New research advances knowledge of the battle between viruses and human cells

The green dots in the picture of this cell indicate the proteins involved in the chemical modification that inhibits virus takeover. The nucleus of the cell is blue. Credit: UMass Amherst

In a lengthy battle between the herpes virus and its human host, a virologist at the University of Massachusetts and her team of students have identified human RNA that can resist virus hijacking and the mechanism by which it occurs.

This finding is described in a paper published on February 15. Minutes of the National Academy of SciencesRepresents an important step in efforts to develop antiviral drugs to combat infectious diseases.

“This paper is about trying to understand how these RNAs escape degradation,” said senior author Mandy Muller, an assistant professor of microbiology. “The next step is to determine if this can be manipulated to your advantage.”

At the Muller Lab, student researchers work with Muller to control human gene expression to complete the viral infection after Kaposi’s sarcoma-related herpesvirus (KSHV) has been hidden inside the human body for years. I’m studying the method. At that point, weakened people Immune system Cancerous lesions of Kaposi’s sarcoma can develop in the mouth, skin or other organs.

Researchers use genome-wide sequencing, post-transcriptional sequencing, and molecular biology to find out how human cells or viruses know how to prevent degradation.

“The virus is very smart, and that’s what I mean,” says Muller. “They don’t do much damage for a very long time because they have many strategies for sticking and it’s one way to hide from the immune system.

“But at some point, often years later, they reactivate. The way to do this is to trigger a large RNA degradation event in which the virus clears the mRNA from the cells. The human system is no longer able to express proteins that need to be expressed, which also means that a lot of resources are suddenly available for the virus. “

A team of lead author and graduate student Daniel Macveigh-Fierro and co-authors and undergraduate students Angelina Cicerchia, Ashley Cadorette, and Vasudha Sharma have investigated how and why some RNA can avoid viral degradation. I have a question. The research In 2020, NIH’s National Institutes of Health supported Mueller with the $ 1.9 million Maximizing Investigators’ Research Award (MIRA).

“We show that RNA that escapes has a different chemical tag (post-transcriptional modification) than other RNAs,” explains Muller. “By attaching this tag, M6A, they can mobilize proteins that protect them from degradation. “

Mueller has been studying KSHV since he was a college student in his native France, and her mission continues.

“We know that this protein is needed to protect RNA from degradation, but we still don’t know how it physically stops degradation, so we’ll look at it now,” she said. Says.

Ultimately, understanding the mechanisms and pathways involved in KSHV infection may lead to the development of RNA therapies for the treatment of viral diseases.

“By identifying the determinants that make mRNA resistant or susceptible to virus-induced disruption, these findings can be used to better design antiviral drugs and reshape the outcome of infection. “Muller said.

Cellular antiviral protection

For more information:
Daniel Macveigh-Fierro et al, m6A leader YTHDC2, is essential for escape from KSHVSOX-induced RNA disruption. Minutes of the National Academy of Sciences (2022). DOI: 10.1073 / pnas.2116662119

Quote: A new study was obtained from on February 18, 2022, between viruses and human cells ( Advance your knowledge (February 18, 2022)

This document is subject to copyright. No part may be reproduced without written permission, except for fair transactions for personal investigation or research purposes. Content is provided for informational purposes only.

New research advances knowledge of the battle between viruses and human cells

Source link New research advances knowledge of the battle between viruses and human cells

Show More

Related Articles

Back to top button