HIV-1 entry into CD4+ cells is mediated by the chemokine receptor CC-CKR-5

Article Abstract:

The entry of the primary, non-syncytium-inducing human immunodeficiency virus 1 (HIV-1) strains requires the activity of the beta-chemokine receptor CC-CKR-5. Cells co-expressing CD4 and CC-CKR-5 are highly susceptible to HIV-1 infection. Cells co-expressing CD4, and CC-CKR-2a, CC-CKR-3 or CC-CKR-4 are resistant to infection. CC-CKR-5 permits fusion of the virus with the cell membrane. Beta-chemokines are proteins that suppress HIV-1 infection by inhibiting membrane fusion and virus replication.

HIV (Viruses), HIV, Proteins, Cell receptors, Cytokines, Virus receptors

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CD4-dependent, antibody-sensitive interactions between HIV-1 and its co-receptor CCR-5

Article Abstract:

The CD4 molecule binding increases the efficiency of antibody-interactions between the human immunodeficiency virus type 1 (HIV-1) glycoproteins gp120 and its beta-chemokine receptor CCR-5. The neutralization of the antibodies against different binding sites on the gp120, inclusive of the V3 loop and the CD4 activated epitopes, fails to influence the gp120 and CD4 binding. However, it suppresses the interaction of gp120 with the co-receptor CCR-5.

Physiological aspects, Observations, Glycoproteins, Chemoreceptors, Binding sites (Biochemistry), Active sites (Biochemistry), CD4 lymphocytes, HIV antibodies

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See a pocket, block it

Article Abstract:

There is hope that D-peptides might be useful in the treatment of the HIV virus. D.M. Eckert and others have discovered that D-peptides, which could stop HIV-1 from entering human cells and fusing with them can be held in a cavity formed in the HIV-1 gp41 transmembrane glycoprotein. D-peptides have been chosen because of their D-amino acid content, which makes them more stable.

Care and treatment, Peptides, Eckert, D.M.

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