Delta variant learned to last for longer duration in the host, CCMB study
Hyderabad: The Delta variant of SARS-CoV-2, which triggered the intense second Covid wave and caused large number of fatalities, had gained the ability to silently replicate in the epithelial cells, which line the surface of the human body, and learned how to last for a longer duration in the host, a recent study by geneticists […]
Published Date - 08:02 PM, Tue - 1 March 22
Hyderabad: The Delta variant of SARS-CoV-2, which triggered the intense second Covid wave and caused large number of fatalities, had gained the ability to silently replicate in the epithelial cells, which line the surface of the human body, and learned how to last for a longer duration in the host, a recent study by geneticists from Hyderabad-based Centre for Cellular and Molecular Biology (CCMB), said.
The ability of the Delta virus to last longer has the potential to cause maximum damage to respiratory and intestinal tissues within the host.
“Absence of support from the adaptive immune response could result in persistent infection resulting in a more severe pathological damage in the respiratory and intestinal tissues. Long-term presence of active SARS-CoV-2 in patients is an indication of such a strategy. Whether this scenario contributed to higher cases of respiratory sickness associated with Delta infection needs further investigation. Higher incidences respiratory support and ICU admissions were reported in Delta prevalent regions, indicating that the lung could have been subject to more serious damage,” the study said.
According to CCMB, “the Delta variant has mastered to trick the antiviral response from infected epithelial cells and gained the capability to replicate silently in epithelial cells. This might allow the virus to remain in the infected tissues for longer than the earlier variants could do. These additional features evolved in Delta might be partially responsible for the distinct pathophysiological conditions in Delta-infected persons”.
The study said, “Our studies reveal that SARS-CoV-2 Delta has integrated multiple mechanisms to silence host innate immune response and evade IFN (interferon) response. Delta’s silent replication and sustained suppression of host innate immune response, possibly resulting in delayed or reduced intervention by the adaptive immune response, could potentially contribute to the severe symptoms and poor recovery index associated with it.”
The study from Krishnan lab clearly helps in understanding how the virus-host relationships evolve over a period of time in a pandemic setting, CCMB added.
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