New York: Scientists have identified a single gene pathway that can disrupt Zika and similar viruses from spreading in the body and also act as a potential drug target for such deadly diseases.
The findings showed that disabling SPCS1 -- in both human and insect cells -- reduces viral infection and does not negatively affect the cells themselves.
"We wanted to find out if we could identify genes present in the host cells that are absolutely required by the virus for infection," said Michael Diamond, Professor at Washington University.
While the absence of SPCS1 gene shut down the spread of flaviviruses, eliminating the gene had no detrimental effect on other types of viruses, including alphaviruses, bunyaviruses and rhabdoviruses, the researchers said.
"In these viruses, without SPCS1 gene the chain reaction doesn't happen and the virus can't spread. So this gene can act as a potential drug target because it disrupts the virus but not the host," Diamond added.
Viruses hijack host cells to replicate and spread, making them dependent upon the genetic material of the organisms they infect.
If a cell lacks a gene that the virus requires for infection, the virus will have to stop in its tracks and will enable the cells to survive. Thus the missing gene becomes vital to spread of the virus.
"Flaviviruses appear to be uniquely dependent particularly on SPCS1 gene to release the viral particle," Diamond noted.
For the study, published in the journal Nature, the team first conducted experiments on West Nile virus and then found that the same results held true for other Flaviviridae family members, including Zika, dengue, yellow fever, Japanese encephalitis and hepatitis C viruses.
Using gene-editing technology called CRISPR that is capable of selectively shutting down individual genes, the researchers identified only nine key genes that the virus relies on for infection or to spread.