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Age-structured viral dynamics in a host with multiple compartments.

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This study models HIV spread between organs, revealing cell migration impacts viral dynamics. Cell-to-cell transmission, unlike cell-free, can promote viral persistence in complex infection networks.

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Area of Science:

  • Virology
  • Mathematical Biology
  • Immunology

Background:

  • HIV infection spreads via cell-free virions and cell-to-cell transmission through virological synapses.
  • Understanding viral dynamics requires analyzing organ connectivity and distinct cellular infection kinetics.

Purpose of the Study:

  • To develop a multi-compartment virus model simulating HIV spread across organs.
  • To analyze how cell migration and infection-age influence viral dynamics and persistence.
  • To establish threshold values for viral persistence or extinction in connected and non-connected systems.

Main Methods:

  • A multi-compartment virus model was developed with distinct infectivity kernels based on cell infection-age.
  • Formulated basic reproduction number for strongly connected systems.
  • Developed sequential threshold values for non-strongly connected systems.
  • Utilized numerical simulations with data-informed intracellular delays and gamma-distributed infectivity kernels.

Main Results:

  • Cell migration significantly affects viral dynamics, not always monotonically with migration rate, in strongly connected systems lacking directional links.
  • In non-strongly connected systems, increased migration can lead to viral extinction, then re-emergence in specific compartments.
  • Faster kinetics (cell-to-cell transmission) promote viral persistence compared to cell-free transmission.

Conclusions:

  • The study provides insights into HIV's complex spread dynamics within and between organs.
  • Cell migration and transmission modes are critical factors influencing viral persistence and extinction.
  • Mathematical modeling is crucial for understanding within-host viral dynamics and developing intervention strategies.