Lethal viruses hijack cellular defences against cancer


Monday, 06 August, 2018


Lethal viruses hijack cellular defences against cancer

Researchers from Monash University’s Biomedicine Discovery Institute (BDI) have identified a new mechanism used by Henipaviruses in infection, and potential new targets for antivirals to treat them. Their findings may also apply to other dangerous viruses.

Led by Monash BDI’s Dr Gregory Moseley, a team of scientists found that Henipaviruses hijack a mechanism used by cells to counter DNA damage and prevent harmful mutations, important in diseases such as cancer.

It was already known that the viruses send a particular protein into a key part of a cell’s nucleus called the nucleolus, but it wasn’t known why it did this, Dr Moseley said.

The researchers showed that this protein interacted with a cell protein that is an important part of the DNA-damage response machinery, called ‘Treacle’, he said. This inhibited Treacle function, which appears to enhance henipavirus production.

“What the virus seems to be doing is imitating part of the DNA damage response,” Dr Moseley said.

“It is using a mechanism your cells have to protect you against things like ageing and mutations that lead to cancer. This appears to make the cell a better place for the virus to prosper,” he said.

It is possible that blocking the virus from doing this may lead to the development of new antiviral therapies, according to Dr Moseley.

Both Hendra and Nipah, which spread from bats to other animals and humans, emerged in the 1990s — Hendra in an outbreak in Brisbane in 1994 and Nipah in Malaysia in 1998. The viruses, which share outcomes including inflammation of the brain and severe respiratory symptoms, have since caused multiple outbreaks of disease. Nipah has killed several hundred people, including at least 17 people in the Indian state of Kerala in June.

“Nipah is not so important in Australia but it’s the one people are concerned about internationally,” Dr Moseley said.

“Like Ebola, if you get a really big outbreak and it’s not containable, it could be disastrous,” he said.

He said the study’s findings add insights into how viruses behave more generally.

“We identified a new way that viruses change the cell, by using the very same machinery that the cell normally uses to protect itself from diseases like cancer,” he said.

“This seems to be heading towards exciting possibilities about what viruses might be doing,” joint first author Dr Stephen Rawlinson said.

“We are now trying to work out exactly how changing the DNA damage response through Treacle is useful to this and other dangerous viruses,” he said.

The findings have been published in the journal Nature Communications. PhD student Tianyue Zhao was the other first co-author.

The multidisciplinary collaboration working on the paper included scientists from Monash University’s Department of Microbiology, physical chemists using a super-resolution microscope in the Monash University School of Chemistry, the CSIRO AAHL high biocontainment facility and the University of Melbourne.

The research was supported by the Australian Research Council and the Australian National Health and Medical Research Council.

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