Use of Viral Resistance Patterns to Antiretroviral Drugs in Optimising Selection of Drug Combinations and Sequences

@article{Moyle2012UseOV,
  title={Use of Viral Resistance Patterns to Antiretroviral Drugs in Optimising Selection of Drug Combinations and Sequences},
  author={Graeme J. Moyle},
  journal={Drugs},
  year={2012},
  volume={52},
  pages={168-185}
}
  • G. Moyle
  • Published 1 August 1996
  • Biology
  • Drugs
SummaryHigh rates of viral replication throughout HIV infection, and the frequency of mutation occurring during each replication cycle due to the inaccuracy of reverse transcriptase, drive the potential for drug-resistant viral variants to appear under the selective pressure of antiretroviral therapy. Loss of antiviral effect with a variety of antiretroviral agents has been reported to coincide with the appearance of viral mutants with reduced drug sensitivity. Additionally, the presence of… 

Antiretroviral Therapy for HIV Infection

3-drug therapy should represent current standard practice in a nontrials setting and may be best guided by measurement of viral load, with a range of other markers having potential utility in individualising treatment decisions.

Human Immuno-Deficiency Virus Drug Resistance, Nuclesoide Reverse Transcriptase Inhibitors, Non-nuclesoide Reverse Transcriptase Inhibitors And Associated Drug Resistance Mutations In The Reverse Transcriptase Gene Of Human Immuno Deficiency Virus-1.

This review mainly focuses on the human immunodeficiency virus-1 drug resistance, nucleoside/nucleotide reverse transcriptase inhibitors, non-nucleoside reverse Transcriptase inhibitors and associated drug resistance mutations in thereverse transcriptase gene of human immuno-deficiencyirus-1.

Discovery and Development of the Anti-Human Immunodeficiency Virus Drug, Emtricitabine (Emtriva, FTC).

In July 2006, the FDA approved Atripla, a once a day, oral, fixed dose combination of emtricitabine, tenofovir disoproxyl fumarate, and efavirenz, which represented the culmination of two decades of research that had transformed AIDS from a death sentence to a manageable chronic disease.

Antiretroviral therapy adherence among treatment-naive HIV-infected patients: A retrospective cohort study.

Low ART adherence observed among treatment naïve patients in this nationally representative study suggests the need for public health interventions to improve adherence among this population.

Saquinavir Soft-Gel Capsule Formulation

Initial results of several trials that used surrogate markers to assess treatment efficacy indicate that the SGC formulation of saquinavir, administered in combination with other antiretroviral drugs, is an effective and well-tolerated treatment for patients with moderate or advanced HIV infection.

A REVIEW ON PATHOLOGY OF AIDS AND ITS TREATMENT REGIMENS

People suffering from HIV have differing needs depending on their personal circumstances and stage of infection, which with antiretroviral treatment may span several decades.

References

SHOWING 1-10 OF 168 REFERENCES

Use of evolutionary limitations of HIV-1 multidrug resistance to optimize therapy

It is shown that several mutations in the HIV-1 reverse transcriptase gene that confer resistance to inhibitors of this enzyme can attenuate viral replication and indicate that evolutionary limitations exist to restrict development of multi-drug resistance (MDR).

Failure of antiretroviral therapy: role of viral and cellular factors.

It is of great importance to investigate the role of cellular factors in 'clinical resistance' to AZT and other anti-HIV agents to help to improve or develop new strategies for antiviral therapy regimens.

Nevirapine resistance mutations of human immunodeficiency virus type 1 selected during therapy

Drug susceptibility and mutations in the reverse transcriptase (RT) gene were analyzed with virus isolates from 38 patients treated with nevirapine, a potent nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) RT, documenting that the circulating virus population can change rapidly, and many alternative mutants can emerge, often in complex mixtures.

Potential mechanism for sustained antiretroviral efficacy of AZT-3TC combination therapy.

In vivo AZT-3TC combination therapy resulted in a markedly greater decreased in serum HIV-1 RNA concentrations than treatment with AZT alone, even though valine-184 mutants rapidly emerged, consistent with in vitro mutation studies.

Zidovudine resistance predicted by direct detection of mutations in DNA from HIV-infected lymphocytes.

A series of infectious HIV variants with specific combinations of mutations in the RT gene were constructed and their sensitivity to zidovudine was assessed by direct detection of specific mutations in DNA from peripheral-blood lymphocyte samples to establish the clinical significance of the resistant isolates.

Resistance of clinical isolates of human immunodeficiency virus to antiretroviral agents

  • D. Richman
  • Biology, Medicine
    Antimicrobial Agents and Chemotherapy
  • 1993
This minireview discusses the molecular biology and clinical implications of the resistance of HIV to zidovudine (AZT) as well as to other nucleoside and nonnucleoside inhibitors of retroviral reverse tran- scriptase.

Resistance to ddI and sensitivity to AZT induced by a mutation in HIV-1 reverse transcriptase.

Analysis of HIV-1 variants confirmed that the ddI resistance mutation alone conferred ddI and 2',3'-dideoxycytidine resistance, and suppressed the effect of the AZT resistance mutation.

Convergent combination therapy can select viable multidrug-resistant HIV-1 in vitro

It is reported here that HIV-1 co-resistant to AZT, ddl and the NNRTI nevirapine and the 'replication incompatible' combinations of resistance mutations, although a mutation conferring oxathiolane-cytosine nucleoside resistance in reverse transcriptase completely sup-pressed AZT resistance in a triple-resistant background.

In vivo emergence of HIV-1 variants resistant to multiple protease inhibitors

Five resistant variants isolated from patients undergoing therapy with the protease inhibitor MK-639 exhibited cross-resistance to all members of a panel of six structurally diverse protease inhibitors, suggesting that com-bination therapy with multiple protease inhibition may not prevent loss of antiviral activity resulting from resistance selection.
...