New Images of Protein Structure Gives Insight Into HIV

 Salk researchers captured the structure of a protein complex called an intasome (center) that lets viruses similar to HIV establish permanent infection in their hosts. The intasome hijacks host genomic material, DNA (white) and histones (beige), and irreversibly inserts viral DNA (blue).

Credit: Salk Institute

 

Retroviruses like human immunodeficiency virus (HIV) operate by inserting their DNA into human DNA, making the previous human cell into a virus making factory. In other words, the retrovirus "hijacks" the host cell. A new study has illuminated the previously unknown structure of the intasome, the mechanism behind the virus that injects the virus' DNA into the host cell.

Previous work on the subject has been done on a virus called prototype foamy virus (PFV), since it is less tricky to study than the HIV virus. The HIV virus affects human immune cells with their intasomes, eventually leading to the death of the immune system. Salk researchers have done this latest study on mouse mammary tumor virus (MMTV), which is more closely related to the HIV virus than PFV. The team used cryo-electron microscopy (cryoEM), a technique that has certain advantages over older methods such as x-ray crystallography. Essentially, the researchers were able to freeze the virus and intasome in time using a frozen liquid solution, all while it was affecting the host cell. They were able to capture an image by measuring how electrons deflected off of the protein.

 

Previous studies on PFV showed that its intasomes were made of four protein components (called integrases) bound by two strands of viral DNA. This recent study has shown that MMTV has eight integrase molecules per two strands of viral DNA. This suggests that HIV may contain a more complex protein structure than previously thought and a different mechanism of entry than PFV. This new framework gives molecular biologists a greater insight into the possible mechanism of how HIV delivers its DNA into the human host cell. 

Overall, more sophisticated imaging techniques will allow us to see the structure of viruses and disease causing bacteria in greater detail. By having a greater understanding of structure, we will be able to make more informed and accurate descriptions of functions. If we know the shape and way in which lethal viruses like HIV move, we will have a much greater chance of curing the disease.

 

Scientists Identify Two Genes that ‘Shut Down’ HIV-1 Virus

An international group of researchers has uncovered the mechanisms of genes that may inhibit the virility of the HIV-1 virus. The two proteins, SERINC5 and SERINC3 are typically found in  the cell membrane of a cell. The HIV-1 virus has 9 genes, one of them coding for the protein HIV-1 Nef, which accounts for much of the viral ability of HIV. HIV-1 Nef also prevents SERINC5 and SERINC3 from reaching the cell membrane or being incorporated into new virions. In the absence of Nef, new virions can leave the host cell and attempt unsuccessfully to infect other cells because the SERINC proteins prevent the HIV virus from leaving the viral envelope. With the presence of SERINC proteins, research say the virility of HIV is reduced by 100-fold.

The research is pointing towards a promising future in viral studies, as HIV has become rampant over the years. Current medicine usually keep the virus at bay and infected individuals manage to have normal, functioning lives. Even so, they still have to live with the stigma of their infection and infected people who do not get diagnosed early may suffer greater consequences. With SERINC's anti-retroviral ability, this could lead to a more effective treatment option for HIV/AIDs and treatment of other enveloped viruses.

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SERINC

HIV/AIDS

Evolution of Ancient Viruses

 

    Research conducted at Stanford University by Doctor Joanna Wysocka, a developmental biologist suggest that ancient viruses are significantly acting on the development of human embryos. The main retrovirus tracked is called HERV-K1. This virus is made by embryonic cells only during the time prior to implantation on the wall of the uterus. The body responds with an immune defense when these new viral genes are present. Thus, the embryonic cell produces surface proteins to prevent additional viruses.

    Experiments were conducted to expose the HERV-K behavior. Scientist found the cells that contained this virus were able to better resist other dangerous viruses' such as influenza virus. In the opinion of Doctor Wysocka these viruses could be fluctuating the proteins throughout vital period of development. Another scientist, from Stephen Goff of Columbia University, recognizes the adaption to ancient viruses further explains the evolution of the human genome.

    It is nothing shy from incredible that our bodies can accept a virus and utilize in in as advantage. It is especially impressive that these retroviruses compose 8 percent of the human genome.  Unfortunately, the writer of this article appears to be presenting the fact this is only a suggestion of how our DNA reacts to ancient viruses. Therefore, the findings are still being discussed and further researched.

The scientific paper can be located in Nature magazine here.

Flu vs. Immunity

The seasonal flu causes 500,000 or more deaths and severe illnesses worldwide every year. Scientists have found a potential way to improve the future flu vaccines but discovering how the flu evolves to escape immunity. The flu vaccine is effective by exposing the body to three major types of inacitive flu, making the immune system develop antibodies that eliminate the flu virus. The flu virus evolves every 2 or 3 years by substitution of amino acids, and different combinations of amino acids. They have found that the seasonal flu develops new strains by substitution of typically one amino acid, when before this research it was thought that there was four. They had also found this substitution occurs at only 7 different sites, when it was previously believed there was 130 sites. These sites were found to be located near the receptor binding site, which is where the virus binds to and infects hosts. The virus needs this site to recognize the cells it needs to cause infection, and would not change so close to the site unless it needed to, as it is important for the virus. 
This research can pave the road for future improvements to the flu vaccine, that could save thousands of live.
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