Education And Debate

Antiretroviral therapy in Africa

BMJ 2004; 328 doi: https://doi.org/10.1136/bmj.328.7434.280 (Published 29 January 2004) Cite this as: BMJ 2004;328:280
  1. Warren Stevens, health economist (wstevens@mrc.gm)1,
  2. Steve Kaye, virologist1,
  3. Tumani Corrah, director1
  1. 1MRC Laboratories, PO Box 273, Banjul, Gambia, West Africa
  1. Correspondence to: W Stevens
  • Accepted 1 December 2003

We should stop and think about the risks of resistance, and ways of minimising them, before increasing access to antiretroviral therapy in Africa

Demands for the introduction of antiretroviral therapy into Africa have been growing over the past few years. On the face of it, the availability of antiretroviral therapy at what seems to be an affordable price is good news. The treatment can produce dramatic clinical improvements in people with symptomatic HIV disease and, when used optimally, can delay the progression of disease. However, the potential short term gains from reducing individual morbidity and mortality may be far outweighed by the potential for the long term spread of drug resistance if the experience of adherence to treatment for tuberculosis is repeated. Without due forethought and planning, antiretroviral therapy is likely to be introduced to Africa in a random and haphazard way, with inconsistent prescribing practices and poor monitoring of therapy and adherence. This risks the rapid development and transmission of drug resistance.

HIV drug resistance

Virus strains with reduced sensitivity to zidovudine, the first drug used to treat HIV infection, were first observed in 1989, three years after it was introduced.1 Subsequently, resistance to every currently licensed antiretroviral drug has been observed.2 Drug resistance within an individual patient is not confined to a single compound, and cross resistance between drugs of the same class is the rule rather than the exception.3

Drug resistance arises by natural selection, mutant strains being selected when the virus replicates in sub-limiting drug concentrations. The only way to prevent resistance is to use a drug regimen that reduces virus replication to virtually zero (commonly equated with a plasma virus load below 50 RNA copies/ml). In this circumstance, the probability of a mutant arising to all the drugs used in a highly active antiretroviral therapy …

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