Independent divergences in the CD4 binding site and V3 loop encoded in two seroprevalent Ugandan HIV-1 clinical isolates

Article Abstract:

UG06c and UG23c are two distinct African subgroups of HIV type 1 (HIV-1). The subgroups have antigens on their surface that are recognized by antibodies from HIV-infected individuals from Africa and North America. A genetic analysis was done of the V3 loop of the gp120 protein and the CD4 T cell recognition site of UG06c and UG23c from African AIDS patients. The V3 loop of gp120 and the CD4 T cell recognition site are two types of antigens on the surface of HIV-1. UG06c and UG23c are both distinct subtypes of HIV-1 with specific types of antigens on their surface. Both subtypes reacted with antibodies in the blood of African and North American individuals with asymptomatic HIV infection.

Binding sites (Biochemistry), Active sites (Biochemistry)

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Helper T-cell recognition of HIV-1 Tat synthetic peptides

Article Abstract:

Tat protein may activate helper CD4+ cells in individuals infected with HIV type 1 (HIV-1). This protein is a regulatory protein that is necessary for replication of HIV-1. A study examined response of helper CD4+ T cells to recombinant (genetically engineered) Tat protein and 12 different Tat protein subunits in 15 HIV-positive individuals and 11 HIV-negative individuals (control group). HIV-positive individuals were more likely to have a response to recombinant Tat than those in the control group. Three Tat protein subunits caused a helper CD4+ T cell response in the HIV-positive individuals but not in HIV-negative individuals.

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Interleukin-10 gene expression induced by HIV-1 Tat and Rev in the cells of HIV-1 infected individuals

Article Abstract:

The production of interleukin-10 in HIV-infected patients could explain the immunosuppression these patients experience. Researchers took blood samples from 8 HIV-infected patients and exposed the samples to proteins from HIV. All but one of the samples produced interleukin-10 upon viral stimulation. This indicates that the T lymphocyte helper type-2 cells were being stimulated. The production of interleukin-10 could cause the defect in cell-mediated immunity, since interleukin-10 is known to suppress the immune system.

Causes of, HIV infection, HIV infections, Interleukins, Immunosuppression

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