Published on April 28, 2020

Ahmedabad: As scientists across the locked down world attempt to target coronavirus, an Ahmedabad-origin researcher in the US is leading the effort to lock out the virus from the human body. 
The popular image of the Covid-19 virus as a sphere with protruding spikes has caught the public imagination. It’s also now public knowledge that these spikes interact with human cells, latch on, and multiply to infect the host.
A team at University of Idaho has decided open an new front in the war on Covid. If one compares the virus to a key and the human cell to a lock, the team has decided to shield the keyhole on the lock so that the key doesn’t fit!

At the forefront of the research is Dr Jagdish Patel, research assistant professor at the university. Patel completed schooling in Ahmedabad and his family lives in the city. He is a molecular modelling specialist and his research focus is on developing and applying computational simulation methodologies to understand protein sequence-structure-function relationship and protein-drug interaction in biomolecular systems. He is also researching drug molecules to prevent Ebola. “Apart from myself, the team at the university that’s working to develop a cure for Covid-19 includes virologist Dr Paul Rowley and evolutionary biologist Dr James Van Levuven,” said Patel. “We have received immediate funding support of $100,000 from National Science Foundation EPSCoR grant issued to University of Idaho Professor Marty Ytreberg.”

Patel said that their inspiration to target the human cell instead of the novel coronavirus came from success of this strategy in the development of a HIV drug. The team said that the spikes of Covid-19 virus interact with ACE2 receptor present on the outer surface of human cells in lungs, heart, kidneys, intestines and arteries. The receptors are responsible for lowering blood pressure.

“The attachment of the spike protein to ACE2 begins the infection process by which the virus transfers genetic material to the cell,” said Patel. “Our approach is to provide a shield — a drug for the ACE2 receptor so that the spike protein cannot attach.” Patel went on to say: “ACE2 is also the preferred receptor for the SARS virus. Thus, this drug can also work in future epidemics involving a virus using the ACE2 receptor.”

The team members at the university said that viruses can rapidly evolve at drug-binding sites to render antiviral drugs ineffective. The team’s strategy to overcome this is to prevent viral entry using inhibitors that can block viral attachment by targeting human cell receptor.

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