Ever since its first eruption late last year, the number of COVID-19 has surged to millions around the world in a matter of a few months. The novel virus has claimed thousands of lives and is spreading fast and furious. For months now, experts around the world are working in harmony to find a solution for the deadly virus. One quick solution is maybe reworking the already existing antiviral drugs. However, it is not an easy task, due to an incomplete biological understanding of the virus and how the host cells react when encountered by it.
To judiciously repurpose drugs, experts are working around the clock to understand the molecular process of the infection and the changes in the host to accommodate the viral replication. By finding the exact viral targets in the host cells, a potential drug can be selected for further testing to avoid patients from exposure to unnecessary drugs lacking validation.
Growth Factor Receptor (GFR) is known to play a crucial role in many viral infections. The GFR signalling activation leads to a change in many cellular processes like adhesion, replication, and differentiation. In the past, various viruses like hepatitis C and influenza have shown to activate GFR signaling to replicate in the host cells. Currently, though COVID-19 is suspected to fall under the same category there is no solid evidence. The authors of this paper tried to establish that COVID-19 infections do activate GFR signaling which in turn aids in the viral replication process. While monitoring the above signalling changes in the host cells, the experts also observed that the activation of GFR signalling was consistent with other viruses relying on the receptors themselves.
The study employed an in-vitro COVID-19 infection model replicating a human cell environment, to study the signalling changes within the host cell to accommodate viral replication. Well into the experiments the authors observed that the changes in the viral protein phosphorylation and phosphorylation driven host signalling was caused upon infection. Both the GFR signalling and downstream pathways were activated.
On further experimentation, by performing drug-protein network analysis experts revealed that GFR signaling pathways is the key for viral replication. The GFR signalling further activates EGFR or PDGFR signalling with a profusion of RhoGTPase associated signalling molecules.
The study does portray a few limitations. The authors had used cancer cells lines to study the virus in-vitro which does not completely speak for other cell lines. The kinetics of infection may be different for different cell lines and needs to be studied further. But taken together the results from the study provides potential novel insights into the molecular process of the viral infection. The proteomic analysis performed by the authors also revealed that several pathways are rearranged when the host cells are infected. By targeting these particular pathways a valid therapy can be found to inhibit the viral replication upon infection.