Two genes have been identified by University of Hong Kong researchers as key to triggering the growth of the deadly Middle East respiratory syndrome (Mers) virus.

The breakthrough provided insights into

the development of more targeted medication in future, as there is no specific vaccine or antiviral treatment for Mers.

READ MORE: A cure for Mers? Hong Kong scientists endorse two drugs they say cured marmosets of the virus

The virus has infected more than 1,600 people around the world since 2012 and killed 587 people.

Compared to Sars, which has a mortality rate of 10 per cent, Mers has a much higher rate of 30 per cent.

Internationally renowned microbiologist Professor Yuen Kwok-yung and his team discovered that two genes – Smad 7 and FGF2 – multiplied much faster in a cell infected by the Mers virus.

“When the two genes multiplied, cells would die. The process of dying helps the proliferation and release of the virus,” said Yuen, who first gained fame in the battle against severe acute respiratory syndrome (Sars) in 2003.

The virus was found to make use of healthy cells and reproduce more by taking them over.

He said this was the first time that researchers had found the death of cells caused by the activation of these two types of genes and the proliferation of the virus.

The research team found up to 58 per cent of Mers patients, mostly from the Middle East and South Korea – the site of a major outbreak last year – had developed kidney failure in addition to respiratory infection. Only 3 per cent of Sars patients experienced the same condition.

READ MORE: South Korea removes last person from quarantine over Mers

While everyone carries the two genes, which affect the life cycle of cells, they are mostly found in the kidney.

“It is very abnormal to see lung cells displaying genes related to kidney failure,” said Yuen.

He estimated the Mers virus was carried from lungs to kidneys through blood circulation, leading to the failure of both organs.

Once the two genes in Mers-infected cells were blocked by chemicals, cells could survive and the level of the virus produced dropped markedly.

The findings have been published in the latest issue of Nature Microbiology.

While the university earlier found two existing drugs used for HIV and sclerosis effective in curing Mers, Yuen said they were not the best. The future development of medication could aim at suppressing the increase of the genes, he said.

“If we can suppress cell death and the growth of the virus, the patient might not die ... This approach has never been considered before,” he said.

It is however not yet known when the medication will be developed, although Hong Kong has been among the leading places for Mers research.

“Firstly, Hong Kong does not have Mers [patients] ... and meanwhile no pharmaceutical firms have shown interest in it,” said Yuen, adding that the drug was less profitable as the number of Mers patients was much lower than those suffering from chronic diseases such as hypertension or diabetes.