A cellular threshold can determine whether herpesvirus becomes active or lies dormant
During the COVID-19 pandemic, we wore masks and kept 2 meters (6.6 feet) apart in an effort to reduce the spread of the tiny droplets we release into the air with every breath, conversation or cough. The main goal was to reduce the number of virus particles—known as virions—to which we were exposed. For each virus, a person must be exposed to a minimum infectious dose to develop disease, and in…
Recent research published in Nature Communications by scientists at the Weizmann Institute of Science has uncovered a cellular threshold that dictates whether a herpesvirus becomes active within a cell or remains dormant. The study focused on herpesviruses, which can either immediately replicate within a cell or wait patiently until conditions are favorable.
Notably, human cytomegalovirus (HCMV), a member of the herpesvirus family, often infects most of the world's population without causing disease, but can become dangerous when the immune system is weakened.
The researchers found that the fate of an infected cell depends on the number of virions (virus particles) that enter it. In a study led by doctoral student Yaarit Kitsberg, they discovered that mature macrophages, the cells that monocytes can differentiate into, tend to undergo active infection, while monocytes can remain dormant. This difference was attributed to macrophages expressing a higher number of proteins on their surface, which viruses use to enter cells.
The researchers labeled the virions with fluorescent markers and observed that macrophages were invaded by far greater numbers of virions compared to monocytes. When they genetically engineered monocytes to express efficient cytomegalovirus receptors, the number of virions entering the cells increased by 15-fold on average, and the proportion of cells undergoing active infection soared.
This suggests that cells in the human body have a minimum infectious dose required for an active infection to develop, and that this dose varies among different cell types.
Understanding this threshold could pave the way for therapies that control the outcome of herpesvirus infections. The research also identified a specific surface protein on macrophages whose deletion significantly reduces the rate of active infection, while adding it to monocytes did not increase their rate of active infection. Further studies are needed to identify other surface proteins that may play a crucial role in determining the fate of herpesvirus infections.
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