Shrayana Ghosh, Amity University Kolkata
A research team from UT Southwestern has recognised a key gene necessary for cells to consume and destroy viruses. The findings which were reported in Nature could lead to ways that could manipulate this process to improve the immune system’s ability to combat viral infections.
The key gene essential for cells to consume and destroy viruses was recently identified by a research team from UT Southwestern. The findings showed the approach could lead to ways of manipulating this mechanism to boost the capacity of the immune system to battle viral infections, such as the current COVID-19 pandemic. Scientists have long understood that to rid themselves of unnecessary material, cells use a mechanism called autophagy. In double-layered vesicles called autophagosomes, autophagy, which translates as “self-eating,” involves isolating cellular waste, which is then fused with single-layered vesicles known as lysosomes to dissolve the materials inside and turn them into building blocks for other purposes. Cells discard old or defective organelles and protein complexes, bacteria, and viral invaders through this process. Researchers have identified clear pathways by which cells initiate and regulate autophagy for a variety of cellular refusal tasks.
Dong and his colleagues for their research, manipulated human cells infected by various viruses in this latest research to deplete more than 18,000 different genes individually, analyzing their effects on autophagy.
The researchers infected cells with the herpes simplex virus type 1(HSV-1) as their initial models. 216 genes that appeared to play a role in viral autophagy were identified by the team’s study. The researchers used bioinformatics to examine biological processes that control these genes to narrow their search for the main players. They soon honed in on a gene named nexin 5 (SNX5) sorting, which generates a protein that allows endosomes recycle plasma membrane-anchored proteins, sorting organelles into cells that often within their cells ferry materials isolated outside cells. When scientists shut down SNX5 in human cells, the capacity of the cells to conduct autophagy on HSV-1 decreased dramatically, but their ability to enable autophagy remained intact as part of regular cell cleaning or bacteria removal, implying that this gene is used exclusively for viral autophagy.
Further studies have shown that deletion of SNX5 has significantly increased vulnerability to infection in laboratory cells as well as in adult and juvenile animals. Nevertheless, they were largely spared when these cells were invaded by viruses manipulated to inhibit their capacity to cause autophagy. The findings indicate that cells have a special viral autophagy pathway that possibly has SNX5 at the helm. This discovery not only solves a long-standing mystery, but it could potentially lead to new ways of combating viral infections.
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