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MERS could be curable..Antibody against MERS found by Scientists


A team of Scientists have recognized a protein that worn out the MERS virus, giving the hope for a potential relief to prevent and treat the incurable disease, according to a report published in Proceedings of the National Academy of Sciences on 27th July. Middle East Respiratory Syndrome (MERS) is an exceptionally lethal pulmonary infection instigated by a formerly unidentified coronavirus (CoV), possibly passed on to humans by infected camels. There is no licensed vaccine or antiviral available so far to treat MERS, which causes symptoms such as fever, cough and shortness of breath. The team isolated a potent MERS-CoV-neutralizing antibody, named LCA60, from memory B cells of an infected patient. LCA60 antibody binds to a novel site on the spike protein and effectively nullifies infection of MERS by meddling with the binding to the cellular receptor CD26. Scientists claim that LCA60 antibody can efficiently be used for prophylaxis, for postexposure prophylaxis of individuals at risk, or for the treatment of human cases of MERS infection. Notably, LCA60, when given to infected mice, dramatically reduced the amount of the MERS virus in the lungs within days. Even in the worst-case scenario, only one virus remained after three days for every 100 viruses at the start of the treatment. In most cases, the virus became untraceable within five days of treatment. The antibody fought the virus whether it was given a day before or a day after the mice were infected. Current MERS outbreak in China and South Korea has caused 186 infections and 36 deaths as of 28th July WHO report.

See in details;

D. Corti et al. Prophylactic and postexposure efficacy of a potent human monoclonal antibody against MERS coronavirus. PNAS. Published online July 27, 2015. doi: 10.1073/pnas.151019912

Pain Sensing’ Gene Discovered – Could Lead to Development of New Pain Treatments

Cambridge, UK (Scicasts) — A gene essential to the production of pain-sensing neurons in humans has been identified by an international team of researchers co-led by the University of Cambridge.

The discovery, reported May 25 in the journal Nature Genetics, could have implications for the development of new methods of pain relief.

Pain perception is an evolutionarily-conserved warning mechanism that alerts us to dangers in the environment and to potential tissue damage. However, rare individuals – around one in a million people in the UK – are born unable to feel pain. These people accumulate numerous self-inflicted injuries, often leading to reduced lifespan.

Using detailed genome mapping, two teams of researchers collaborated to analyse the genetic make-up of 11 families across Europe and Asia affected by an inherited condition known as congenital insensitivity to pain (CIP). This enabled them to pinpoint the cause of the condition to variants of the gene PRDM12. Family members affected by CIP carried two copies of the variant; however, if they had only inherited one copy from their parents, they were unaffected.

The team looked at nerve biopsies taken from the patients to see what had gone wrong and found that particular pain-sensing neurons were absent. From these clinical features of the disease, the team predicted that there would be a block to the production of pain-sensing neurons during the development of the embryo – they confirmed this using a combination of studies in mouse and frog models, and in human induced pluripotent stem cells (skin cells that had been reset to their ‘master state’, which enables them to develop into almost any type of cell in the body).

PRDM12 had previously been implicated in the modification of chromatin, a small molecule that attaches to our DNA and acts like a switch to turn genes on and off (an effect known as epigenetics). The researchers showed that all the genetic variants of PRDM12 in the CIP patients blocked the gene’s function. As chromatin is particularly important during formation of particular specialised cell types such as neurons, this provides a possible explanation for why pain-sensing neurons do not form properly in the CIP patients.

“The ability to sense pain is essential to our self-preservation, yet we understand far more about excessive pain than we do about lack of pain perception,” says Professor Geoff Woods from the Cambridge Institute for Medical Research at the University of Cambridge, who co-led the study. “Both are equally important to the development of new pain treatments – if we know the mechanisms that underlie pain sensation, we can then potentially control and reduce unnecessary pain.”

PRDM12 is only the fifth gene related to lack of pain perception to have been identified to date. However, two of the previously-discovered genes have already led to the development of new pain killers that are currently been tested in clinical trials.

“We are very hopeful that this new gene could be an excellent candidate for drug development, particularly given recent successes with drugs targeting chromatin regulators in human disease,” adds Dr. Ya-Chun Chen from the University of Cambridge, the study’s first author. “This could potentially benefit those who are at danger from lack of pain perception and help in the development of new treatments for pain relief.”

Article adapted from a University of Cambridge news release. The original article is licensed under a Creative Commons Licence.

Publication: Transcriptional regulator PRDM12 is essential for human pain perception. Chen, Y-C et al. Nature Genetics; (May 25, 2015)

Source: http://scicasts.com/genomics/2029-functional-genomics/9466-pain-sensing-gene-discovered-could-lead-to-development-new-pain-treatments/?utm_source=newsletter_1849&utm_medium=email&utm_campaign=scicasts-on-cancer-research

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