Estimating drug efficacy and viral dynamic parameters: HIV and HCV

@article{Perelson2008EstimatingDE,
  title={Estimating drug efficacy and viral dynamic parameters: HIV and HCV},
  author={Alan S. Perelson and Ruy M. Ribeiro},
  journal={Statistics in Medicine},
  year={2008},
  volume={27}
}
Mathematical models have proven valuable in understanding the in vivo dynamics of human immunodeficiency virus type 1 (HIV‐1), the virus that causes AIDS, and hepatitis C virus (HCV), the virus that causes hepatitis C infection. By comparing mathematical models with the data obtained from patients being treated with antiviral drugs, it has been possible to determine many quantitative features of these infections. The most dramatic finding has been that even though AIDS and hepatitis C are… 

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References

SHOWING 1-10 OF 41 REFERENCES

Mathematical Analysis of HIV-1 Dynamics in Vivo

It is shown how dynamical modeling and parameter estimation techniques have uncovered important features of HIV pathogenesis and impacted the way in which AIDS patients are treated with potent antiretroviral drugs.

Modeling viral and drug kinetics: hepatitis C virus treatment with pegylated interferon alfa-2b.

Models incorporating pharmacokinetic/pharmacodynamic analysis into a model of viral dynamics are needed to correctly interpret viral load changes and estimate drug effectiveness in treatment protocols using peginterferon alfa-2b.

Hepatitis C Viral Dynamics in Vivo and the Antiviral Efficacy of Interferon-α Therapy

Findings show that infection with hepatitis C virus is highly dynamic and that early monitoring of viral load can help guide therapy, with blocking efficacies of 81, 95, and 96% for daily doses of 5, 10, and 15 million international units, respectively.

Differences in viral dynamics between genotypes 1 and 2 of hepatitis C virus.

The better response rate of patients infected with HCV genotype 2 is multifactorial, the first finding of a difference in viral dynamics between subtypes of the same virus and demonstrates the importance of subtype-specific virus-host-drug interactions.

Modeling Long-Term HIV Dynamics and Antiretroviral Response: Effects of Drug Potency, Pharmacokinetics, Adherence, and Drug Resistance

A drug efficacy threshold for each patient is estimated that can be used to assess whether an ARV regimen is potent enough to suppress HIV viruses in the individual patient and the proposed mathematic models and statistical techniques may provide a framework to simulate and predict antiviral response for individual patients.

Modeling plasma virus concentration during primary HIV infection.

It is illustrated that two possible immune response mechanisms, cytotoxic T lymphocyte destruction of infected target cells and cytokine suppression of viral replication, could account for declines in viral load data not predicted by the original target-cell-limited model.

Effect of ribavirin on hepatitis C viral kinetics in patients treated with pegylated interferon

The third‐phase decay of initial viral kinetics was more pronounced in patients treated with peginterferon α‐2a plus ribavirin, suggesting that combination treatment leads to a better restoration of the patient's immune response.

Viral dynamics and response differences in HCV‐infected African American and white patients treated with IFN and ribavirin

The failure of IFN response in African American patients infected with genotype 1 HCV is in part due to an impaired ability to inhibit viral production.