Yep, this seems to be a very important research as current drugs to halt the spread of the HIV on infected individuals can't reach such dormant ones and, once solved this puzzle, AIDS might reach its cure.

Regards,


Dan60

An old article dating back to 2003 but may be of significance in light of a very recent discovery which is also included in this post

http://www.jleukbio.org/content/74/5/821.short

"Human immunodeficiency virus type 1 (HIV-1) Nef activates STAT3 in primary human monocyte/macrophages through the release of soluble factors: involvement of Nef domains interacting with the cell endocytotic machinery

Increasing evidence indicates that the expression of the human immunodeficiency virus-1 (HIV-1) Nef protein significantly influences the activation state of the host cell. Here we report that Nef specifically activates STAT3 in primary human monocyte-derived macrophages (MDM). This was demonstrated by both single-cycle infection experiments driven by Vesicular Stomatitis virus glycoprotein (VSV-G) pseudotyped HIV-1 and treatment with exogenous recombinant Nef. The analysis of the effects of Nef mutants revealed that domains of the C-terminal flexible loop interacting with the cell endocytotic machinery are involved in the STAT3 activation. In particular, our data suggest that the Nef-dependent STAT3 activation relies on the targeting of Nef to the late endosome/lysosome compartment. In addition, we found that Nef activates STAT3 through a mechanism mediated by the release of soluble factor(s), including MIP-1α, that requires de novo protein synthesis but appears independent from the activation of src tyrosine kinases. The results presented here support the idea that the first intervention of Nef in the intracellular signaling of monocyte-macrophages could generate, by means of the release of soluble factor(s), a secondary wave of activation that could be of a potential pathogenetic significance."

http://www.medicalnewstoday.com/articles/206044.php

"Article Date: 29 Oct 2010

Promising New Compound Could Aid Fight Against Cancer -- Trials Could Be A Year Away
A promising cancer-fighting compound could be a year away from clinical trials thanks to a licensing agreement announced this month.

The University of Central Florida and Moffitt Cancer Center signed an agreement with GLG Pharma, LLC to take the compound to the next level of development and perhaps someday to use it against a variety of cancers, including breast cancer.

UCF Associate Professor James Turkson and a team at Moffitt Cancer Center co-developed GLG-302, a compound that has been shown to prevent the uncontrolled activity of the STAT3 protein. This protein, when hyperactive, has been implicated in human cancer, particularly breast cancer...

In addition to its involvement in cancer cells, hyperactivated STAT3 is also involved in immune cells. The body's immune system is tricked by the abnormally active STAT3 into thinking the tumor cells are harmless. In the presence of our compound, the immune system should recognize that something is wrong, re-activate, recognize that remaining cancer cells are harmful and destroy them..."

Aids immunity mystery may be solved

http://www.eurekalert.org/pub_releases/2010-11/rumc-dih111810.php

"18-Nov-2010

Discovery in how HIV thwarts the body's natural defense opens up new target for drug therapies
CHICAGO -- Natural killer cells are major weapons in the body's immune system. They keep the body healthy by knocking off tumors and cells infected with viruses, bombarding them with tiny lethal pellets. But natural killer cells are powerless against HIV, a fact that has bedeviled science for over 20 years.

Now, researchers at Rush University Medical Center have discovered the reason why..."

http://www.eurekalert.org/pub_releases/2010-11/chb-dme111910.php

"19-Nov-2010

Designing more effective anti-HIV antibodies
Trapping a shape change during the infection process could lead to new vaccine strategies

Boston, Mass. – Although people infected with HIV produce many antibodies against the protein encapsulating the virus, most of these antibodies are strangely ineffective at fighting the disease. A new study suggests why some of the most common of these antibodies don't work: they target the protein in a form it takes after the virus has already invaded the cell, when it's too late, report researchers at Children's Hospital Boston and their colleagues..."