A 60 kD heat-shock protein-like molecule interacts with the HIV transmembrane glycoprotein gp41.

The heat-shock protein hsp60 is typically found in mitochondria, but, in smaller amounts, also in the cell cytoplasm and associated with the cell membrane. Since heat-shock proteins are known to interact with a variety of molecules and since purified HIV-1 particles were described to contain hsp60 molecules, we tested the possibility that a previously described putative receptor for HIV transmembrane protein gp41 is identical to hsp60. The gp41-binding human protein P62 was purified from H9 and Raji cell lysates by a gp41-coupled affinity column.

Modulation of cell surface protein expression by infection with HIV-1.

The examples discussed above show the profound influence of HIV infection on expression pattern of cell surface proteins and the functional relevance thereof. Altered cell surface pattern is involved in all aspects of HIV-induced pathogenesis such as viral spreading viral adhesion and cellular apoptosis and is an important parameter for therapeutical approaches. The regulatory mechanism is not homogenous for all proteins but includes divergent effects like modulation of gene transcription and proteolytic cleavage.

Human immunodeficiency virus type 1 derived from cocultures of immature dendritic cells with autologous T cells carries T-cell-specific molecules on its surface and is highly infectious.

During the budding process, human immunodeficiency virus type 1 (HIV-1) acquires cell surface molecules; thus, the viral surface of HIV-1 reflects the antigenic pattern of the host cell. To determine the source of HIV-1 released from cocultures of dendritic cells (DC) with T cells, immature DC (imDC), mature DC (mDC), T cells, and their cocultures were infected with different HIV-1 isolates. The macrophage-tropic HIV-1 isolate Ba-L allowed viral replication in both imDC and mDC, whereas the T-cell-line-tropic primary isolate PI21 replicated in mDC only.

Acquisition of host cell-surface-derived molecules by HIV-1.

Objective: To determine the acquisition of host cell-membrane-derived molecules by HIV-1 during the budding process, and to investigate whether the uptake of these molecules is cell-type-specific and selective.

Design: Virions, propagated by four different cell types were analysed for the presence of adhesion molecules, glycosylphosphatidylinositol (GPI)-anchored proteins and various cell-surface markers. The pattern was compared with the phenotype of the HIV-1-infected cell.