and contribute to accelerated disease progression. In order to
investigate the effects of concurrent infection on chronically infected HIV
patients under treatment with highly active antiretroviral therapy (HAART), we
extend a simple dynamic model of the effects of vaccination on HIV infection
[Jones and Perelson, JAIDS 31:369-377, 2002] to include growing pathogens. We
then propose a more realistic model for immune cell expansion in the presence
of pathogen, and include this in a set of competing models that allow low
baseline viral loads in the presence of drug treatment. Programmed expansion of
immune cells upon exposure to antigen is a feature not previously included in
HIV models, and one that is especially important to consider when simulating an
immune response to opportunistic infection. Using these models we show that
viral blips with realistic duration and amplitude can be generated by
concurrent infections in HAART treated patients.
