- Summary: Resistance to anti-HIV drugs
- What is resistance?
- Resistance to nucleoside and nucleotide reverse transcriptase inhibitors
- Resistance to non-nucleoside reverse transcriptase inhibitors
- Resistance to protease inhibitors
- Resistance to fusion inhibitors
- Limiting the chance of resistance
- Transmission of resistant HIV
- Resistance in non-B HIV sub-types
- Resistance in tissue and other compartments
Resistance to fusion inhibitors
Great natural diversity in susceptibility to fusion inhibitors has been noted. A much more substantial number of viruses from treatment-naive patients show reduced susceptibility to fusion inhibitors in vitro compared to other drug classes, where susceptibility tends to be tightly clustered around the mean. In the case of T-20 (enfuvirtide, Fuzeon), up to a quarter of isolates appear either hypersusceptible to T-20 or to have reduced susceptibility compared to wild-type.
This variability in susceptibility is likely to be more pronounced for agents targeting gp120 and its interactions, since regions of gp120 are hyper-variable. This means that there will be differences in susceptibility within and between individuals.
Baseline analysis of TORO 1 and 2 participants found that 15% had a polymorphism at position N42S in gp41, but this was not associated with reduced susceptibility to T-20. The mutations V38A, V38V/A, G36D, N43D, V38M were associated with mean reductions in susceptibility of 15- to 42-fold. N43N/D was associated with a mean fivefold reduction in susceptibility (Greenberg 2003).
Research into coreceptor inhibitors and resistance is ongoing. There is evidence from a study of maraviroc that resistance to one CCR5 inhibitor does not necessarily produce resistance to all CCR5 inhibitors (Westby 2005). In regard to drugs which target the CXCR4 co-receptor, there is evidence that AMD070 has antiviral effect on virus which has been previously exposed to AMD3100 (Schols 2005).
References
Greenberg ML et al. Baseline and on-treatment susceptibility to enfuvirtide seen in TORO 1 and TORO 2 to 24 weeks. Tenth Conference on Retroviruses and Opportunistic Infections, Boston, abstract 141, 2003. Labrosse B et al. Baseline susceptibility of primary human immunodeficiency virus type 1 to entry inhibitors. J Virol 77: 1610-1613, 2003. Lalezari JP et al. Enfuvirtide, an HIV-1 fusion inhibitor, for drug-resistant HIV infection in North and South America. New England Journal of Medicine. N Engl J Med 348: 2175-2185, 2003. Schols D et al. Multi-drug resistant HIV-1 is sensitive to inhibition by chemokine receptor antagonists. Twelfth Conference on Retroviruses and Opportunistic Infections, Boston, abstract 545, 2005. Westby M et al. Structurally related HIV co-receptor antagonists bind to similar regions of CCR5 but have differential activities against UK-427,857-resistant primary isolates. Twelfth Conference on Retroviruses and Opportunistic Infections, Boston, abstract 96, 2005.
latest aidsmap news
- Fluconazole shown to be more effective against cryptococcal meningitis at higher dose
- Promising early results for large-scale study of community-level HIV prevention initiative
- GNP+ launches website documenting global HIV exposure / transmission laws and prosecutions
- Widespread resistance to antiretrovirals among children in the Central African Republic
- Children starting HIV treatment in sub-Saharan Africa have a low risk of death
- Different paediatric responses to antiretroviral therapy in Uganda and the United Kingdom/Ireland may reflect differences in nutrition and access to cotrimoxazole
- Rare abacavir liver side-effects reported
- Abacavir treatment doesn't cause changes in biomarkers linked to heart attack, suggests small study
- Traditional healers could play key role in ART rollout
- HIV testing for mothers and children must expand, UN report shows
