This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: 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 many cases, the larger the dose, the more severe the illness. Until now, virologists have addressed the infectious dose mainly at the level of the whole organism, but scientists from the laboratory of Noam Stern-Ginossar at the Weizmann Institute of Science have discovered that the fate of an individual infected cell, too, depends on the number of virions that enter it. In a study published in Nature Communications and focusing on herpesviruses, the researchers reveal that the cellular infectious dose determines whether a virus will become active in the cell or enter a dormant state.
These findings pave the way for therapies that could control the outcome of infection. While most viruses invade a living cell and immediately exploit its machinery to replicate, herpesviruses and HIV have another option: They can wait patiently in a dormant state inside the cell until conditions become favorable. For example, human cytomegalovirus (HCMV), a member of the herpesvirus family, infects most of the world's population, usually without causing disease.
But when the immune system is weakened, the dormant virus can reawaken and cause severe infections. Moreover, HCMV is one of the most common infections transmitted from mother to fetus, and in a minority of cases, it can cause serious harm, including developmental delays and hearing loss. Among the hiding places for dormant cytomegalovirus in the body are blood-system cells called monocytes.
By contrast, macrophages—cells into which monocytes can differentiate—tend to undergo active infection. Since the 1990s, scientists have been trying to understand what accounts for this difference between the two cell types. The leading hypothesis was that monocytes, unlike macrophages, are capable of packaging viral DNA into an especially compact structure that silences it.
In the new study, led by doctoral student Yaarit Kitsberg under the supervision of Stern-Ginossar and staff scientist Dr. Michal Schwartz, the researchers examined which genes are expressed in human monocytes. They then differentiated the monocytes into mature macrophages and looked for what had changed.
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