New Zealand-made “virus decoy” is promising

A team led by Associate Professor Rohan Ameratunga, an immunology professor at Auckland Hospital, is investigating whether a designer’bait’ molecule delivered through an inhaler can prevent the SARS-CoV-2 virus from attaching to lung cells. doing.

“At this time, there is no proven cure for Covid-19,” said Ameratunga, who has worked with prominent researchers such as Dr Davide Comoletti of the University of Victoria and Professor Miguel Quiñones-Mateu of the University of Otago.

“We are investigating the vulnerabilities of the virus and thought that the most vulnerable part was the cell-binding part.”

The virus attaches to lung cells by binding an outer “spike” protein. This plays a big role in the speed at which the virus spreads to our bodies and to other people.

Like the threat, a receptor called ACE2 happens to be highly expressed in respiratory cells, allowing the virus to penetrate deep into the lungs.

ACE2 previously hosted this havoc and acted as a receptor for the Sars coronavirus, which infected more than 8,000 people and killed 800 in the early 2000s.

To block the process, Ameratunga and his team created a unique designer ACE2 protein that sheds the virus from the actual receptor attached to sensitive cells.

When the virus was coated with a false receptor, researchers hoped it would be cleared through the sputum, just like other particles like dust and bacteria.

Their decoys not only reduce the amount of virus that passes through them and attach to cells, but they also help protect the front line health care workers.

“What we’re trying to do is target the virus very early in the infection, essentially letting people inhale these proteins, thus flattening the virus’ exponential infection curve. “

“Thus, if you are infected, it is much milder than otherwise.”

This week, his team tested the decoy at Wellington Labs in Comoretti and found it to work.

“It actually blocks the virus, and it works as we expected it to do,” he said.

“What we want to do now is make these clinical grade drugs and eventually do human trials. We don’t have Covid-19 here, so we almost have to do it overseas.”

He expected it to mean working with large pharmaceutical companies to enable trials in multiple countries.

But in order to maintain the core of research in New Zealand, the team needs to look for government funding.

“Everyone has done a great job, but at some stage we need some serious funding to get it going.

“The worst scenario is that we have to go abroad. That’s important, and so many people are dying from it. As a scientist, I need this to work. We want to make it available to everyone.”

This project is endorsed by the Australian Society of Clinical Immunoallergy and the New Zealand Immunodeficiency Foundation.

New Zealand scientists reveal virus’weakness’

Meanwhile, another team discovered a potential target point on the viral genome, or its complete genetic organization. This may point the way to new treatments.

During the lockdown period, PhD students Ali Hosseini and Professor Alex McLellan of the Department of Microbiology and Immunology at the University of Otago have begun to analyze the recently deciphered SARS-CoV-2 genome.

They have discovered a previously unrecognized weakness – a “target site” that is picked up by a nucleic acid-based “immune system” that operates in every cell of our body called microRNAs, or miRNAs.

MiRNAs, which are essential for the regulation of gene expression in cells, also play an important role in virus recognition and destruction.

One target site for SARS-2 matched a specific miRNA called miR197. The miRNA was found to be present at very high levels in patients with cardiovascular complications or respiratory viral infections.

The viral miR197 binding site has been independently mutated almost 40 times since March of this year. This mutation is now present in over 75% of SARS-CoV-2 global isolates.

“Patients with cardiovascular complications have been shown to be at risk for Covid-19,” McLellan said.

“Our study suggests that the normal defense pathways in these patients may have been blocked by this mutation in the virus.”

But it’s too early to say whether such mutations are useful for the virus, or simply “neutral hitchhikers” who don’t benefit the virus, he said.

“We need a direct approach with live viruses and further research into the transmission of such variants worldwide,” he said.

“Still, it was amazing to find the frequency of mutations in the miR197 target site in different SARS-2 isolates.

“Our research keeps an eye out for these sites and see what happens to them in the future.”

Researchers say their findings also open the possibility to design at artificial miRNA sites.

This may help weaken the virus for vaccine studies, and has been done successfully ly for other respiratory viruses.

-Jamie Morton