Research conducted at the laboratory of the University of Pennsylvania, provides data to the first change in the targeted gene, which leads to the creation of genetically modified immune cells impermeable to the HIV virus.

The study focuses on the use of a technique known as targeted gene editing.

The aim is to change conformation of the CC chemokine receptor type 5 (CCR5) delta32, which represents a protein on the surface of T - cells that HIV uses to connect to and infect healthy cells.

If the protein is changed even slightly, the virus is unable to continue its development. Although the modification of the protein is not able to kill the virus, its ability to proliferate is suppressed, generally used in drugs used for treatment of patients diagnosed with HIV.

Only a small portion of the world population carries an allele that cause this conformational change in CCR5 - delta32.

Basically everyone should copy inherited from both parents, which therefore does not allow inoculation with the virus. The fact is, however, that allele is owned by only 14% of the European population and carriage in African and Asian populations is even more rare.

It is this mutation serves as inspiration for the study.

There are involved only 20 subjects diagnosed as HIV positive by 2 persons they fell, due to the very low levels of T cells.

In the remaining 18 patients, the T cells are subjected to the modification, and then monitor their response to the match, and the virus.

In 6 th patient has seen a sharp rise in resistance to the virus, which even led to the discontinuation of drug therapy.

Although immune cell lives on average about six weeks, the modified cells can be detected several months later.

These changes have not eradicated the virus from the body, and although best results patients are not cured.

Yet to be made additional tests and studies, the researchers, however, have an optimistic attitude and better predict outcome.

A powerful mixture of antibodies fighting against the AIDS virus attack pulls strong form of the virus in monkeys and then " hold off " weeks , Reuters reported , citing a research team of the U.S. government , led by researchers at Harvard University . Experts have presented findings from two studies in this direction in the journal " Nature "

Researchers found that the rare antibodies produced by 10 to 20 percent of people with HIV, such as to counteract many of the strains of the virus. Such antibodies adhere to those areas of the virus, which are critically important to him, and which are monitored in any strain of HIV. And are attached to the virus , the antibodies do unable to infect other cells.

In the past decade, scientists have tried to develop a vaccine that can cause the body to produce this type of specific antibodies to HIV , but it was quite difficult.

Scientists describe the above antibodies as Ferraris antibody indicates Dr. Dan Baruch , a professor at the Medical College of Harvard University , participated in the research.

For the purpose of both research scientists experienced antibodies on monkeys of the species rhesus infected monkey version of HIV. Rare antibodies were collected from HIV -infected people were then grown in large quantities in the laboratory and were infused in large doses to monkeys. Researchers tested various combinations of antibodies in 35 monkeys. Best working antibody called PGT 121 . Alone or with other antibodies , it gives great results.

Generally antibodies reduced the virus to very low levels in 16 to 18 monkeys within seven days, and this effect was maintained for up to three months. In three animals carry the virus, but in small quantities after treatment he did not reappear.

The effect of the antibodies to be tested on humans. Furthermore, it has not been studied in combination with antiretroviral drugs, which are the standard anti-HIV drugs, used by many thousands of patients in order to control the virus.

According to scientists, however, the combination of antibodies with antiretroviral drugs would make sense because the two treatments have different mechanisms of action. Antiretroviral drugs only attack the mechanism of HIV virus to create copies, while antibodies can directly attack the particles of the virus in blood and in cells that are infected with the virus.

It is not clear whether the antibodies can attack the dormant HIV cells that are hidden in the body and allow the virus to reappear when treatment is discontinued.

Untreated HIV infection destroys a person's immune system by killing infection-fighting cells, but precisely when and how HIV wreaks this destruction has been a mystery until now. New research by scientists at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, reveals how HIV triggers a signal telling an infected immune cell to die. This finding has implications for preserving the immune systems of HIV-infected individuals.

HIV replicates inside infection-fighting human immune cells called CD4+ T cells through complex processes that include inserting its genes into cellular DNA. The scientists discovered that during this integration step, a cellular enzyme called DNA-dependent protein kinase (DNA-PK) becomes activated. DNA-PK normally coordinates the repair of simultaneous breaks in both strands of molecules that comprise DNA. As HIV integrates its genes into cellular DNA, single-stranded breaks occur where viral and cellular DNA meet. Nevertheless, the scientists discovered, the DNA breaks during HIV integration surprisingly activate DNA-PK, which then performs an unusually destructive role: eliciting a signal that causes the CD4+ T cell to die. The cells that succumb to this death signal are the very ones mobilized to fight the infection.

According to the scientists, these new findings suggest that treating HIV-infected individuals with drugs that block early steps of viral replication -- up to and including activation of DNA-PK and integration -- not only can prevent viral replication, but also may improve CD4+ T cell survival and immune function. The findings also may shed light on how reservoirs of resting HIV-infected cells develop and may aid efforts to eliminate these sites of persistent infection.