HIV Structure and Function
The mature virus consists of a bar-shaped electron dense core containing the viral genome--two short strands of ribonucleic acid (RNA) about 9200 nucleotide bases long--along with the enzymes reverse transcriptase, protease, ribonuclease, and integrase, all encased in an outer lipid envelope with 72 surface projections containing an antigen, gp120, that aids in the binding of the virus to the target cells with CD4 receptors. By electron microscopy, the plasma membrane of an infected CD4+ lymphocyte exhibits budding virus particles approximately 90 to 100 n in diameter. The genome of HIV, similar to retroviruses in general, contains three major genes--gag, pol, and env.
The major structural components coded by env include the envelope glycoproteins, including the outer envelope glycoprotein gp120 and transmembrane glycoprotein gp41 derived from glycoprotein precursor gp160. Major components coded by the gag gene include core nucleocapsid proteins p55, p40, p24 (capsid, or "core" antigen), p17 (matrix), and p7 (nucleocapsid); the important proteins coded by pol are the enzyme proteins p66 and p51 (reverse transcriptase), p11 (protease), and p32 (integrase). Although most of the major HIV viral proteins, which include p24 (core antigen) and gp41 (envelope antigen), are highly immunogenic, the antibody responses vary according to the virus load and the immune competence of the host. The antigenicity of these various components provides a means for detection of antibody, the basis for most HIV testing.
HIV has the additional ability to mutate easily, in large part due to the error rate of the reverse transcriptase enzyme, which introduces a mutation approximately once per 2000 incorporated nucleotides. This high mutation rate leads to the emergence of HIV variants within the infected person's cells that can resist immune attack, are more cytotoxic, can generate syncytia more readily, or can resist drug therapy. Over time, different tissues of the body may harbor differing HIV variants.
The transmission of HIV-2 is similar to that for HIV-1, though perinatal transmission is much less frequent. HIV-2 infection has a longer latent period before the appearance of AIDS, a less aggressive course of AIDS, and a lower viral load with higher CD4 lymphocyte counts than HIV-1 infection until late in the course of the disease when clinical AIDS is apparent. This may explain the limited spread of HIV-2, both in West African countries and elsewhere, due to less efficient transmission, particularly via heterosexual and perinatal modes. The mortality rate from HIV-2 infection is only two-thirds that for HIV-1.
The major structural components coded by env include the envelope glycoproteins, including the outer envelope glycoprotein gp120 and transmembrane glycoprotein gp41 derived from glycoprotein precursor gp160. Major components coded by the gag gene include core nucleocapsid proteins p55, p40, p24 (capsid, or "core" antigen), p17 (matrix), and p7 (nucleocapsid); the important proteins coded by pol are the enzyme proteins p66 and p51 (reverse transcriptase), p11 (protease), and p32 (integrase). Although most of the major HIV viral proteins, which include p24 (core antigen) and gp41 (envelope antigen), are highly immunogenic, the antibody responses vary according to the virus load and the immune competence of the host. The antigenicity of these various components provides a means for detection of antibody, the basis for most HIV testing.
HIV has the additional ability to mutate easily, in large part due to the error rate of the reverse transcriptase enzyme, which introduces a mutation approximately once per 2000 incorporated nucleotides. This high mutation rate leads to the emergence of HIV variants within the infected person's cells that can resist immune attack, are more cytotoxic, can generate syncytia more readily, or can resist drug therapy. Over time, different tissues of the body may harbor differing HIV variants.
HIV-2
A second HIV designated HIV-2 has been isolated. Most cases have appeared in West Africa and have appeared only sporadically in other parts of the world. The genetic sequences of HIV-1 and HIV-2 are only partially homologous. HIV-2, or other as yet uncharacterized members of the HIV-group of viruses, will not necessarily be detected by using the various laboratory tests for HIV-1 antibody. HIV-2 is genetically more closely related to simian immunodeficiency virus (SIV) than HIV-1.The transmission of HIV-2 is similar to that for HIV-1, though perinatal transmission is much less frequent. HIV-2 infection has a longer latent period before the appearance of AIDS, a less aggressive course of AIDS, and a lower viral load with higher CD4 lymphocyte counts than HIV-1 infection until late in the course of the disease when clinical AIDS is apparent. This may explain the limited spread of HIV-2, both in West African countries and elsewhere, due to less efficient transmission, particularly via heterosexual and perinatal modes. The mortality rate from HIV-2 infection is only two-thirds that for HIV-1.
