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Drug target for Ebola-like viruses identified

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drugToronto: A potential mechanism to combat diseases caused by haemorrhagic fever viruses such as Ebola has been discovered, scientists say.

These diseases present a dramatic risk to human health as they often spread quickly and kill a high percentage of infected individuals, as demonstrated by the recent Ebola outbreaks, researchers said.

Effective treatments such as vaccines and drug therapies are not available for many of these infections since the outbreaks mostly occur in developing countries with limited financial resources.

Moreover, the genomes of many haemorrhagic fever viruses mutate rapidly, enabling them to quickly adapt to potential drug treatments and evade the immune system.

“Although our work does not directly lead to treatments on a short term, it does identify a process where the virus could be vulnerable to drug therapy, or how we might design an attenuated viral strain for vaccine development,” said first author Normand Cyr, a postdoctoral researcher at the University of Montreal.

“Identification of the Achilles heels of haemorrhagic fever viruses like the Rift Valley fever virus will help inspire additional research and eventually lead to the development of new therapeutic strategies to treat these deadly tropical infections,” said Cyr.

Researchers used Nuclear Magnetic Resonance (NMR) spectroscopy studies to investigate the structural properties of an important viral protein required for virulence of the Rift Valley fever virus, a virus that causes infections in both humans and livestock similar to the Ebola virus.

Viral proteins such as the Non-structural protein (NSs) studied in the research bind to the transcription machinery of human cells via the p62 subunit of the TFIIH protein complex, which leads to the formation of nuclear filaments that are essential for propagation of the virus.

“The structural details reported show that the viral protein uses a simple so-called OXaV motif that is similar to that found in human DNA repair proteins, and blocking this binding event with drugs would certainly weaken the virulence of the virus,” said senior co-author Professor James Omichinski, who supervised the research.

The research was published in the journal PNAS.


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