"Molecule-Abridora" of HIV exposes the most vulnerable parts of the virus; which means a "possible development of a vaccine. "

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Highlights First Half 2015 Immune System | CD4 and CD8
Can Opener merely illustrative
An old example of an opener. In this case, cans

By testing a newly developed molecule, JP-III-48, on patient blood samples HIV-positives, researchers at the University of Montreal, Canada observed something innovative. The molecule had the ability to open HIV "like a flower." Although this finding is still in its early stages, the team hopes they can define a basis for new preventive measures and possibly even a way to eliminate the virus from people. already infected with HIV.

Part of the reason scientists find difficulty in creating a vaccine for HIV is that the virus has a unique way of escaping the immune system. Although the host creates antibodies against HIV, there is no way to physically reach the virus, it is difficult for the human body to mount an effective immune response against it. A study recently published by National Academy of Sciences, suggests a way around HIV defenses.

The virus is similar to a hermetically sealed package. Finding a way to "open" HIV would allow antibodies to reach more vulnerable regions of the virus and thus eliminate infection.

Harvard and the University of Pennsylvania researchers developed JP-III-48, but in Montreal, Canada, researchers were the first to successfully test HIV-positive patients. The molecule mimics the CD4, a protein located on the surface of T lymphocytes. The CD4 protein, which gives its name to the specific cells of the immune system that HIV infects, functions as a gateway to T cells and allows HIV to enter and infect cells. It was in Montreal the first study in which researchers added the JP-III-48 molecule to patients infected with HIV-1 (the most common form of the virus) and witnessed the "opening of viral structures like flowers".

"The addition of the small viral molecule involves the forces necessary to open the virus like a flower," said study author Jonathan Richard, explaining in a Press release. The molecule forces the virus to expose the parts that are recognized by the host's antibodies. The antibodies then create a kind of bridge with some cells in the immune system and form an attack. "Antibodies that are naturally present after infection can target cells infected by the virus so that they are killed by the immune system," added Richard.

HIV virus
Graphical representation of “open” HIV.

So far, the effects of the JP-III-48 molecule on HIV have only been seen in the serum of HIV-positive patients, but the researchers hope that soon the test of this "opening molecule" in primates with a simian version of the virus.

Researchers speculate that this finding could have huge potential for research into developing an HIV / AIDS vaccine.AIDS. Another factor that makes the fight against HIV so difficult is that even if the virus is completely eliminated from the bloodstream, there are still latent traces of HIV in reservoirs, waiting to return as soon as treatment ceases.

The team believes that the "molecule-opener" can play an important role in overcoming this viral defense. If scientists can develop a form of “shock patrol” against viruses, in order to force them to leave their reservoirs they can be killed using the “opening molecule” as in the strategy explained at the beginning of this article, using antibodies that the organism is capable of generating.

Claudius el guapissimoTranslated by Cláudio Souza, from the original English of Medical Daily website, at the link: http://www.medicaldaily.com/hiv-can-opener-molecule-exposes-viruss-most-vulnerable-parts-what-it-means-vaccine-331996#.VUqNhvtgMsk.google_plusone_share

Is this stuff fills your heart with hope? Read this and connect the dots 🙂 🙂 pontos Scientists say they are on the verge of finding a cure for HIV infection and the AIDS vaccine

Source of the original article:

Source: Richard J, Veillette M, Brassard N, et al. CD4 mimetics sensitize HIV-1-infected cells to ADCC. PNAS 2015.

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