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An experimental genetically engineered medication that works completely differently from other drugs for HIV holds out hope for HIV-positive people who are on salvage therapy.

Modern HIV treatment is, compared to what was available in the 1980's and 1990's, highly effective. It is so effective that doctors and nurses now usually spend less time explaining the side effects of the medications used to control the virus, and more time persuading patients to stay on needed medications despite the fact they feel good. A minority of HIV patients, however, experience multiple-drug resistance, a phenomenon that greatly complicates their care.

What is Multiple-Drug Resistance?

Drug resistance is the failure of a medication that previously controlled an infection to continue to control that infection. Multiple-drug resistance is a condition in which more than one medication to control the same infection that once worked becomes ineffective.

The human immunodeficiency virus HIV multiplies at a very rapid rate. Unlike more complex organisms, it does not have proteins that correct errors in its DNA. Some of these mutations will enable HIV to produce new and different enzymes.

The drugs that are used to treat HIV target the enzymes that the virus needs to attach to T-cells and then to multiply inside them. There are drugs that target reverse transcriptase, integrase, protease, and gp41. If a mutation causes slight changes in these enzymes so that they still function for the virus but they do not respond to drugs, then the virus is able to resist the drug.

How Do HIV+ People Acquire Drug-Resistant HIV?

The more viruses there are in the bloodstream of an HIV+ person, the more opportunities there are for genetic mutations and the resulting drug resistance. The golden rule of prevention of drug-resistant HIV is very simple: Keep viral load (the number of copies of the virus per ml of blood) as low as possible. To keep viral load as low as possible, it is critically important that:

  • No doses of medication are ever skipped. When the concentrations of a needed medicine in the bloodstream go down, viral load and mutations go up.
  • HIV patients can never pick and choose prescription medications. That's because the doctor chooses the cocktail of drugs carefully to avoid interactions. For instance, For example, if the nucleoside/nucleotide reverse transcriptase inhibitor Viread (tenofovir) is combined with the protease inhibitor Revataz (atazanavir), blood levels of Reyataz can fall to dangerously low levels. This is why the protease inhibitor Norvir (ritonavir), which boosts Reyataz levels in the bloodstream, must be taken when Viread is also prescribed. Taking one medication and missing another may make a third medication less effective.
  • Medication must be absorbed into the digestive tract. If vomiting and diarrhea are a problem, the doctor has to know. Some medications have to be taken with or without food to be absorbed properly.
  • The doctor has to know all the drugs, legal and illegal, the patient is taking. Some drugs have to be activated by the liver. Other drugs are broken down by the liver. The doctor needs to know if there is something that makes a medication ineffective, or overly effective, due to the liver's total burden of processing drugs.

Viral load isn't the only factor in acquiring drug-resistance. HIV patients who have unprotected sex may acquire drug-resistant strains of the virus from their partners. HIV-negative people who have unprotected sex while on Truvada sometimes are infected with a strain that is resistant to the prophylactic drug, and assuming they are OK they don't get treatment before the virus mutates into resistant forms. Even in the HIV window period, before the virus is even detectable, it can mutate to evade drug treatment.

Continue reading after recommendations

  • Reichert JM. Antibodies to Watch in 2016. MAbs. 2016. 8(2):197-204. doi: 10.1080/19420862.2015.1125583. PMID: 26651519.
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