HIV requires multiple gp120 molecules for CD4-mediated infection

Article Abstract:

The entry of the human immunodeficiency virus (HIV) into cells involves the binding of the glycoprotein gp120 molecule of the outer coat of the virus to the CD4 molecule of T lymphocytes. A method of preventing invasion of the virus is to block all the gp120 molecules so they cannot bind to the CD4 molecules on cells. One of the ways this is done is to use CD4 molecules that are soluble or free from the cell surface. The blocking of this binding of the virus to the cells was quantitatively examined. At low concentrations of CD4, the inhibition of binding was proportional to the amount of gp120 present. That is, one molecule of soluble CD4 molecule was bound to one molecule of gp120. This was true for three strains of HIV, although two of the strains had stronger binding to CD4 than the other strain. However, at greater concentrations of CD4, binding was not proportional to the amount of gp120 that was available. When half of the gp120 molecules were occupied, it took less CD4 to block the binding. It appears that HIV requires more than one gp120 molecule for binding to CD4. This was evident in all three strains of HIV examined. It is possible that the initial binding of virus by the interaction of gp120 molecule and CD4 requires one molecule of each. However, more than one gp120 molecule may be needed for adsorption of the virus and penetration into the cell. The gp120 molecules may interact with each other on the viral coat. Other viruses such as polio and influenza virus have subunits on their coats that interact with each other. Only a few sites are important in the inactivation of these viruses. The mechanism of the inactivation of HIV appears to be different. Further study on the interactions of gp120 with CD4 and with itself are necessary. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, gp120 (Medication)

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In vivo emergence of HIV-1 variants resistant to multiple protease inhibitors

Article Abstract:

The in vivo drug-resistant human immunodeficiency virus type 1 (HIV-1) variants appear to be emerging because of the inhibition of HIV-1 protease through drug therapy. Multiple resistant variants are generated during the combination of therapy with multiple protease inhibitors showing that the inhibitors cannot restrict resistance selection that end the drugs' antiviral activity. Five variants, obtained from patients under therapy, are resistant toward a set of six structurally diverse protein inhibitors.

Protease inhibitors, Drug resistance

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HIV-1 and HCV sequences from Libyan outbreak

Article Abstract:

Molecular phylogenetic techniques were used to analyze new sequences from outbreaks of human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection reported in children attending Al-Fateh Hospital in Benghazi, Libya. It was found that the HIV-1 and HCV strains were already circulating and were prevalent in the hospital and its environs before the arrival of the foreign medical staff that stand accused of transmitting the HIV strain to the children.

Science & research, Libya, Prevention, HIV infection in children, Pediatric HIV infections, Hepatitis C virus

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