Latest news with #TexasBiomedicalResearchInstitute
News18
2 days ago
- Health
- News18
Covid Virus's Bodyguard: How Pathogen Protects Itself While Replicating
Last Updated: US study highlights that disrupting this protective shield significantly reduces the virus's ability to spread, which could be key to developing more effective antiviral treatments Scientists from the Texas Biomedical Research Institute and the University of Chicago have made a significant breakthrough in understanding SARS-CoV-2, the virus responsible for Covid-19. Their collaborative efforts have identified a crucial self-protective mechanism that the virus uses within the human body, enabling it to replicate effectively and infect more cells. The study highlights that disrupting this protective shield significantly reduces the virus's ability to spread, emphasising its critical role in viral propagation. The research reveals that SARS-CoV-2 is not just an invading pathogen but a sophisticated entity that actively protects itself during the infection process. This newly discovered mechanism allows the virus to survive and multiply within host cells, bypassing the body's natural defences. Scientists observed a direct correlation: interference with this shielding process led to a significant drop in the viral infection rate. This finding, published in the journal Nature Communications, strongly suggests that understanding and potentially targeting this protective strategy could be key to developing more effective antiviral treatments. While the initial report does not delve into the specific molecular or cellular details of how this mechanism operates, its identification marks a pivotal moment in Covid-19 research. Scientists emphasise its profound importance in deciphering the intricate ways the virus spreads at a cellular level. Unravelling this protective shield could open new avenues for therapeutic intervention, potentially leading to drugs that disarm the virus's ability to protect itself, thereby limiting its replication and spread within an infected individual. This discovery holds promise for a more targeted approach to combating Covid-19. By understanding the virus's internal defences, researchers can work towards developing antiviral therapies that specifically dismantle this protective mechanism, rather than relying solely on broad-spectrum approaches. (With agency inputs) First Published: June 06, 2025, 18:46 IST
Hans India
3 days ago
- Health
- Hans India
Study shows how Covid virus shields itself during replication
US researchers have identified a mechanism that SARS-CoV-2 -- the virus that causes Covid-19 -- uses to protect itself inside the body as it works to replicate and infect more cells. Without this protective mechanism, viral infection is dramatically reduced, said the team from the Texas Biomedical Research Institute and the University of Chicago. The finding, published in the journal Nature Communications, not only provides a potential target for new Covid therapies but also offers insights that could inform future vaccine and antiviral development. The study builds on earlier work from Texas Biomed that identified ORF3a, a type of viral protein most important for the virus's pathogenicity, or ability to cause disease. Specifically, the team found that SARS-CoV-2 ORF3a appears to play a vital role in protecting structural proteins, most notably the spike protein that facilitates spread into other cells, as they are assembled on the surface of viral particles. It does this by driving the formation of a dense group of proteins that surround the spike protein and provide protection while in transit, much like security detail protecting a person or an armoured vehicle carrying cash to the bank, the researcher said. Jueqi Chen, Assistant Professor at the University of Chicago, termed these protective complexes "3a dense bodies" or 3DBs for short. It appears that 3DBs help prevent the spike protein from being cut into smaller components. When ORF3a is missing, these 3DBs fail to form, and the spike protein often arrives damaged, severely impairing the nascent virus's ability to infect new cells, the expert said. "ORF3a could therefore be a good target for drugs to block the virus," said Luis Martinez-Sobrido, Professor at Texas Biomed. "This discovery could also be instrumental for vaccine development, as we illustrated previously," Martinez-Sobrido added.
