A team of scientists led by researchers at the Hebrew University in Jerusalem have discovered a potential way to resist deadly viral infections such as hepatitis C and Zika by blocking their means of regeneration.
Viruses, themselves a form of parasite, are unable to reproduce and multiply on their own, and instead rely on hijacking their host’s metabolic machinery: the components that produce the chemical processes on which we rely to stay alive.
Scientists still don’t have a clear sense of exactly how viruses achieve this, due to the complexity of the relationship between metabolism and human genes.
In the Nature Chemical Biology study between researchers at the Hebrew University in Jerusalem, Harvard Medical School, Broad Institute of MIT and Harvard, University Duisburg-Essen and the University of Dusseldorf, scientists teamed up to identify a number of genetic switches that control the body’s response to the Flaviviridae family of viruses, which includes hepatitis C, yellow fever, West Nile, dengue and Zika.
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The team found that: “Viral infection dramatically affects host metabolism, but not always for the benefit of the virus.
“The results show that virus needs can conflict with the host’s requirement for energy and that virus replication might be tightly controlled by positive and negative interactions with the host.”
In other words, while many metabolic interactions may be beneficial for the propagation of viruses, by blocking elements of these processes with carefully targeted drug therapies, we may be able to lessen and even stop their replication.
Director of the Alexander Grass Centre for Bioengineering at the Hebrew University of Jerusalem, Yaakov Nahmias, said: “This is the first indication that our cells can block replication of Flaviviridae viruses like HCV and Zika by denying them from critical building blocks the viruses need to survive.
“Our results present a new approach to treat virus infection by targeting the genetic regulation of metabolic processes on which the virus rely.”
Researchers in the wider chemical biology field now hope that the findings will offer the chance for a new methodology on tackling metabolic liver cancer, and a host of secondary illnesses associated with the hepatitis C infection such as fatty liver disease and diabetes.
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