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Written By: Editorial Team | Updated : August 29, 2018 10:23 AM IST
This study could be quite helpful © Shutterstock
Human cytomegalovirus is a leading cause of birth defects and transplant failures. As it has evolved over time, this virus from the herpes family has found a way to bypass the body's defense mechanisms that usually guard against viral infections. Until now, scientists couldn't understand how it manages to do so. Normally, when a virus enters your cell, that cell blocks the virus's DNA and prevents it from performing any actions. The virus must overcome this barrier to effectively multiply.
Cytomegalovirus doesn't simply inject its own DNA into a human cell. Instead, it carries its viral DNA into the cell along with proteins called PP71. After entering the cell, it releases these PP71 proteins, which enables the viral DNA to replicate and the infection to spread.
The researchers found that, while PP71 is still present in the cell, it activates another protein known as IE1. This happens within the first few hours of the virus entering the cell, allowing the IE1 protein to take over after PP71 dies and continue creating a new virus.
The first author of the new study Noam Vardi said, "We noticed that when the IE1 protein degrades slowly, as it normally does, the virus can replicate very efficiently. But if the protein breaks down faster, the virus can't multiply as well. So, we confirmed that the virus needs the IE1 protein to successfully replicate."
The new study could lead to a new therapeutic target to attack cytomegalovirus and other herpesviruses, such as Epstein-Barr virus that causes mononucleosis and herpes simplex virus 1 and 2 that produce most cold sores and genital herpes, concluded the study published in the journal Proceedings of the National Academy of Sciences.
Earlier in the year, another research conducted at the University of California had shown that low levels of cytomegalovirus had a significant impact on the microbe and immune cell populations and how the immune system responded to the influenza vaccine.
(With inputs from ANI)
