Breakthrough in Bacterial Infection Mechanisms Unveiled by Virginia Tech Team

Virginia Tech researchers have identified how Shigella flexneri bacteria manipulate host molecules to ensure survival against human defenses. This discovery could offer insights into broader bacterial infection strategies. The study by Daniel Capelluto's team is published in the journal Structure.


Devdiscourse News Desk | Updated: 20-09-2024 22:46 IST | Created: 20-09-2024 22:46 IST
Breakthrough in Bacterial Infection Mechanisms Unveiled by Virginia Tech Team
Representative Image. Image Credit: ANI
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Researchers at Virginia Tech have unlocked the secrets of how bacteria manipulate molecules to infect their hosts, focusing on the pathogen Shigella flexneri, known to cause dysentery. The groundbreaking study led by Daniel Capelluto has been published in the open-access journal Structure by Cell Press.

This infection strategy could be common among other bacteria, presenting a foundational understanding of the molecular mechanisms that drive bacterial infections, according to Capelluto, an associate professor of biological sciences. Insights from this research pave the way for more precise preventive measures against bacterial diseases.

Shigella flexneri, transmitted through contaminated food or water, targets the intestinal lining by replicating and invading host cells. Capelluto pointed out that dysentery predominantly affects children under 5 in developing countries, responsible for around 160,000 deaths annually. He noted that bacteria manipulate host cell metabolism to facilitate infection, releasing proteins that disrupt cellular balance and create an acidic environment rich in lipids.

In normal conditions, proteins like TOM1 and TOLLIP help degrade unneeded membrane proteins. However, during a bacterial infection under acidic conditions, these proteins bind to bacterial lipids, aiding bacterial survival. Using advanced biochemical techniques, the research identified the lipid-binding site in TOM1, showing how it is prevented from its normal function.

(With inputs from agencies.)

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