摘要: Highly active antiretroviral therapy (HAART) reduces the viral burden in human immunodeficiency virus type 1 (HIV-1) infected patients below threshold of detectability. However, substantial evidence indicates that replication persists these individuals. In this paper we examine ability several biologically motivated models HIV-1 dynamics to explain sustained low loads. At or near drug efficacies result steady state loads detectability, most are extremely sensitive small changes efficacy. We argue if reflect reality many should have cleared virus, contrary observation. find a model which cell death rate is dependent on density does not suffer shortcoming. The shortcoming also overcome two more conventional include populations cells less effective than main population, suggesting difficulties with penetrance and maintenance intracellular concentrations all susceptible HIV infection may underlie ongoing replication.