The Zika virus is highly lethal virus in today’s time which is highly infecting the new born brain’s making them underdeveloped.
As zika is spreading throughout the world, it is calling for rapid development in therapeutics for treating Zika rings loud and clear. For taking a further step in identifying a possible therapeutic candidate.
Team of researchers from the Duke-NUS Medical School with the collaboration with scientists from the University of North Carolina, have discovered the mechanism by which C10, a human antibody previously identified for reacting with the Dengue virus. It is thus preventing Zika infection at cellular level.
Process of Neutralizing Zika Virus:
For infecting a cell, virus particles can usually undergo two main steps, docking and fusion. It is also common target for disruption and developing viral therapeutics.
During docking process, virus particle is identifying specific sites over the cell and further binds to them. With infection of Zika, docking then further initiating the cell to further take virus in via an endosome, a separate compartment within the cell body.
Proteins within the virus coat will undergo changes in structure for fusing with the membrane of endosome. It is thereby releasing the virus genome into the cell and thus completing the fusion step of infection.
Using the method which is known as cryoelectron microscopy, it is allowing for the visualization of extremely smaller particles and their interactions.
Team has visualized C10 interacting with the Zika virus under different pHs. It is so as to mimic the different environments both the antibody and virus which will find themselves in throughout infection.
They even showed that C10 is binding to the main protein which is making up the Zika virus coat, regardless of pH. It is thus locking these proteins into place while preventing structural changes required for fusion step of infection.
Without the fusion of the virus to the endosome, viral DNA is prevented from entering the cell and infection is thwarted.
Dr Lok commenting over the same says, “Hopefully, these results will further accelerate the development of C10 as a Zika therapy to combat its effects of microcephaly and GuillainBarré syndrome. This should emphasise the need for further studies of the effect of C10 on Zika infection in animal models.”
Ralph Baric, PhD, professor in the Department of Epidemiology at UNC’s Gillings School of Global Public Health says, “By defining the structural basis for neutralization, these studies provide further support for the idea that this antibody will protect against Zika infection, potentially leading to a new therapy to treat this dreaded disease.”
These findings have suggested that C10 may have developed as a therapy for Zika infection and thus should be further explored.
In addition to that disrupting fusion with C10 may prove to be more effective in preventing Zika infection with therapeutics which is attempting to disrupt docking.
This is because this fusion step is quite critical for Zika infection while the virus may develop other mechanisms for overcoming disruptions to docking step.
With the call for rapid development of Zika therapies, C10 has quite emerged as a front runner for answering this call.