During sexual transmission, the virus penetrates the thin, moist surface of the vagina, urethra or rectum of another person during sex. Special protective white cells called macrophages usually patrol just beneath these surfaces and usually protect against invading organisms. Unfortunately, HIV is able to infect these exact defender cells or macrophages, which then carry the virus into the blood circulation.

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Once in the blood, the virus spreads throughout the body and has access to another type of white cell, called a T-helper lymphocyte. HIV gets into these cells by attaching to a specific protein on their surface, known as CD4 (so these cells are also called CD4 cells). T-helper lymphocytes circulate in the blood, but most of them are found in the lymph glands, where they stimulate other cells of the immune system to go into action.

In addition to the CD4 receptor, another co-receptor is required for the HIV virus to enter the CD4 cell successfully. The co-receptors are called CCR5 and CXCR4 and are also protein markers on the surface of these types of cells. Certain people have genetically defective CCR5 receptors that make them relatively resistant to HIV infection. CCR5 defects are more common in Northern European populations but unfortunately are not common in South Africans.

HIV multiplies best inside T-helper lymphocytes and the infected lymphocytes eventually deteriorate and die, releasing more viruses to infect new lymphocytes.

The virus takes about two weeks to start multiplying efficiently in the body. At about three weeks after infection the immune system will recognise the "invasion" and start to produce antibodies to HIV. The battle between the virus and the immune response causes the symptoms of the seroconversion illness when antibodies are produced. Amazingly, the immune system will get the upper hand at this stage and limit multiplication of the virus, so that symptoms resolve in a week or two. Thereafter most people will have partial control over the virus with no symptoms of HIV infection for several years, 10 on average.

However, the virus hides out in an individual's lymphocytes and slowly but surely evades the control measures of the immune system, mostly because it is genetically changeable and therefore keeps presenting a new appearance to the immune system which cannot keep up with the virus. All this time T-helper cells are not functioning properly or are destroyed whenever the virus multiplies. Initially the body is able to replace the T-helper cells as fast as they are destroyed and there is no significant effect on their numbers. However, after several years the body's ability to replace the T-lymphocytes begins to fall off. T-helper cells play a crucial part in the proper functioning of the immune system and the depletion of these cells drastically reduces the effectiveness of the immune system.

AIDS is first diagnosed when an HIV-positive person gets a characteristic opportunistic infection or an AIDS-related tumour. Very common opportunistic infections in AIDS are Pneumocystis carinii pneumonia (PCP) now known as Pneumocystis jerovici pneumonia and tuberculosis (TB), which can even occur in sites in the body outside the lungs, bones or gut. The common tumours in AIDS are Kaposi's sarcoma, usually visible in the skin, and certain tumours of the lymph glands (lymphoma). Infection of the brain by HIV itself or other viruses and certain types of parasites, can cause dementia and stroke-like problems.

Some people progress to AIDS quickly within two years, whereas others remain symptom-free for 15 years or more. This latter group of people are known as "long-term non-progressors" and scientists are very interested in what advantage they have for withstanding HIV. In developing countries, where people may be malnourished and have many other illnesses to contend with as well, HIV disease tends to progress to AIDS more quickly than the 10-year average for people living in the better circumstances of the developed world.

Reviewed by Dr Craig Corcoran, Clinical Virologist, National Health Laboratory Service and University of Cape Town, October 2006.

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