Military scientists have determined that the body’s immune system contributes to the severity of the disease in rats infected with the Crimean-Congo malaria virus (CCHFV), which causes a highly contagious viral infection in in people. Their works, published May 19, 2022 in PLoS pathogensprovides a deeper understanding of how the virus causes disease and lays the groundwork for the provision of medical preventive measures to prevent and treat infection.
CCHFV is endemic in Asia, Africa and Eastern Europe, and there have been recent outbreaks in Western Europe. For these reasons, the World Health Organization considers the priority of the disease. Currently not available accept drugs or CCHFV vaccine, which causes diseases that resemble a lack of symptoms to disaster and death. While it is not known why some patients become ill others also become infected. epidemiological studies suggest that the host inflammatory response– a complex physical reaction that develops when tissues invade it virus– may be an important factor in regulating disease outcomes. To date, however, the significance of the host’s response in disease management has not been demonstrated.
To investigate this method, Joseph W. Golden, Ph.D. and colleagues at the US Centers for Disease Control and Prevention (USAMRIID) initially suggested that rats that did not have “critical equipment” were not at risk for CCHFV infection. These mice do not have a protein called mitochondrial antiviral protein signal (MAVS) and the study took place even when type I interferon, an important component of immune response, and not activated. This is an interesting study, according to Golden, who said that rats should be more susceptible to infection because they do not have the basic immune system.
“In fact, in small MAVS mice, the virus fails to produce a inflammatory response, and bacterial levels are reduced in the liver, a key type of virus,” he said. This has led USAMRIID researchers to suspect that increased production of inflammatory cytokines, a type of signal involved in immune responses, may contribute. disease progression.
By studying infection in mice without significant cytokine pathways, the researchers determined that the TNF-mai receptor signaling is a major driver of CCHFV-.. They can protect beraye infection with CCHFV using antibodies aimed at TNF-α. Surprisingly, they also determined that while low-grade CCHFV strains caused a simpler response than viral strains, both strains caused lower levels of liver damage. Essentially, their work reflects that inflammatory response help bring out the effects of CCHFV.
USAMRIID has been studying CCHFV for many years, and with the recent development of an appropriate animal modeling system, Golden and his team have focused their research on two aspects: understanding how the virus causes disease and producing vaccines and medicines to prevent or treat infection. The team has previously identified an important protein called glycoprotein 38 (GP38) as an important immunosuppressive agent. That study paved the way for the development of vaccines that could be used to protect people infected with the virus. They have also developed a DNA barrier that can protect against viruses that are currently in development before hospitalization. With this new study, USAMRIID team identified the inflammatory response as the new target of drug intervention.
Their functional body allows for a combination of therapeutic approaches that both attack the virus and regulate the host’s response to help prevent it. severe disease, according to study author Aura Garrison, Ph.D. “With this recent development, we hope that vaccines and vaccines for the benefit of humanity will soon be available to reduce the risk of CCHFV,” she said.
Joseph W. Golden et al, Inflammatory Host contributes to the severity of the disease in the Crimean-Congo hemorrhagic fever infection mice, PLOS DISEASES (2022). DOI: 10.1371 / journal.ppat.1010485
U.S. Army Medical Center for Infectious Diseases
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