Episome partitioning and symmetric cell divisions: quantifying the role of random events in the persistence of HPV infections
Thomas Beneteau, Christian Selinger, Mircea T. Sofonea, Samuel Alizon

TL;DR
This study develops a stochastic model to understand how random cellular events like episome partitioning and division symmetry influence HPV persistence, highlighting the importance of stochasticity in infection outcomes.
Contribution
It introduces a detailed stochastic model of HPV dynamics that emphasizes the role of random cellular events in viral persistence, advancing understanding beyond deterministic approaches.
Findings
Random episome partitioning impacts HPV persistence
Symmetric cell divisions increase likelihood of infection persistence
Stochastic effects are crucial in HPV infection outcomes
Abstract
Human Papillomaviruses (HPV) are one of the most prevalent sexually transmitted infections (STI) and the most oncogenic viruses known to humans. The vast majority of HPV infections clear in less than 3 years, but the underlying mechanisms, especially the involvement of the immune response, are still poorly known. Building on earlier work stressing the potential importance of stochasticity in HPV infection clearance, we develop a stochastic mathematical model of HPV dynamics with an explicit description of the intracellular level. We show that the random partitioning of virus episomes upon stem cell division and the occurrence of symmetric divisions greatly affect viral persistence. These results call for more detailed within-host studies to better understand the relative importance of stochasticity and immunity in HPV infection clearance.
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