Chromatin is folded into compartments, loops, and domains. It has two types of compartments; A and B. The A compartment has active genes and the B compartment silenced genes. The two are separate.
However, infected lung cells show a mingling of the compartments. These genes are activated in response to viral infection. This could explain why infected patients release fewer interferons than in other viral infections.
The infected cells have depleted cohesin proteins. This results in loosely folded domains that are not activated. This is a manipulation that may make the virus interfere with cellular defenses.
Infected cells lack the acetyl group that is associated with transcriptional activation. This is likely to suppress neighboring genes. Interestingly, the virus mimics the host’s histones to hinder acetylation, further disrupting the chromatin structure.
These alterations may have long-lasting effects on the lung cells. The persistence of the observed changes may form the basis needed to establish potential targets for therapeutic interventions.
While the findings above have shed light on the mechanisms that underlie most COVID symptoms, further research is necessary to determine whether similar changes will be observed within the cells of the entire organism. The results of this finding will be instrumental in better understanding what the long-term effects of COVID will be in the structure of people who have contracted it. Researchers believe that we may be studying the impact of COVID decades from now because its lasting impacts on some cells, such as lung cells, are far from being established.