The coronavirus is spreading faster despite several efforts and measures to contain, almost 10 times more than the SARS 2003 virus. But why? In a quest to find answers, researchers, using genetic and structural analyses have identified a key a protein on its surface.
"Understanding transmission of the virus is key to its containment and future prevention," David Veesler, a structural virologist at the University of Washington in Seattle told Nature.
How does a virus enter the cell?
Receptors on the cell membrane, which are the protein structures, that receive and transduce signals which are the gateways recognised by the virus, to enter into the host cell. The virus hijacks the cellular processes producing a virally encoded protein such that it gets activated by the cell, later entering the cell to replicate itself.
If researchers can know how exactly the coronavirus enters the receptors, they may succeed to develop a drug to stop it. Usually, the cell receptor as well as the virus protein can act as potential targets for drugs to block the pathogen. However, this is not sure in case of the novel coronavirus.
What about coronaviruses?
There are a group of coronaviruses among which the novel coronavirus is one. Among these known coronaviruses, it creates a viral envelope, called spike (S) protein, that undergoes a biochemical modification to enter through the receptor. This is called S protein priming. However, the new coronavirus has its S protein different from other coronaviruses with a protein site on it that is activated by a host cell's enzyme called furin.
Li Hua, a structural biologist at Huazhong University of Science and Technology in Wuhan, China told Nature that Furin is found in lots of human tissues, like the lungs, liver and small intestines, meaning that the virus can potentially attack multiple organs as observed in the COVID-19 patients. Li co-authored a genetic analysis of the virus that was posted on the ChinaXiv preprint server (not peer reviewed).
"Camostat mesylate" could block the infection.
However, evidence that the novel coronavirus protein binds to the same receptor as the SARS virus' S protein is published in the journal Cell. The receptor is called angiotensin-converting enzyme 2 or ACE2. The paper further showed that "camostat mesylate, an inhibitor of the enzyme that is used by the novel coronavirus for S protein priming, blocks COVID-19 infection of lung cells.
Stefan Pöhlmann (professor for Infection Biology at Georg-August-University and Head of the Infection Biology Unit of the German Primate Center, Germany) and his colleagues wrote in the study: "This compound or related ones with potentially increased antiviral activity could thus be considered for off-label treatment of SARS-CoV-2-infected patients." However , testing and clinical trials have not happened.
Gary Whittaker, a virologist at Cornell University in Ithaca, New York said, "Coronaviruses are unpredictable, and good hypotheses often turn out to be wrong,"
In the Cell journal's paper it was found that antibodies against the SARS coronavirus protein reduced how well a lab's model virus with novel coronavirus protein could infect cells. Further finding similar results with antibodies against S proteins made in rabbits but "confirmation with infectious virus is pending," the paper added.
David Veesler, an assistant professor in Biochemistry at the University of Washington in Seattle and his team showed that antibody serum from four different mice could reduce infection with a lab model virus containing the novel coronavirus by 90%. The team showed evidence that the virus enters target cells via ACE2 in a paper published in Cell, which is similar to the Pöhlmann's paper.
All these can greatly help in a creation of vaccine, until proven by clinical trials, which could take months.