Viral dynamics in vivo: limitations on estimates of intracellular delay and virus decay.
Viral life cycle
DOI:
10.1073/pnas.93.14.7247
Publication Date:
2002-07-26T14:43:20Z
AUTHORS (5)
ABSTRACT
Anti-viral drug treatment of human immunodeficiency virus type I (HIV-1) and hepatitis B (HBV) infections causes rapid reduction in plasma load. Viral decline occurs several phases provides information on important kinetic constants replication vivo pharmacodynamical properties. We develop a mathematical model that takes into account the intracellular phase viral life-cycle, defined as time between infection cell production new particles. derive analytic solutions for dynamics following with reverse transcriptase inhibitors, protease or combination both. For HIV-1, our results show decay (days 2-7) allows precise estimates turnover rate productively infected cells. The initial quasi-stationary 0-1) transition 1-2) are explained by combined effects pharmacological delays, clearance free particles, Reliable first three quantities not possible from data load only; such require additional measurements. In contrast HBV predicts frequent early sampling will lead to reliable half-life properties administered drug. On other hand, cells cannot be estimated decay.
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