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    1-trickyprotei

    This illustration shows how the envelope proteins covering the surface of an HIV virion (1, 2) bind to a host cell (3, 4). The trimeric MPER region of gp41 is shown in red and can be disabled by antibodies, shown in light blue

    Duke scientists have taken aim at what may be an Achilles' heel of the HIV virus.
    Combining expertise in biochemistry, immunology and advanced computation, researchers at Duke University have determined the structure of a key part of the HIV envelope protein, the gp41 membrane proximal external region (MPER), which previously eluded detailed structural description.
    The research will help focus HIV vaccine development efforts, which have tried for decades to slow the spread of a virus that currently infects more than 33 million people and has killed 30 million more. The team reported the findings online in the Jan. 13 early edition of Proceedings of the National Academy of Sciences.
    "One reason vaccine development is such a difficult problem is that HIV is exceptionally good at evading the immune system," said Bruce Donald, an author and professor in Duke's computer science and biochemistry departments. "The virus has all these devious strategies to hide from the immune system."
    One of those strategies is a dramatic structural transformation that the virus undergoes when it fuses to a host cell. The envelope protein complex is a structure that protrudes from HIV's membrane and carries out the infection of healthy host cells. Scientists have long targeted this complex for vaccine development, specifically its three copies of a protein called gp41 and closely associated partner protein gp120.
    The authors said they think about a particular region of gp41, called MPER, as an Achilles' heel of vulnerability.
    "The attractiveness of this region is that, number one, it is relatively conserved," said Leonard Spicer, senior author and a professor of biochemistry and radiology. In a virus as genetically variable as HIV, a successful vaccine must act on a region that will be conserved, or similar across subtypes of the virus.
    "Second, this region has two particular sequences of amino acids that code for the binding of important broadly neutralizing antibodies," said Spicer. The HIV envelope region near the virus membrane is the spot where some of the most effective antibodies found in HIV patients bind and disable the virus.

    trickyproteiWhen the virus fuses to a host cell, the HIV envelope protein transitions through at least three separate stages. Its pre- and post-fusion states are stable and have been well studied, but the intermediate step—when the protein actually makes contact with the host cell—is dynamic. The instability of this interaction has made it very difficult to visualize using traditional structure determination techniques, such as x-ray crystallography and nuclear magnetic resonance (NMR) spectroscopy.
    That's where Duke's interdisciplinary team stepped in, solving the structure using protein engineering, sophisticated NMR and software specifically designed to run on limited data.
    First author Patrick Reardon spent years engineering a protein that incorporated the HIV MPER, associated with a membrane and behaved just like gp41 in the tricky intermediate step, but was stable enough to study. Reardon, then a PhD student under Spicer, is now a Wiley postdoctoral fellow at the Environmental Molecular Sciences Laboratory, a scientific facility in the Department of Energy's Pacific Northwest National Laboratory.
    The result captured the shape of the three-parted MPER in its near-native state, but the protein needed to be more than structurally accurate—it had to bind the broadly neutralizing antibodies.
    "One of the most important aspects of the project was ensuring that this construct interacted with the desirable antibodies, and indeed, it did so strongly," Reardon said.
    The team validated the initial structure using an independent method of data analysis developed by Donald's lab, which showed alternate structures were not consistent with the data.
    "The software took advantage of sparse data in a clever way that gave us confidence about the computed structure," Donald said. It used advanced geometric algorithms to determine the structure of large, symmetric, or membrane-bound proteins—varieties that are very difficult to reconstruct from NMR data.
    Donald's lab has been perfecting the method for a nearly decade, and Donald said its application in this paper represents a culmination of that work, demonstrating how the two-pronged approach can illuminate the structure of complex protein systems.
    The next steps of this research have already begun. In December, Duke received a grant of up to $2.9 million from the Bill & Melinda Gates Foundation to fund the development of an HIV vaccine that will build on these findings.

    Published in News
    Wednesday, 20 November 2013 09:19

    Super antibodies almost won HIV

    In AIDS patients as there is only one hope - to antiretroviral therapy, which is based on drugs that prevent HIV from reproducing. Genome recorded in the virus RNA and thus enter the cell it with reverse transcriptase enzyme (reverse transcriptase) makes a copy of its own DNA template RNA. Then, this DNA was self proteins cells begin RNA viral clone. If, for example, to suppress the work of the reverse transcriptase of the virus, it can not reproduce.

    But even cocktails of antiretroviral drugs only help to translate the acute phase of the disease chronic. Such therapy can not do anything with the virus, which floats in the blood or in the cell is dormant. Therefore, researchers are looking for a way to get rid of the virus, rather than just suppressing its ability to reproduce. (By the way, the usual anti-HIV therapy is theoretically allows to get rid of the virus, but only under special conditions, and such cases are, unfortunately, rare.)

    630b-teratoma-service-ipsc-transgenic-mouse-dr4-stem-cell-differentiation-neural-stem-cells-rat-models-gene

    HIV and human lymphocyte

    When it comes to completely banish HIV, all agree that the best anti tool to be found here. On the one hand, it's simple: just find the immunoglobulins, which would learn viral envelope protein have been associated with him and would have signaled an immune killer cells that this complex must be destroyed. The problem, however, is that HIV has enormous variability, and antibodies usually catch only a certain proportion of the virus particles, for the same protein they endowed with a number of differences that make antibodies do not see it.

    However, our immune system is still able to cope with such a variety of the virus , creating a broad-spectrum antibodies . The fact that the immune system can produce immunoglobulins that recognize more than 90 % of the species of HIV , scientists discovered in 2010, and this discovery , of course, has given all hope that AIDS is about to fall . But over time it became clear that such antibodies are rare and a huge amount of time , then only in response to a real infection - that is to provoke a synthesis of a vaccine of killed pathogen will not work.

    Nevertheless, scholars have continued to work with the likes of antibodies. And not so long ago have found universal antibodies that appear much earlier and look simpler than those observed before - however, proved their versatility and low. But be sure to make yourself immune to produce such antibodies? The experiments showed the two research groups - Deaconess Medical Center Beth Israel and the National Institute of Allergy and Infectious Diseases (both - USA) - immunoglobulins broad-spectrum, just introduced into the blood, effectively reduce the level of HIV.

    858b-teratoma-service-ipsc-transgenic-mouse-dr4-stem-cell-differentiation-neural-stem-cells-rat-models-gene

    HIV between epithelial cells (bottom) and lymphocyte (top)

    Immediately it should be said that the group of Dan Baruch (Dan Barouch) and Malcolm Martin (Malcolm Martin) experimented with monkeys: macaques infected with simian-human hybrid HIV, which multiply in monkeys, but looked like a human virus. He served as a weapon against a broad-spectrum antibodies obtained from patients with AIDS.

    Dan Baruch and his colleagues used a cocktail of three types of antibodies, and, as the researchers write in Nature, in the week of the virus level down so that it can not be detected! A similar result was also when used instead of a mixture of immunoglobulins only one of their kind. Once the content of such antibodies in the blood began to decline, the concentration of the virus rose again, but some monkeys it was still indistinguishably low even without the introduction of additional portions of antibodies.

    In another study carried out by Malcolm Martin and his colleagues, we are talking about the same thing , but here researchers have used different types of antibodies against HIV. Again, the concentration of the virus in macaques fell for seven days prior to the indiscernible ( again: undetectable !) Level and remained so for 56 days, until the antibodies do not begin to fade. Then it all depended on how much virus was originally in monkeys , if small, following the disappearance of virus antibodies remained under the control of its own immunity of animals , and if it was originally much, the level began to rise.

    Thus, as emphasized by the researchers, the virus disappeared from both the blood and other tissues, and no resistance to the administered antibodies, it appeared. (However, there was one exception: when the second study administered only one antibody and experimental monkey was a 3-year experience of cohabitation with the virus, it has a sustained viral strain.)

    In both cases, scientists are not too long treated the virus with human antibodies because they were afraid that the immune system begins to resent monkeys against foreign immune proteins , and perhaps that was the reason that in most cases, the virus recovered . That is, it is not clear whether it is possible to make the effect of the " long-playing ". All this is clear only after a clinical trial , and as for the results described above , the enthusiasm of researchers can understand the first time in a living organism could so much lower level of viremia (alas , previous experiments with antibodies that were placed on humans and mice had a very unimpressive results ) .

    What's next? The cost of antibodies is much higher than the anti-retroviral drugs, and to treat them more difficult. But the authors of the work suggest that such antibodies should be connected to conventional anti-HIV drugs: it will reduce the cost of treatment, and is likely to increase its efficiency - if antibodies to add substances harmful to reproduction of the virus in the cell.

    Published in News

    vaccine-gentaur-bullet-blender-gold-kronos-dio-targattThe dream of many scientists to create a vaccine against AIDS has failed. National Institutes of Health in the U.S. announced that it attempts to immunize volunteers with an experimental vaccine known as HVTN 505 is officially terminated, since it is clear that it does not prevent infection.

    Clinical trial began in 2009 and since then, 1,250 voluntary participants received vaccine and 1244 others - control infusion of placebo, both groups over a period of 24 weeks. Among all the volunteers in total, so far has 41 infected with HIV than those who received the vaccine and 30 infected than those who received placebo. The study focused mainly people who have unprotected sex.

    Vaccine strategy using "double whammy" that aimed to strengthen the immune system. Three initial injections are placed initially, and after 16 weeks - another injection containing genetic material which creates a molecule of the type produced by HIV in order to induce a response in the immune system against viruses. Scientists say the vaccine itself did not cause infection. After presenting the matter collected data and results collected until mid-April at the National Institute of Allergy and Infectious Diseases, which sponsored the clinical trial recommended stopping the attempt to create the vaccine. Volunteers will be monitored for 5 years, and the data will be analyzed for further information.

    Published in News
    Wednesday, 03 April 2013 16:56

    Roadmap to an HIV Vaccine

    HIV-vaccine-gentaur-antibodiesBy investigating an African patient’s HIV infection, researchers have traced the development of an antibody that is effective at neutralizing many strains of HIV, according to a study published today (April 3) in Nature. The researchers—who identified the original HIV variant as well as the broadly neutralizing antibody, and pieced together their evolution over the course of infection—hope that a vaccine mimicking this process could encourage the development of such effective HIV-fighting antibodies.

    The new research provides “really in-depth information on how a particular type of broadly neutralizing antibody emerges over the course of a natural HIV infection,” said Leonidas Stamatatos, an immunologist at Seattle Biomedical Research Institute who did not participate in the study.

    Broadly neutralizing antibodies—able to block many strains of HIV from binding target cells—are notoriously rare: only about 20 percent of HIV-positive people ever generate such antibodies. One of the most attractive neutralizing targets is the HIV envelope protein (Env) that binds T cells, which is present on every variant of HIV. But Env is covered in sugar molecules that often mimic host structures, making it hard for the immune system to distinguish virus from self. In order to avoid an adverse autoimmune reaction, the body produces few B cells whose antibodies can recognize these common structures. One approach to developing an effective HIV vaccine is to stimulate these rare B cells, but because Env’s sequence can vary widely between HIV strains, researchers didn’t know much about the right Env variant for the job.

    In order to find an Env that could stimulate an antibody with broadly neutralizing potential, Barton Haynes at Duke University and researchers at the Center for HIV-AIDS Vaccine Immunology (CHAVI) set up eight acute infection clinics in Malawi, South Africa, Tanzania, Uganda, and one in North Carolina, where they could watch antibody and virus develop within weeks of infection.

    Haynes and his team found one patient who developed a broadly neutralizing antibody within 3 years of infection. The antibody, dubbed CH103, could block infection of target cells by 55 percent of the HIV virus particles they tested, which expressed a total of 196 different types of Env. Because the team had blood samples from the patient starting 4 weeks after infection, they could isolate the original antibody, CH103’s predecessor, as well as determine the sequence of the original Env protein that first spurred the antibody’s production.

    As HIV proteins accrue mutations during an infection, antibodies evolve to increase specificity and adapt to changing targets. Finding the antibody that bound the original Env allowed researchers to identify which mutations conferred broadly neutralizing activity to CH103 and identify mutations in Env that could have contributed to CH103’s development. Haynes and his colleagues hope to recreate the evolution of CH103-like antibodies using the right combination of Env variants in a vaccine.

    “The study provides important information on how one might design a rational vaccination strategy,”Dennis Burton, an immunologist at The Scripps Research Institute who did not participate in the study, wrote in an email to The Scientist. “[It’s] a significant leap.”

    An effective vaccine will need to elicit more than one type of antibody to block HIV infection, so Haynes and his team are also examining the evolution of broadly neutralizing antibodies and their corresponding HIV proteins in other patients, as well.

    Indeed, the bulk of the work is just beginning, said Stamatatos, who noted that the possible combinations of Env “are nearly infinite.” It’s also not clear yet whether the Env mutants should be given together, or provided sequentially in a fashion more akin to a natural infection. Haynes and his colleagues are currently beginning to test both strategies with different Env combinations in macaques and mice engineered to express human antibodies.

    H.-X. Liao et al., “Co-evolution of a broadly neutralizing HIV-1 antibody and founder virus,”Nature, doi:10.1038/nature12053, 2013.

     

    Published in News