In a breakthrough that could potentially lead to a cure for HIV infection, scientists have discovered a way to remove the virus from infected cells, a study released Thursday said.

The scientists engineered an enzyme which attacks the DNA of the HIV virus and cuts it out of the infected cell, according to the study published in Science magazine.

The enzyme is still far from being ready to use as a treatment, the authors warned, but it offers a glimmer of hope for the more than 40 million people infected worldwide.

"A customized enzyme that effectively excises integrated HIV-1 from infected cells in vitro might one day help to eradicate (the) virus from AIDS patients," Alan Engelman, of Harvard University's Dana-Farber Cancer Institute, wrote in an article accompanying the study.

Current treatments focus on suppressing the HIV virus in order to delay the onset of AIDS and dramatically extend the life of infected patients.

What makes HIV so deadly, however, is its ability to insert itself into the body's cells and force those cells to produce new infection.

"Consequently the virus becomes inextricably linked to the host, making it virtually impossible to 'cure' AIDS patients of their HIV-1 infection," Engelman explained.

That could change if the enzyme developed by a group of German scientists can be made safe to use on people.

That enzyme was able to eliminate the HIV virus from infected human cells in about three months in the laboratory.

The researchers engineered an enzyme called Tre which removes the virus from the genome of infected cells by recognizing and then recombining the structure of the virus's DNA.

This ability to recognize HIV's DNA might one day help overcome one of the biggest obstacles to finding a cure: the ability of the HIV virus to avoid detection by reverting to a resting state within infected cells which then cease to produce the virus for months or even years.

"Numerous attempts have been made to activate these cells, with the hope that such strategies would sensitize the accompanying viruses to antiviral drugs, leading to virus eradication," Engelman wrote. "Advances with such approaches in patients have been slow to materialize."

New experiments must be designed to see if the Tre enzyme can be used to recognize these dormant infected cells, he wrote.

"Although favorable results would represent perhaps only a baby step toward eventual use in patients, the discovery of the Tre recombinase proves that enzymatic removal of integrated HIV-1 from human chromosomes is a current-day reality," he said.

The researchers who developed the enzyme were optimistic about their ability to design additional enzymes which would target other parts of the virus's DNA.

However they warned that there were significant barriers to overcome before the enzyme could be used to help cure patients.

"The most important, and likely most difficult, among these is that the enzyme would need efficient and safe means of delivery and would have to be able to function without adverse side effects," wrote lead author Indrani Sarkar of the Max Planck Institute for Molecular Cell Biology and Genetics in Dresden.

"Nevertheless the results we present offer an early proof of principal for this type of approach, which we speculate might form a useful basis for the development of future HIV therapies," Sarkar concluded.

A popular theory on how HIV attacks the body's immune system is wrong, a new study has found.

Scientists have long believed that HIV causes the slow depletion of healthy white blood cells -- the T cells which recognize infections so the body can fight them off -- by causing infected T cells to produce virus particles before dying.

This ongoing cycle of infection, HIV production, reinfection and cell destruction has been called the "runaway" hypothesis.

But if this were so, the T cells would be killed off far too quickly, the researchers found.

Using a simple mathematical model, researchers in the United States and Britain showed the "runaway" model would deplete the body's healthy T cells in a matter of months, instead of the years it actually takes.

The results show that a "slow process must be active" in the depletion of the T cells, the authors wrote in the current issue of the journal PLoS Medicine.

Identifying this process "will provide a key insight into the nature of HIV disease and indicate potential new approaches to therapy," they concluded.

A potential explanation for the slow process could be that the virus slowly adapts over the course of the infection, the authors said.

"The virus is constantly mutating and there may be selection - in a Darwinian sense -- over time for 'fitter' mutants of the virus in an infected person," said lead author Andrew Yates of Emory University in Atlanta, Georgia.

"There are several ways the virus could become fitter - for example by being able to infect new cells more readily, or by infected cells producing more new virus, or producing it more rapidly," he said in an e-mail interview.

"The virus adaptation hypothesis requires a lot more experimental investigation, however, and is only a tentative conclusion."

Conflict, wide-scale rape and mass displacement of people in sub-Saharan Africa do not necessarily lead to a higher rate of HIV/AIDS, the United Nations refugee agency said on Friday.

Contradicting a "common belief" of such a link, a new study by the UN High Commissioner for Refugees (UNHCR) said that out of 12 refugee camps where HIV prevalence was surveyed, nine actually had a lower rate than surrounding host communities.

The study, led by Paul Spiegel of the UNHCR's Public Health and HIV section, looked at population data in the Democratic Republic of Congo, southern Sudan, Rwanda, Uganda, Sierra Leone, Somalia and Burundi.

"Data from these countries did not show an increase in prevalence of HIV infection during periods of conflict, irrespective of prevalence when conflict began," said the study, which was published in British medical journal The Lancet.

"Although every occurrence of rape is abhorrent and could increase an individual's risk of contracting HIV infection, there are no data to show that wide-scale rape raised the overall prevalence of infection" in the seven countries surveyed, it added.

There is also no evidence that refugees exacerbate the HIV epidemic in host communities, the report said.

UNHCR spokesman Ron Redmond stressed however that the findings did not mean the agency was taking a complacent attitude towards the problem.

"This does not mean that conflict in all countries would mean lower HIV infection than non-conflict countries... Nor should the findings be interpreted to mean we shouldn't worry about HIV or rape in conflict," he told journalists.

Mass killings, forced displacement and hiding from conflict can all lower the level of infections and consensual sexual encounters, and reduce social networks in which individuals might be exposed to HIV.

Moreover, most refugees tend to come from rural areas where HIV is lower than in urban areas, the report noted.

Spiegel and the other authors did stress the study's limitations, however, saying it was "restricted by the nature and quality of the work in displaced populations and countries affected by conflict."

More research is needed among people displaced by conflict and the host communities where they find refuge in order to fully explain the nature of HIV transmission in such environments, they concluded.