A new study by researchers at the Weizmann Institute of Science has revealed that each cell has its own threshold for sensitivity to the virus, which explains why the virus remains dormant in some cells and multiplies in others.
The study focused on herpesviruses, pathogens capable of actively replicating within cells or entering a dormant state. Human cytomegalovirus (CMV) is a prime example, infecting most of the world's population and often showing no symptoms until the immune system is weakened. Among its reservoirs are monocytes, blood cells where the virus can remain dormant without causing active infection, while macrophages, which monocytes may transform into, are susceptible to full-blown infection.
The researchers pointed out that scientists had believed for many years that monocytes suppressed the virus by compressing its DNA, but they discovered that it was different. The body's cells have an infectious dose necessary to develop an active infection, and this dose varies according to the type of cell. Infecting a cell with a viral dose below this threshold leads, in some cases at least, to the virus going into a dormant state.
Subsequent studies have shown how the virus overcomes cellular defenses. Early proteins destroy the nucleosomes that encapsulate the viral genome and force the cell to assemble the building blocks of DNA, which are then transferred to the virus. The destruction of the nucleosomes is sufficient to activate a latent herpes virus. The more defensive structures a cell has and the fewer free building blocks it possesses, the higher the viral dose threshold the virus needs to exceed.
Based on these findings, researchers believe that assessing the risk of infection is not limited to the level of the entire organism, but extends to the level of the single cell, which may open new horizons for understanding how viruses transition from a dormant state to an active state.
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