Last month, researchers fromSouth Africa's KwaZulu Natal, Oxford and Harvard universities announced the results of a collaborative study designed to explore in greater depth the interaction between Human Immunodeficiency Virus (HIV) and the immune system. The results, published in the scientific journal Nature, identify a gene which is involved in combating the virus.

HIV is dangerous, attacking the very heart of the body's ability to resist infection. This leaves sufferers weak and susceptible to a range of opportunistic diseases, which take advantage of the feeble state of the body's defences leading to Acquired Immune Deficiency Syndrome (AIDS).

Like all viruses, HIV cannot replicate single-handedly. It requires a host cell from which it can multiply and spread. Inside the body, white blood cells are responsible for dealing with invading viruses like HIV. Cruising around in the bloodstream, their task is to identify, attack and destroy any cells they encounter which the virus has infected.

HIV targets specialised white blood cells known as 'CD4' cells. After injecting genetic material into a CD4 cell, the virus hijacks the machinery of the CD4 cell to make many copies of itself, killing the host CD4 cell in the process. Once the resources of the host are used up and the CD4 cell is dead, the virus moves on to a new cell. As more of the CD4 white blood cells die, a victim becomes weak and increasingly prone to other infections which capitalise on the diminished ability of the body to fight off attack.

Although the virus is a killer in most people, a tiny minority of HIV positive individuals exhibit immunity to its effects. They live as carriers, completely free of symptoms, and have immune systems which can control the virus. During this control phase, HIV is constantly mutating to change the way it looks. Attempting to avoid the immune resistance of the body, they are analogous to a guilty criminal on the run drastically altering a hairdo or changing their appearance in another way to deceive pursuers.

People with such immunity possess advantages which enable them to combat a marauding HIV infection more effectively than others. They can detect and react to changes in the virus, whereas the immune systems of others fail to keep track of what HIV looks like as it mutates. Researchers found that the battle for supremacy between the immune system and HIV in these people is occurring far faster with HIV than for other viruses - the body is adapting rapidly to the makeovers of HIV and recognising the new disguises, and HIV is in turn altering itself quickly to evade the immune defences.

HIV detection is achieved using molecules called HLAs (Human Leukocyte Antigens). One particular group of HLAs, consisting of 3 types of molecule, is vital in the identification of HIV and other viruses. HLAs are located on the surfaces of certain body cells. If HIV infects a cell, the HLAs display tiny fragments of chopped-up virus at the cell surface. Another type of white blood cell known as a T 'killer' cell then recognises the sign that the HLA is sending out; realising that the body cell is infected, the T killer cells destroy it.

The data for this investigation was collected from South Africa, which suffers more HIV infections than any other nation. It showed that of the 3 HLAs involved in HIV recognition, type 'B' HLAs performed much better than the other two HLA types at showing killer T cells which body cells were infected with HIV. To use an example if the HLAs were lamps then the type 'B' HLAs would be the brightest and would attract the most attention of moths (killer T cells).

The ability to control HIV infection, and therefore the speed of progression to AIDS, furthermore depends on what subtype of HLA 'B' an individual has - this is determined by the HLA 'B' gene that an individual possesses.

Although genetic links to HIV infection resistance can be predicted, the vital knowledge is establishing exactly which genes are involved. Searching for the right genes is difficult, but now scientists can start looking in the right place to obtain a more detailed understanding of how genetic resistance to HIV works.

Currently, antiretroviral drugs are the main weapons in the arsenal against HIV. By disrupting the viral life cycle, they delay immune deterioration and the onset of AIDS. Antiretroviral drugs are prescribed in complex combinations, and inhibit enzymes that play key roles in the HIV life cycle to impede the spread of HIV through the body. The process of administering the drugs in combination may change; two weeks after this research was published, the pharmaceutical titan GlaxoSmithKline (GSK) announced that it has received EU consent to promote a new drug against HIV called Kivexa. GSK are marketing Kivexa as the first integrated HIV medication to be created - taken as one pill daily with no food or fluid requirements, Kivexa comprises two antiretroviral drugs in the same tablet.

Vaccines are seen as the ultimate solution to stopping HIV proliferation, but no such vaccine exists as yet. Given its ability to change frequently, HIV is a difficult virus against which to construct a vaccine. Design is also held back by ethical questions about methods of development and testing of vaccines. Scientists are looking at different types of vaccine to raise the immune responses of people to HIV infection.

Traditional vaccines work by injecting material from dead or harmless fragments of infectious microorganisms, causing the immune system to produce antibodies to fight back. Other vaccines stimulate immune cells in the body to deal with viruses in other ways. For example, a potential HIV vaccine might not be able to actually prevent infection, but once HIV is in the body it could stop progression to full-blown AIDS.

The main researcher in the group that made the findings was Dr Philip Goulder, a paediatrician working at Oxford University. Commenting on the results on the University website, he emphasized the importance of continuing scientific studies into HIV.

"This study identifies the genetic battleground where the struggle between HIV and the human immune response occurs. The findings will help in understanding precisely how the immune system can succeed or fail against HIV, a prerequisite for a rational approach towards the design of an HIV vaccine."