Seja bem vindo, Thomas! Talvez possamos utilizar esses novos conhecimentos nos projetos do FAAH no futuro. Thank you.

http://www.sciencedaily.com/releases/2013/09/130912143210.htm

Molecular Structure Reveals How HIV Infects Cells

Sep. 12, 2013 — In a long-awaited finding, a team of Chinese and US scientists has determined the high-resolution atomic structure of a cell-surface receptor that most strains of HIV use to get into human immune cells. The researchers also showed where maraviroc, an HIV drug, attaches to cells and blocks HIV's entry. [...]

The CCR5 receptor is one of the most sought-after targets for new anti-HIV drugs. Although the AIDS-causing virus was initially discovered to infect cells via another receptor, CD4, researchers found in 1996 that HIV infection also requires a co-receptor -- usually CCR5, which sits alongside CD4 on a variety of immune cells.

CCR5's importance to HIV infection is underscored by the fact that certain genetic variants of it can dramatically raise or lower HIV infection risk, as well as the speed of the disease process after infection. One shortened CCR5 variant, found in about 10 percent of Europeans, is not expressed at all on immune cell surfaces -- and people who produce only this variant are almost invulnerable to HIV infection.

Scientists therefore have sought to develop anti-HIV drugs that block the virus from binding to CCR5 or otherwise render the receptor inactive. [...] A minority of HIV strains use CXCR4 instead of CCR5 as a co-receptor with CD4 for their initial infiltration of cells. [...] As in most receptor-structure projects, Wu and her colleagues further stabilized CCR5 with a compound that is known to bind to it, in this case the Pfizer drug maraviroc (sold under the brand name Selzentry® or Celsentri® outside the US). Marketed for HIV infection since 2007, maraviroc grabs hold of CCR5 in a way that prevents HIV from using the receptor to get into cells. [...]

The resulting crystallography data provided that fine-grained picture of CCR5's HIV-resistant conformation. The data also revealed maraviroc's precise binding site on CCR5 -- a site from which the drug molecule clearly influences how the receptor works, even though it is separate from the sites on the receptor that are thought to be used by HIV. The maraviroc binding site is also different from the site used by CCR5's natural binding-partners, a set of immune proteins called chemokines. Maraviroc thus appears to work against HIV indirectly -- not by physically blocking the virus, but by locking the receptor structure into an HIV-insensitive conformation. [...]

Comparison of the CCR5 structure with the previously determined CXCR4 structure also provided hints about an important aspect of HIV evolution during infections. Most HIV infections start by using only CCR5 as a co-receptor for cell entry, but in time the virus often switches its co-receptor usage from CCR5 to CXCR4. That opens up more cell types to HIV infection, and the further spread of the virus inside the body is liable to speed up the disease progression towards full-blown AIDS and death.

The new data suggest that the distinction between CCR5 and CXCR4 as co-receptors for HIV infection boils down to relatively subtle differences in structural shapes and electric charge distributions in the HIV binding region -- differences that will be of interest to HIV drug developers. "Knowing the CXCR4 structure and now the CCR5 structure at this level of detail should accelerate the development of drugs that can block HIV by using both of these co-receptors," said Wu. [...]

http://www.gizmag.com/hiv-aids-vaccine-ohsu/2...362bd-f91328a98f-90441497

I guess this the same news about the vaccine. But easier to understand...
I like gizmag...

Thanks so much Safak
Effectively, it's much more clear in this article
Here's the correctly popularized science and thus made understandable for the neophyt
This vaccine is really carrier of hope
Let us hope that his declension to the man will be so much successful

http://www.sciencedaily.com/releases/2013/09/130918132448.htm

"Sep. 18, 2013 — A team of researchers led by King's College London has for the first time identified a new gene which may have the ability to prevent HIV, the virus that causes AIDS, from spreading after it enters the body.

Published in Nature today, the study is the first to identify a role for the human MX2 gene in inhibiting HIV. Researchers say this gene could be a new target for effective, less toxic treatments where the body's own natural defence system is mobilised against the virus."