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World Community Grid Forums
Category: Completed Research
Forum: FightAIDS@Home Phase 2
Thread: Interesting news articles about HIV / AIDS |
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Thread Status: Active Total posts in this thread: 55
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Jim Slade
Veteran Cruncher Joined: Apr 27, 2007 Post Count: 664 Status: Offline Project Badges: 
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First New HIV Vaccine Efficacy Study in Seven Years Has Begun
South Africa Hosts Historic NIH Supported Clinical Trial The first HIV vaccine efficacy study to launch anywhere in seven years is now testing whether an experimental vaccine regimen safely prevents HIV infection among South African adults. The study called HVTN 702, involves a new version of the only HIV vaccine candidate ever shown to provide some protection against the virus. HVTN 702 aims to enroll 5,400 men and women, making it the largest and most advanced HIV vaccine clinical trial to take place in South Africa, where more than 1,000 people become infected with HIV every day. http://blog.aids.gov/2016/11/first-new-hiv-va...even-years-has-begun.html  |
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Seoulpowergrid
Veteran Cruncher Joined: Apr 12, 2013 Post Count: 815 Status: Offline Project Badges: 
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@Papa3
----------------------------------------As there is no other way to contact you except through here, I wanted to let you know that Phase 1 has officially restarted. You still have a chance to cross 200 years! link  |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges: 
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CRISPR kills HIV and eats Zika 'like Pac-Man'. Its next target? Cancer.
http://www.wired.co.uk/article/crispr-disease-rna-hiv |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges:
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In a decades-long game of hide and seek, scientists from Sydney's Westmead Institute for Medical Research have confirmed for the very first time the specific immune memory T-cells where infectious HIV 'hides' in the human body to evade detection by the immune system. "Previously it was thought that HIV was hiding primarily in central memory T-cells, but our new HIV genetic sequencing test has revealed that the majority of replication-competent virus is actually hiding in effector memory T-cells. "HIV is really very clever. Essentially, it is hiding in the exact same cells within the immune system that are meant to attack it," she said. Effector memory T-cells are the cells in the body that 'remember' previous infections and how to defeat them. These are the cells that provide life-long immunity to infections such as measles or chicken pox.
https://www.sciencedaily.com/releases/2017/10/171019100818.htm |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges:
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Researchers have solved the last unknown protein structure of HIV-1, the retrovirus that can cause AIDS. Knowledge of this structure, called the cytoplasmic tail of gp41 protein, will help researchers further understand how the virus infects human cells and how progeny viruses are assembled and released from infected cells. The cytoplasmic tail appears to play a key role in virus assembly to help incorporate the envelope spike structures into the surface of viral particles. "If we are able to inhibit incorporation of the envelope protein, we inhibit viral replication," Saad said. "This would disarm the virus and prevent disease. The cytoplasmic tail is a critical component of infectivity."
Instead of intact product, a bacterial enzyme was cutting the protein during protein expression. "We have never seen this for any other protein," Saad said. The researchers found that they had to limit protein expression to just two hours. Even then, 70 percent of the cytoplasmic tail was cut and only 30 percent was left intact. They found that the N-terminal end of the cytoplasmic tail of gp41, measuring 45 amino acid residues, lacked a regular secondary structure and was not associated with the membrane, which wraps around an HIV-1 viral particle like the leather cover of a baseball. The C-terminal end of the cytoplasmic tail of gp41, measuring 105 amino acid residues, was tightly associated to the membrane and had three alpha-helixes with portions that were hydrophobic and portions that were hydrophilic. The UAB group also showed the preferred topology of the cytoplasmic tail when bound to the membrane. Saad says the structure opens up whole new areas of research: How the cytoplasmic tail stabilizes the envelope protein structure, how it affects membrane mobility of the envelope protein structure, and how it helps coordinate membrane-binding and the association of 2,000 HIV-1 Gag polyproteins underneath the membrane surface. The Gag polyproteins are later cut inside the maturing virus to form multiple smaller matrix, capsid and nucleocapsid proteins that produce the condensed viral core. Saad says knowledge of the gp41 cytoplasmic tail structure will also open comparative studies of 10 different retroviruses that have similar tails to learn why some tails are shorter and some tails are longer. "The cytoplasmic tail of gp41 has been of interest for a long time, and nobody understands how it functions in infection or how it helps incorporate the envelope protein into the membrane," Saad said. https://www.sciencedaily.com/releases/2017/10/171019123742.htm |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges:
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New algorithm speeds up protein folding simulations
Conventional simulations, using molecular dynamics and Monte Carlo methods, have been successful overall at modeling biological molecules like proteins. To determine how proteins fold, the simulation searches for configurations that correspond to lower and lower energy states. Eventually, it finds the lowest energy state, which gives a stable fold. But as the simulation searches, it may encounter a configuration with a slightly higher energy, which forms a barrier that impedes the algorithm. As a result of these slowdowns, conventional methods can only simulate molecular behaviors occurring over short time scales of a few hundred microseconds. Many phenomena, such as certain protein folds or a drug binding to a potential target, happen over the course of a few seconds, minutes or even days. Simulating such long timescales would take too much computation time with just conventional approaches. To speed up the simulations, researchers can inject energy into the system, which pushes the model over any energy barriers. But one of the biggest challenges to these methods is in defining the coordinates that describe the system -- which, for example, can be the length between atoms in the molecule, and the angles between bonds. Traditionally, researchers define the coordinates before they start the simulation. Every time step along each coordinate depends on the previous step. But this dependency can bias the simulation. Peter's new algorithm avoids this bias. He found a generalized coordinate system in which each time step doesn't rely on the previous step. "Only few parameters are needed, and no human intuition is required, which can potentially bias the simulation result," he said. https://www.sciencedaily.com/releases/2017/12/171205120032.htm |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges:
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Scientists have just discovered a new mechanism by which HIV evades the immune system, and which shows precisely how the virus avoids elimination. ... "We discovered that HIV promotes the destruction of the anti-viral Interferon signalling pathway. Essentially, HIV uses the machinery in our own cells to do this, and the virus is thus able to reduce the production of many important anti-viral molecules. Without these anti-viral molecules, our immune system can't clear viral infections."
https://www.sciencedaily.com/releases/2018/04/180417115716.htm |
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Papa3
Senior Cruncher Joined: Apr 23, 2006 Post Count: 360 Status: Offline Project Badges:
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Scientists at the University of Virginia School of Medicine have revealed how a cancer-causing virus anchors itself to our DNA. That discovery could pave the way for doctors to cure incurable diseases by flushing out viruses, including HPV and Epstein-Barr, that now permanently embed themselves in our cells.
"The reason we can't get rid of these [viruses] is because we can't figure out a way to get their DNA out of the nucleus, out of the cell," explained UVA researcher Dean H. Kedes, MD, PhD. "They depend on this 'tether' to remain anchored to the DNA within our cells, and to remain attached even as the cells divide. This tether is a key factor to disrupt in devising a cure." Now that scientists can understand this vital infrastructure, they can work to disassemble it. https://www.sciencedaily.com/releases/2018/04/180419130908.htm |
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TheBizii
Advanced Cruncher Slovenia Joined: Jan 4, 2016 Post Count: 51 Status: Offline Project Badges: 
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Scientists have identified a key molecule exploited by HIV when the virus infects human cells, and the discovery could represent a major step forward in defeating the deadly disease.
https://www.sciencealert.com/we-discovered-ho...sphate-ip6?share=b433bc7c |
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Dan60
Senior Cruncher Brazil Joined: Mar 29, 2006 Post Count: 185 Status: Offline Project Badges:
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The guardians at the city gates were induced deep in sleep as the enemy slipped past and into the heart of the city’s control center. The invader’s blueprint for takeover usurped city resources while city attendants, deceived by the enemy, unwittingly enabled the deadly enemy force to multiply and spread to neighboring city-states by arresting and executing the guardians.
http://www.oyageninc.com/layscience/the-sentinel |
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