The molecular biology of human immunodeficiency virus type I infection

Article Abstract:

Infection with human immunodeficiency virus type 1 (HIV-1) causes AIDS, a fatal disease that has been diagnosed in more than 132,000 people in the US alone. Many more are infected with HIV-1; predictions place the number of these people at 15 to 20 million worldwide by the year 2000. The virus is transmitted by sexual contact, exposure to infected blood or blood products, and from mother to child; more than 60 percent of all cases involve heterosexual transmission. Effective drug treatments will depend on learning more about HIV and the ways it infects its host. A review is presented of current knowledge related to the molecular biology of the infection. HIV is a lentivirus (a class of viruses that cause slowly-developing infections) of the retrovirus family (viruses that copy their RNA into DNA, which is then inserted into the host genome). Besides causing characteristic symptoms (nervous system involvement, weak immune responses), lentiviruses have complex viral genomes. The viral structure is depicted and described. Its life cycle, from infection of host CD4-positive T cells (immune system cells), the main viral target, and other immune system cells, is described. The steps covered include: attachment of the virus to host cells; internalization into the cell; transcription of viral RNA and integration of DNA into the host cell; the latent period, when the HIV-1 infection may lie dormant; late and early expression of the aberrant genes; and construction of new viral particles. The ways HIV-1 kills and damages cells are not understood; hypotheses are briefly listed. Development of an HIV-1 vaccine has been hindered by the structural variability in one of the proteins that form the viral envelope (coat); however, recent developments in research concerning SIV-1 (simian immunodeficiency virus, type 1) are more encouraging. An effective vaccine should induce an immune response from both the cellular (T cell) and humoral (B cell) components. A great deal of basic information has been gathered about HIV-1 in a short time; the task now is to develop ways of halting the disease it causes. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Development and progression, HIV infection, HIV infections, Genetic aspects, Viral genetics

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Denying HIV safe haven

Article Abstract:

The replication of HIV inside T cells appears to be dependent on T cell activation. A 1996 study found that vaccinating HIV-infected people with tetanus toxoid caused blood levels of HIV to increase. In addition, blood cells from healthy people were more easily infected with HIV after the volunteers were vaccinated with tetanus toxoid. When HIV infects a resting T cell, the virus does not completely convert its RNA into DNA. The incomplete DNA transcripts are then destroyed by the cell. Activation of the T cell causes an increase in the levels of deoxynucleotides, which are used by the virus to transcribe its RNA. The drug hydroxyurea can reduce the level of these deoxynucleotides and this has been shown to reduce HIV replication. Giving HIV-positive people immunosuppressive drugs early in the infection could also reduce T cell activation and thereby block HIV replication. However, these drugs could also abolish the immune response to the virus.

Editorial, Virus replication

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T-cell function and migration: two sides of the same coin

Article Abstract:

A review of T cell movement is discussed, focusing on how T cells find antigens and destroy infectious organisms, how some organisms can evade the immune system, and why T cells sometimes attack the body's own tissues. Insights into T cell migration can be used to design effective treatments for many diseases.

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