Аннотация
Within its host cell, a complex coupling of transcription, translation,
genome replication, assembly, and virus release processes determines
the growth rate of a virus. Mathematical models that account for
these processes can provide insights into the understanding as to
how the overall growth cycle depends on its constituent reactions.
Deterministic models based on ordinary differential equations can
capture essential relationships among virus constituents. However,
an infection may be initiated by a single virus particle that delivers
its genome, a single molecule of DNA or RNA, to its host cell. Under
such conditions, a stochastic model that allows for inherent fluctuations
in the levels of viral constituents may yield qualitatively different
behavior. To compare modeling approaches, we developed a simple model
of the intracellular kinetics of a generic virus, which could be
implemented deterministically or stochastically. The model accounted
for reactions that synthesized and depleted viral nucleic acids and
structural proteins. Linear stability analysis of the deterministic
model showed the existence of two nodes, one stable and one unstable.
Individual stochastic simulation runs could access and remain at
the unstable node. In addition, deterministic and averaged stochastic
simulations yielded different transient kinetics and different steady-state
levels of viral components, particularly for low multiplicities of
infection (MOI), where few virus particles initiate the infection.
Furthermore, a bimodal population distribution of viral components
was observed for low MOI stochastic simulations. The existence of
a low-level infected subpopulation of cells, which could act as a
viral reservoir, suggested a potential mechanism of viral persistence.
Описание
The whole bibliography file I use.
Линки и ресурсы
тэги
- 12381432
- Animals,
- B,
- Gov't,
- Linear
- Models,
- Non-P.H.S.,
- P.H.S.,
- Processes,
- Replication,
- Research
- Stochastic
- Support,
- U.S.
- Virus
- Viruses,
- iological,