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Home > Press > Sweet 'quantum dots' light the way for new HIV and Ebola treatment Abstract: A research team led by the University of Leeds has observed for the first time how HIV and Ebola viruses attach to cells to spread infection. The findings, published today in the journal Angewandte Chemie, offer a new way of treating such viruses: instead of destroying the pathogens, introduce a block on how they interact with cells. Lead author Dr Yuan Guo, from the Astbury Centre for Structural Molecular Biology at the University of Leeds, said: "Until now, how these viruses attach to cells was a 'black box' to chemists. We knew that the viruses were interacting with healthy cells, but the way in which they bound together was still a mystery." In the study, the researchers used nano-sized crystals (about a millionth of a millimetre in size) called 'quantum dots' that mimicked the shape of the viruses and acted as technological stand-ins in experiments to reveal how they bind to cells. Quantum dots are fluorescent crystals in which the colour of the emitted light is dependent on the size of the crystal - one of several properties that has led to them becoming the most desirable component for the latest generation of televisions. They have also emerged as an advanced type of fluorescent probe for biomolecular and cellular imaging, making them useful for studying how viruses spread. Using the fluorescence of the quantum dots, the research team behind the new study were able to illuminate the physical binds that attach them to the cells, also revealing how the viruses would bond. In order to allow the quantum dots to bind to cells, they first had to be coated in sugar - a new technique that was developed at the University of Leeds for this study. Study co-author Dr Bruce Turnbull, also from the Astbury Centre, and the University's School of Chemistry, said: "We often only hear about sugar in a negative light, about how consuming it is bad for our health. But there are many different types of sugars that play a vital role in human biology. In fact, all of our cells are coated in sugar and they interact with other cells by proteins binding with these sugars. Indeed, the reason why we have different blood types is because of the different types of sugar coating on our red blood cells. "Viruses also attach to the surface of healthy cells through interactions between proteins and sugars. These interactions are weak individually, but can be reinforced by forming multiple contacts to offer the viruses a 'way in'. We want to understand what factors control this binding process and, eventually, develop a range of inhibitors designed to target specific viral bindings." The study has already revealed the different ways in which two cell surface sugar binding proteins that were previously thought to be almost indistinguishable - called 'DC-SIGN' and 'DC-SIGNR' - bind to the HIV and Ebola virus surface sugars, thereby spreading the viruses. Study co-lead author Dr Dejian Zhou, also from the Astbury Centre and the University's School of Chemistry, said: "These proteins are like twins with different personalities. Their physical make-up is almost identical, yet the efficiency with which they transmit different viruses, such as HIV and Ebola, varies dramatically and the reason behind this had been a mystery. "Our study has revealed a way to differentiate between these proteins, as we have found that the way in which they bind to virus surface sugars is very different. They both attach via four binding sites to strengthen the bond, but the orientation of these binding pockets differs." A pioneering tradition in structural biology Further progress in this area will be boosted by the state-of-the-art facilities in the Astbury Centre, enabling researchers to better understand life in molecular detail. The University of Leeds has played a key role in the birth of structural biology as a scientific discipline, with the development of X-ray crystallography by Nobel Laureates William and Lawrence Bragg in Leeds in 1912-13. A recent £17 million investment in some of the best nuclear magnetic resonance and electron microscopy facilities in the world is now enabling scientists to remain at the forefront of research into complex proteins. A new academic symposium, the Asbury Conversation, is being hosted at the University of Leeds from 11 - 12 April 2016, to bring together leading researchers from across the globe to discuss the most recent innovations, new techniques and technologies in the field of structural molecular biology. A public exhibition and lecture on Tuesday 12 April follows the symposium, aimed at helping people understand the secret life of molecules, including an exhibit called "The complex life of sugars". Professor Michael Levitt, who was awarded the 2013 Nobel Prize in Chemistry for developing computer-based tools to better understand and predict chemical reactions, will be delivering the talk, "How modelling molecules builds our understanding of life." The research was funded by the Wellcome Trust, with additional funding from the Biotechnology and Biological Sciences Research Council (BBSRC). For more information, please click If you have a comment, please us. Issuers of news releases, not 7th Wave, Inc. or Nanotechnology Now, are solely responsible for the accuracy of the content.

Millions of those infected with HIV worldwide are young women, ages 15-24, according to the World Health Organization. Because the HIV epidemic overlaps with an epidemic of intimate partner violence (IPV) against women and girls, researchers have suspected a correlation between inequities in relationship power and the risky sexual behavior that can lead to HIV transmission.

News Article | August 31, 2016
Site: motherboard.vice.com

There are good reasons that transmissible cancer isn't really a thing. This mostly has to do with the immune systems of advanced organisms—while our own cancer evades immune responses by virtue of being, well, part of us, cancer from other individuals is recognized as an invader. Thus, outside cancer is quickly rooted out and eliminated. Cases of transmissible cancer in humans are extreme novelties, occurring rarely in immunocompromised patients, such as those with HIV. In nature, a few species are unlucky enough to have infectious cancer as an everyday threat. Shellfish get it thanks to weak immune systems and an existence based on the constant ingestion and filtering of seawater shared by other shellfish. Dogs get it thanks to the swapping of tissues that occurs in rough dog sex. Tasmanian devils get it because of the tissue swapping involved in constantly fucking up each other's faces. That's a prerequisite for transmissible cancer occurring at all: the transmission of full-on tissue. A cancer cell doesn't behave like a bacterium or virus—cancer needs to be transplanted en masse for it to gain footing elsewhere. In most cases, devil facial tumour disease (DFTD) is fatal. Over the past two decades, some 80 percent of the entire Tasmanian devil population has been decimated by the cancer. The disease has spread across nearly 95 percent of the island of Tasmania and has affected all known devil populations. Epidemiological models have predicted that DFTD likely portends the end of the entire Tasmanian devil species. Read More: The Adorably Ferocious Tasmanian Devils Are Being Driven to Extinction by Face-Melting Disease There may be hope, however. No, the devils don't seem to be learning to interact socially without destroying each other's faces, but their immune systems are learning to fight back against the infection via phenomenally rapid adaptations. This is according to a paper published on Tuesday in Nature Communications by disease ecologist Andrew Storfer and colleagues at Washington State University. "Overall, our results reflect a rapid evolutionary response to this strong selection imposed by DFTD, and such a response to a highly lethal, novel pathogen has rarely, if ever been documented in wild populations," Storfer and co. write. "The only other well-studied example, the evolution of rabbit resistance to myxomatosis following its release in Australia, took place over a much larger number of host generations." The swapping of tissues is a necessary but not sufficient condition for transmitting cancer. There is still the issue of immune responses. What helps DFTD is that Tasmanian devils all happen to look pretty similar genetically. This is the result of various "population bottlenecks" occurring through the species' history. At various points, the species shrank to a very small population size, which then recovered to normal levels. The effect is that the post-bottleneck devils all descend from a relatively small number of ancestors. Because DFTD is fairly new, Storfer and his team were able to compare DNA from Tasmanian devils from before its emergence (based on archived tissue) with DNA from devils alive eight to 16 years after the disease appeared. Genetic variations began appearing in as few as four generations of the animals, which is remarkable given that rapid evolution usually requires some amount of pre-existing genetic variation, which the devils don't really have. The researchers found five genes in two regions relating to cancer or immune function that are likely indicative of genetic selection. "The functions of these genes suggest that the devil immune system may be adapting to be able to recognize tumour cells," the paper notes. This functionality will need to be fleshed out further in future research. This gives hope for the devils not just in their own adaptability, but because we may be able to incorporate the genes into captive populations that may one day be necessary for repopulation efforts. "First and foremost, this gives us hope for the survival of the Tasmanian devil," Storfer offered last week in a press briefing. The findings may also have implications for wildlife disease in general and also human cancer. "Because this cancer moves from host to host it's effectively like one very long-lived human tumor within a single individual," he explained. "This may give us some insights into cancer recurrence and remission in humans."

Cotrimoxazole (CTX) discontinuation is inferior to CTX continuation among ART-treated, immune-reconstituted HIV-infected adults living in a malaria-endemic region, according to results of a recent trial. These trial findings were important for December 2014 WHO guidelines recommending that CTX prophylaxis be continued regardless of CD4 cell count or HIV/AIDS clinical stage in settings where malaria is endemic and/or severe bacterial infections are common.

News Article | April 21, 2016
Site: www.sciencedaily.com

Thanks to combination antiretroviral therapy, many people with HIV can be expected to live decades after being infected. Yet doctors have observed that these patients often show signs of premature aging. Now a study has applied a highly accurate biomarker to measure just how much HIV infection ages people at the biological level -- an average of almost 5 years.

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