HIV

A minority of scientists continue to question the connection between HIV and AIDS and even the very existence of HIV (see Duesberg hypothesis).

As of February 12, 2003, there were an estimated 50 700 000 worldwide HIV infections.

Pathogenesis

HIV causes disease by infecting the CD4+ T cells. These are a subset of leukocytes (white blood cells) that normally coordinate the immune response to infection. By using CD4+ T cells to replicate itself, HIV spreads throughout the body and at the same time depletes the very cells that the body needs to fight the virus. Once a HIV+ individual's CD4+ T cell count has decreased to a certain threshold, they are prone to a range of diseases that the body can normally control. These opportunistic infections are usually the cause of death.

There are several reasons that HIV is so hard to fight. First, the virus is an RNA virus, using the reverse transcriptase enzyme to convert its RNA into DNA. During that process there is a large chance of mutation. Therefore, the virus becomes quickly resistent to therapy. Second, the common notion that HIV is a killer feasting on T cells is not true. If HIV were a killer virus, it would have died out soon because there would be too little time for new infections. Now, HIV stays in the body for years, infecting people through unsafe sex and blood transfusions while the patient sometimes doesn't know. HIV can survive even when drugs kill all viruses in the blood. It integrates itself into the DNA of the host cell and can stay there for years, lying dormant, immune to all kinds of therapy because it is just DNA. When the cell divides and the DNA is copied, the virus is copied too. After years, the virus can become active again, seize the cell's machinery and replicate. In recent years, the notion that the CD4+ T cells decrease because of direct HIV infection has become doubted as well. The HIV coating protein readily detaches from virus particles. The blood becomes filled with these proteins, which can stick to the CD4+ T cells, glueing them together. In addition, they are recognized by the immune system, causing the immune cells to attack their own CD4+ cells. In summary, HIV is a guerrilla terrorist, keeping low and seeking shelter when threatened, but always ready to hit where it hurts.

Treatment

Patients today are given a complex regime of drugs that attack HIV at various stages in its life cycle. These are known as antiretroviral drugs. They include:

• Protease inhibitors[?] (PIs) inhibit activity of protease, an enzyme used directly by HIV, and so prevent virus replication.
• Reverse transcriptase inhibitors[?] (RTIs) inhibit activity of reverse transcriptase, an enzyme HIV needs to reproduce. Lack of this enzyme prevents HIV from building RNA and DNA. They come in three forms:
  • Nonnucleoside reverse transcriptase inhibitors[?] (NNRTIs)
  • Nucleoside analog reverse transcriptase inhibitors[?] (NARTIs or NRTIs)
  • Nucleotide analog reverse transcriptase inhibitors[?] (NtARTIs or NtRTIs)
• Entry inhibitors[?] inhibit the viral entry into the cell interacting directly with the viral receptor and avoiding the fusion of the viral membrane with the target cell membrane.

Many problems are involved in establishing a course of treatment for HIV. Each effective drug comes with side effects, often serious and sometimes life-threatening in themselves. Common side effects include extreme nausea and diarrhea, liver damage and failure, and jaundice. Any treatment requires regular blood tests to determine continued efficacy (in terms of T-cell count and viral load) and liver function.

See also : OraQuick, List of HIV patients