A UT Southwestern team has identified a crucial gene for cell consumption and viral destruction. The results may lead to ways of manipulating this process in the battle against viral infections in the immune system.

Autophagy, which means "self-eating," isolates cellular waste from double-layered vesicles called autophagosomes. This process helps extract old and damaged organelles, protein complexes, bacteria, and viral invaders from cells. Researchers have found specific pathways by which cells induce and control autophagy for a variety of cell refusal tasks.

216 genes were identified that seem to play a role in viral autophagy. The researchers used bioinformatics to examine biological processes controlled by these genes. They quickly produced a gene called Sorting Nexin 5 (SNX5), which produces a protein to facilitate recycling. The team considered SNX5 may be essential for autophagic since viruses often enter cells via this pathway. However the cells' ability to conduct autophile on HSV-1 and Sindbis viruses decreased considerably when scientists shut off the gene.

"By learning how cells naturally take up and degrade viruses," said study leader Xiaonan Dong, Ph.D, "we could discover ways to augment this process, creating a more general strategy for developing broad-spectrum antiviral therapeutics that combat an array of different viral infections."

Transmission electron microscopic image of an isolate from the first U.S. case of COVID-19, formerly known as 2019-nCoV. The spherical viral particles, colorized blue, contain cross-sections through the viral genome, seen as black dots.
Photo by CDC / Unsplash

These findings together indicate that cells have a special viral autophagy pathway that is possibly regulated by SNX5. Not only does this discovery solve a mystery of a long history of basic biology, but it may potentially lead to new approaches to treat viral infections. Most current methods target viruses via their weaknesses – a method which calls for a single strategy for each viral form to be created.