N. L. Komarova

Dynamically adjusted cell fate decisions and resilience to mutant invasion during steady state hematopoiesis revealed by an experimentally parameterized mathematical model

The paper uses an experimentally parameterized mathematical model to show how hematopoietic stem cells dynamically adjust and resist mutant invasion during steady state hematopoiesis.

Mutant fixation in the presence of a natural enemy

This study investigates how infection affects mutant fixation probability in populations, finding that infection weakens selection and alters fixation probabilities for advantageous and disadvantageous mutants.

A hybrid stochastic-deterministic approach to explore multiple infection and evolution in HIV

This paper introduces a hybrid stochastic-deterministic algorithm to simulate HIV mutant evolution, showing it can accurately model dynamics with reduced computational cost and reveal evolutionary outcomes not captured by deterministic models.

Quantifying the dynamics of viral recombination during free virus and cell-to-cell transmission in HIV-1 infection

This study quantifies how HIV-1 recombination dynamics differ between free virus and cell-to-cell transmission, finding faster recombination with cell-to-cell transmission due to increased infection multiplicity and co-transmission of viral strains.

Effect of synaptic cell-to-cell transmission and recombination on the evolution of double mutants in HIV

This study investigates how synaptic and free-virus transmission modes affect the evolution of HIV double mutants using a stochastic agent-based model, finding that each mode influences mutant persistence and spread differently based on mutant fitness.

Determinants of stem cell enrichment in healthy tissues and tumors: implications for non-genetic drug resistance

This study uses mathematical models to analyze how feedback loops influence cancer stem cell fractions in tumors and healthy tissues, identifying conditions that promote or reduce stem cell enrichment.

Multiple infection of cells changes the dynamics of basic viral evolutionary processes

This paper uses computational models to show that multiple viral infections alter mutant dynamics, increasing short-term mutant presence but decreasing long-term fixation probability.