The widespread availability of
antiretroviral therapy has made the fight against
HIV a great deal easier. But these medications can’t go the distance alone. Working closely with your doctor, you’ll need to choose and monitor your treatment carefully. This is because of obstacles that can arise before and during treatment—one of the most important is
HIV drug resistance. Fortunately, we now know a lot about how to reduce the risk of drug resistance and treat drug-resistant virus. We also have access to important technologies that look for drug-resistant
virus and help us make important treatment decisions. These drug-resistance tests have become a routine part of
HIV care. In simple terms, drug resistance refers to the ability of disease-causing germs—such as bacteria and viruses—to continue multiplying despite the presence of
drugs that usually kill them. With HIV, drug resistance is caused by changes (mutations) in the virus’s genetic structure. These mutations can lead to changes in certain proteins, most commonly enzymes, which help
HIV reproduce (replicate). Mutations are very common in HIV. This is because
HIV replicates at an extremely rapid rate and does not contain the proteins needed to correct the mistakes it makes during copying. Mutations occur randomly, on a daily basis, but many are harmless. In fact, most mutations actually put
HIV at a disadvantage—they reduce the virus’s “fitness” and slow its ability to infect CD4
cells in the body. However, a number of mutations can actually give
HIV a survival advantage when
HIV medications are used, because these mutations can block
drugs from working against the
HIV enzymes they are designed to target. These are the mutations we are concerned about when we talk about drug resistance.
HIV relies on many
enzymes to replicate inside a human cell. It also relies on proteins, including gp41, to latch on to CD4
cells and infect them. Mutations can occur in any of these parts of the
virus and cause drug resistance.
Relevant Topics in Neuroscience & Psychology