Could Herpes Speed Up AIDS?

Jun 10

A common herpes virus could hasten the onset of AIDS in HIV-positive people by helping HIV to attack the immune system. The claim comes from the group of Researchers.

The findings do not change the picture of HIV as a cause of AIDS. Some Researchers had claimed that HIV alone does not because AIDS and that another agent is necessary for the virus to harm the body. Such claims have been widely discounted by evidence from animal studies.

It is still believed that HIV is the necessary factor and root cause of AIDS. But it may be that in some people the disease could be caused by co-factors.

Scientists have often suggested that the human herpes virus 6 might be such a co-factor, but there has been no proof of the claim. HHV-6, a member of the class of herpes viruses that includes herpes simplex type 1 and Epstein-Barr, is very common: at least 70 per cent of the population have antibodies to it. This has made it impossible to tell whether it affects the course of disease in HIV-positive people because it is being found everywhere.

Researchers that cultured T cells infected with HHV-6 (but not HIV) produce dramatically larger amounts of CD4 than normal. CD4 is the molecule that is the main receptor for HIV on cells. More importantly, they have also found that HHV-6 seems to induce certain other T cells, which normally lack CD4, to make the molecule. This increases the number of cells that are vulnerable to contagion through HIV.

This seems to be a new and peculiar virus to virus reaction; one virus is regulating the expression of the receptor for the other. HHV-6 seemed to be inducing genes in the T cells to switch on, probably at an early stage in infection. The team tested other herpes viruses and found no such effect, which suggests that it is specific to HHV-6.

So far, the only evidence comes from the behaviour of cells in the laboratory. Studies in people and animals will be necessary to confirm the importance of the results.

HIV’s main targets in the immune system are a type of T cell, often known as T-helpers but more accurately described as CD4-positive, as they have the receptor on their surface. Another family of T cells called cytotoxic T or killer T cells, lack CD4 and have another molecule, CD8 which distinguishes them. These are not normally susceptible to HIV.

The team found that cloned and purified CD8-positive cells, which produce no CD4, began to produce CD4 in the presence of HHV-6. They measured the amount of the molecule using standard techniques of immunofluorescence and fluorocytometry. The number of CD4-positive cells in the culture correlated well with the number expressing antigens to HHV-6.

Finally the team exposed CD8-positive cells infected with HHV-6 to HIV. As a control, cells uninfected with HHV-6 were also exposed to HIV. After repeated washing, the team detected genetic material from HIV in the infected cells but not in the uninfected cells.

To find out how important HHV-6 really is in people with HIV, the scientists need to study its effects in humans.

No one exactly knows how genes govern the expression of CD$ and CD* on mature T cells, but as the immature T cells in the thymus possess both receptors; all cells must have the genetic potential to produce both CD4 and CD8.

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