Infection with HIV-1 results in a slow, progressive deterioration of the immune system. Over time, during the course of HIV infection, infected subjects harbor a severe immune-suppression due predominantly to the selective depletion of the CD4+ T cell population. The discovery that CD4 is the primary cellular receptor that HIV uses to enter T cells provided the rationale to explain why CD4+ T cells progressively declined. According to this view, HIV infects CD4+ T cells and then lyses them during the productive phase of the viral life cycle. However, this removal of virus-infected cells is certainly not the only mechanism of CD4+ T lymphocyte depletion, since naive CD4+ T cells are relatively resistant to productive HIV infection. It is also well-documented now that during the early stages of HIV disease, CD4+ T cell counts decline whereas total CD8+ T cell compartment expand. However, this increase of CD8+ T cells is comprised entirely of memory and activated T cells, while naive CD8+ T cells decline at the same rate as naive CD4+ T cells. Since HIV does not usually infect CD8+ T cells, unless expressing transiently the CD4, and these declines are hardly attributable to HIV-mediated cytolysis, other mechanisms could be responsible for this decline of naive CD4 and CD8 T cells in HIV-infected subjects.

Interestingly, functional defects in the immune system can be demonstrated long before CD4+ depletion occurs. Studies have shown a progressive deterioration of T cell function at all stages of infection with HIV. Among abnormalities caused as a result of HIV-1 infection, T cell proliferation induced by specific antigen, antibodies or non specific mitogens is significantly decreased. Although an increasing number of studies confirm a direct correlation between impairment of T cell function and progression of HIV, the mechanism responsible for gradual deterioration of T cell function remains to be elucidated. Mymetics has made an important discovery that may explain the important immune system damage caused by HIV-1.