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Lab.Equipment has sourced a new article from the Biotech industry for you. This one is published by GEN – Genetic Engineering and Biotechnology News:
Marburg virus, a member of the filovirus family—which also contains the five species of Ebola virus—typically causes a serious disease of hemorrhagic fever, with a fatality ratio of up to 88%. There is no treatment for Marberg infection and although experimental treatments have been validated in nonhuman primates models, they have never been tried in humans.
A detailed study of the monoclonal antibodies from a person who survived a Marburg infection led researchers to identify novel mechanisms that contribute protection against the disease, according to the latest findings of a collaborative team led by the University of Texas Medical Branch (UTMB) at Galveston and Vanderbilt University Medical Center.
The findings are now available in a paper titled, “Non-neutralizing Antibodies from a Marburg Infection Survivor Mediate Protection by Fc-Effector Functions and by Enhancing Efficacy of Other Antibodies” in Cell Host & Microbe.
In an earlier study, the research team had isolated a large panel of monoclonal antibodies (mAbs) from B cells of a human survivor with previous naturally acquired Marburg virus infection. In this new study, they characterized functional properties of these mAbs and identified non-neutralizing mAbs targeting the glycoprotein (GP) of the virus.
“Antibodies are currently the most promising platform for developing post-exposure treatments for Marburg virus infection and are critical tools for the design of improved vaccines,” said Alex Bukreyev, a UTMB virologist in the departments of pathology and microbiology & immunology and senior author on the study. “Understanding the mechanisms of antibody-mediated protection during Marburg virus infection is also useful for understanding antibody protection against other viral pathogens, including SARS-CoV-2, which causes... Find the full article at the GEN – Genetic Engineering and Biotechnology News Blog.
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