Major AIDS breakthrough; No one cares.. TMO CHEATS

[Langrisserx]

More than one happening whilst u twiddle ur pixels... be glad for the singularity.




http://www.washingtonpost.com/nation...02c_story.html

Scientists have speculated that the virus-producing infected cells become so full of the virus they were producing that they die. Or they realize something was very wrong, and perform a clean programmed cell death called apoptosis.

The deaths of these CD4 T-cells are offset by the body producing more of them in response. But after a while, the body can’t keep up, and the T-cell count drops leading to the onset of AIDS. Then, diseases that used to be easy to fend off can take over.

“It’s really a race between production and destruction,” said Fauci.

For 30 years, scientists have thought that AIDS was brought on solely by the virus-producing infected cells, rather than the resting cells. But there weren’t enough of these infected cells to explain the huge swaths of T-cells being wiped out in patients developing AIDS.

“It is much more a cellular suicide than a viral murder,” said Greene. “The cells are committing suicide in a vain attempt to kill the virus.”

Because of its explosive and messy nature, pyroptosis is a good way of signalling to the troops to help clean up. But inflammation of these cells during death causes the new cells to fall to the same grim fate.

“This process just becomes a gristmill for chewing up CD4 cells,” Greene said.

From there, they wanted to find the molecule that was the pyroptosis instigator. The team analyzed the DNA of the resting CD4 T-cells using a technique called mass spectroscopy to find every protein that was bound to it. From the original laundry list of proteins, they picked the most likely candidates and progressively knocked out each one in newly made T-cells to tease out what each protein did. When they knocked out one in particular, IFI16, the cells no longer self-destructed.




http://www.tgdaily.com/general-scien...us-replicating
http://onlinelibrary.wiley.com/doi/1...09856/abstract


Bilaterally substituted p-terphenyl molecules reproduce the interactions of an α-helix of the HIV-1 protein Rev with its RNA receptor and block Rev function and virus replication. In their Communication on page 13405 ff., J. Alcamí, S. Fustero, and J. Gallego et al. report the structure-based design of p-terphenyl molecules that inhibit the Rev-mediated transport of HIV-1 RNA from the nucleus to the cytoplasm by binding to the RNA loop that is recognized by Rev