Australian researchers have made an exciting discovery that could lead to the better treatment of those with mosquito-borne diseases like Ross River virus.
The current Ross River outbreak along the east coast of Australia has left many of those infected with severe joint pain due to the arthritis associated with the virus.
Researchers at QIMR Berghofer Medical Research Institute have now discovered an enzyme in the immune system that promotes the arthritis following infection of chikungunya virus, a mosquito-borne disease related to Ross River virus.
Professor Andreas Suhrbier from the Inflammation Biology Laboratory at QIMR Berghofer led the international study and says the finding is a massive step forward in their understanding of the disease.
The mouse study has also led to hope that existing drugs may already be available to target the debilitating and “hard to treat” inflammation it causes.
“We’ve got a brand new drugable target that will hopefully lead to better treatment for this kind of disease and hopefully also related diseases like Ross River disease,” Prof Suhrbier told AAP.
“And perhaps also other viral arthritic disease,” he said.
Like Ross River virus, chikungunya virus can cause severe, chronic polyarthritis – inflammation in multiple joints – and/or polyarthralgia (pain in multiple joints).
Standard anti-inflammatory drugs are usually not very effective in reducing the inflammation or pain.
Researchers at QIMR Berghofer used RNA-sequencing technology to examine inflammatory responses following infection with chikungunya in the immune system.
It found the granzyme A enzyme promotes arthritis following infection with chikungunya virus.
When granzyme A was missing, chikungunya virus caused far less swelling and arthritis, said Prof Suhrbier.
“We also found that when we inhibited the enzyme, there was far less swelling and arthritis,” he added.
This is very significant because for a long time there has been debate about what granzyme A actually did, said Prof Suhrbier.
Prof Suhrbier says the evidence is “clear as day” that the enzyme actually causes inflammation.
“Get rid of granzyme A and the arthritis is much reduced, ” he said.
While the drugs used to inhibit granzyme A in the mice don’t work in humans, there may already be existing anti-inflammatory drugs that inhibit the very thing the enzyme targets to cause the inflammation, said Prof Suhrbier.
“That would be a shortcut to a treatment because those drugs have already been developed and we don’t have to start from scratch to try to make a human granzyme A inhibibtor” Prof Suhrbier said.
However he did acknowledge more research is needed to confirm the findings, published in journal PLOS Pathogens.