Several studies have revealed how viruses infect the body!

June 13, 2019 news / BIOON / - this issue brings you the latest research progress on virus infection, and we will learn how the virus infects the body together 【1】 Nat Microbiol: it is the first time to find that influenza virus and respiratory bacteria can work together to promote host infection doi: 10.1038/s41564-019-0447-0 Recently, an international journal Nature In the report on microbiology, scientists from the St Judas children's research hospital found that influenza virus might function like Velcro to help common respiratory bacteria stand firm in the respiratory tract In this paper, the researchers found for the first time that influenza virus can adhere to the surface of common respiratory bacteria, and significantly enhance the ability of bacteria to adsorb on the organ wall Compared with mice only infected with bacteria or influenza virus, mice infected with bacteria virus complex tend to have a higher death rate Photo source: Dr Jason Rosch, a nature researcher, said that bacteria seem to use influenza viruses to decorate their surfaces, so as to enhance the ability of bacteria to adsorb on respiratory tract tissues in the early stage of infection, and it seems to be a way for bacteria and viruses to work together to promote infection in the early stage of infection The results are expected to help researchers design more effective vaccines, after researchers found that there may be a beneficial interaction between different bacteria and viruses in the gut and organs When an infected person coughs or sneezes or spreads pathogens, bacteria and viruses will take advantage of the interaction They will use different receptors to absorb into the host respiratory system tissues, and work together to cause the patient's condition to worsen, said researcher Rosch The bacteria in this study usually exist in the nasal cavity, which will spread to the lung tissue of infected patients and lead to pneumonia or ear canal infection, and the direct effect of influenza virus and bacteria will also promote the spread of the virus 【2】 ELife: how do key proteins help H1N1 virus infect humans? DOI：10.7554/eLife.43764 Recently, in a research report published in the International Journal eLife, scientists from the University of California clarified how two proteins help influenza A virus particles fight against human cells In this paper, researchers clarified how influenza A virus hosts the mucosal defense barrier in the body's trachea and causes infection Relevant research results are expected to help open Develop new measures to interfere with the activity of influenza A virus The mucosal barrier is the first defense barrier against influenza A virus, which contains sialic acid that can induce the virus to bind In order to infect cells and not be fooled, influenza A virus depends on the balance between two proteins on the surface of virus particles, namely hemagglutinin and neuraminidase Up to now, researchers have not known that these proteins are assembled on virus particles And how it promotes the virus to penetrate into the host's mucosal layer According to researcher Michael Vahey, we speculate that the shape of virus particles and the packaging and assembly of hemagglutinin and neuraminidase will affect the adsorption and separation balance of virus by allowing the virus to invade the mucosal barrier effectively The researchers studied the assembly patterns of hemagglutinin and neuraminidase in influenza A virus by using fluorescent labeling and super-resolution fluorescent microscopy The results showed that the two proteins can be distributed in an asymmetric way, and they can combine and divide to lead to long-lasting directional movement H1N1 seems to work like a Brownian ratchet The assembly of this protein enables it to pass through the host mucosa in a thermally driven manner, which solves the conflicting needs of viruses, that is, it can not only penetrate the mucosa, but also stably adsorb on the cells below Later researchers will carry out more in-depth research to understand whether there is a certain correlation between the assembly characteristics of A-virus and its infectivity during host host transmission and individual infection The relevant research results may help researchers to develop new interventions for effective treatment of A-virus infection and transmission 【3】 Nat commun: the virus in the "protein coat" is more infectious, which can accelerate the occurrence of Alzheimer's disease doi: 10.1038/s41467-019-10192-2 the latest research of Stockholm University and Karolinska Institute shows that the interaction between the virus and the protein in the host biological fluid will form a layer of protein on the surface of the virus The protein coat makes the virus more infectious and promotes plaque formation in neurodegenerative diseases such as Alzheimer's disease Kariem ezzat and his colleagues studied the protein crown of respiratory syncytial virus (RSV) in different biological fluids RSV is the most common cause of acute lower respiratory tract infection in children all over the world, resulting in 34 million cases and 196000 deaths every year "The protein crown characteristics of RSV in blood are very different from those in lung fluid It's also different between humans and other species, such as rhesus monkeys, which also have RSV, "ezzat said "The virus remains unchanged at the genetic level It just accumulates different protein canopy on the surface to obtain different identity, which depends on its environment This makes it possible for viruses to benefit from extracellular host factors, and we have shown that many different coronal experiences make RSV more infectious "Researchers at Stockholm University and Karolinska college also found that viruses such as RSV and HSV-1 can bind to a specific protein called amyloid Amyloid protein aggregates into plaques and plays a role in Alzheimer's disease, leading to neuronal cell death So far, the mechanism of the connection between the virus and amyloid plaques is hard to find, but ezzat and his colleagues found that HSV-1 can accelerate the transformation of soluble amyloid protein to the linear structure that makes up amyloid plaques In an animal model of Alzheimer's, they found that mice developed the disease within 48 hours of brain infection In the absence of HSV-1 infection, this process usually takes several months 【4】 Nat Immunol: during chronic viral infection, killer T cells cause cachexia to produce doi: 10.1038/s41590-019-0397-y in a new study, researchers from Austria, Germany, the United States and Switzerland identified the mechanism of viral infection leading to cachexia In mice infected with a specific virus, killer T cells cause fat tissue and weight loss, but how they do that is still unclear Photo source: Nature Immunology in order to understand how infection can promote the production of cachexia, the researchers studied an established viral infection model: mice infected with lymphocytic choriomenitis virus (LCMV), a rodent borne pathogen that can also infect humans They observed that within a week of exposure, the mice showed symptoms of human cachexia: they moved less, lost 20 percent of their weight, and some muscle and fat tissue disappeared The researchers conducted a number of experiments to understand what promotes cachexia production in their mouse models They first blocked "common and suspicious" proteins, such as IL-6 and TNF α, known to cause cachexia in mouse models But surprisingly, there was no improvement in tissue wasting in animals, suggesting a different mechanism at work Further experiments show that killer T cells need to be activated by LCMV virus to trigger cachexia, and they need to be activated by specific antiviral cytokines However, it is not clear how killer T cells promote the production of cachexia Bergthaler said he believes that these T cells may be releasing a soluble factor to guide fat tissue to start burning fat, or they may first pass this information through another type of cell He said, "this is one of the major issues that we have left behind We know T cells work, but we don't know how they work "Bergthaler suggests that cachexia may not always be bad in an infected situation: it may be a way to quickly release energy stored in fat tissue to help the immune system fight infection These are speculations, he stressed, but important considerations still need to be taken, especially in developing methods to treat cachexia "We think this is an interesting case: at the whole biological level, you will see how the immune system communicates with metabolism, and it is likely to feed back into the immune system again We are trying to understand the physiological and evolutionary reasons "[5] cell: Chinese scientists reveal the mechanism of Chikungunya virus invading host cells doi: 10.1016/j.cell.2019.04.008 In a new study, the research team of George F Gao, Beijing Academy of Biological Sciences, Institute of Microbiology, Tianjin Institute of industrial biotechnology, Institute of genetics and developmental biology, Chinese Academy of Sciences, Feng The crystal structure of mouse mxra8, human mxra8 and Chikungunya virus E protein when they are combined, as well as the low-temperature electron microscope structure of human mxra8 and Chikungunya virus like particles were analyzed by Gao group The results of the study were recently published online in the journal Cell Image source: cell the researchers found that mxra8 has two Ig like domains with unique topologies This receptor binds to the canyon between the two E-protein monomers of the spike protein on the surface of Chikungunya virus particles The atomic details of the binding interface between the E protein of Chikungunya virus and mxra8 revealed that the two Ig like domains of mxra8 and the hinge region connecting the two domains were involved in the interaction with the amino acid residues of E1-E2 protein from chikungunya virus In addition, the stalk region of mxra8 is very important for chikungunya virus to invade host cells These findings provide important information for the development of treatment strategies for these arthritis A viruses They can help to screen experimental drugs, evaluate whether the antibodies produced by experimental vaccines are likely to prevent infection, and analyze whether mutations in viruses will affect their virulence 【6】 Cell: to reveal the three-dimensional structure of Chikungunya virus when it binds to mxra8 receptor, which is expected to develop new vaccines and drugs doi: 10.1016/j.cell.2019.04.006 In a new study, researchers from Washington University and paxvax company in the United States found information that may help prevent this debilitating disease They photographed high-resolution structural images of the virus when it combined with a protein found on the surface of cells in the joint (mxra8 below) The protein used in this study came from mice, but humans also had the same protein, and the virus interacted with the protein in mice and humans in almost the same way These structures show in detail at the atomic level how chikungunya virus binds to the cell surface protein - data that are expected to accelerate the design of drugs and vaccines to prevent or treat arthritis caused by the virus or related viruses Related research