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Weekly Alibi Nurse Ratchett

The Mechanics of Resistance

By Mike Ratchett, Staff Nurse

DECEMBER 8, 1997:  With all the talk lately of protease inhibitors and "cocktail" regimens, it's important that people reading the statistics and latest news in the treatment of HIV and AIDS have a basic understanding of what's behind the breaking stories. AIDS deaths are decreasing, and many people with the disease are indeed living longer, more productive lives; but we must be careful to remember what we're dealing with here. Despite the aforementioned good news, there's also quite a bit of bad. HIV infection is on the rise-- especially among minorities and hetero- sexuals. And with more people acquiring the virus, knowledge of how it works in the body is vital.

One of nature's simplest and most perfect lifeforms, viruses are minute parasites that are able to replicate only once inside the cells of the host. Viruses consist of a core of either ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) surrounded by a protein coat. Once viral genes are integrated into the host's genes, they instruct the host cell to produce viral protein, and replication of the virus takes place rapidly--perhaps millions of times per day--causing various symptoms and illness in the host.

HIV, like all other viruses, cannot, as of yet, be "cured" by modern medicine. While certain antibiotics and antiviral medications can, for a time, control replication of viruses including HIV, the virus generally wins in the end. These organisms are able to do so due to slight mutations that cause them to become resistant to certain medications. It is estimated that every single-point HIV mutation may occur more than 10,000 times a day in an infected individual. Some of these mutations, or changes in the genetic coding of the virus, are fatal to it, while others cause insignificant changes. Still others, though, have an advantageous effect on viral behavior, resulting in increased virulence, faster replication and decreased sensitivity to antiviral drugs and other treatments.

The genes of all lifeforms undergo occasional mutations, usually the result of a slight change in a protein. Antibiotic and antiviral drugs work by interfering with protein manufacture in bacteria and viruses by inhibiting the production of vital enzymes, proteins that initiate and control chemical reactions in cells. In an individual who takes these drugs, the wild-type organism, or natural form of a viral or bacterial gene, is killed off or prevented from multiplying further. But spontaneous mutations take place with great frequency in bacteria and viruses, the population of the infecting organisms is likely to include several slightly different forms, some with natural resistance to the drugs used to destroy the predominant wild type. In turn, a resistant type can quickly become the dominant form because resistance can be passed from generation to generation.

As viruses go, HIV is characterized by a high rate of replication, eventually leading to the depletion of CD4 cells, lymphocytes (commonly known as T-cell lymphocytes) vital to the body's immune system to which HIV attaches itself. Cells infected with HIV are killed by non-infected lymphocytes, resulting in a low CD4 cell count. This renders the body increasingly more susceptible to any number of diseases, a certain collection of which make up the group of diseases and complications under the AIDS umbrella.

Combination therapy, the recently hailed miracle treatment of patients with HIV/AIDS, is far more effective than traditional monotherapy because several different drugs are used in an attempt to kill the dominant strain of the virus and slow replication of the mutated forms. The harrowing news in light of all the hope is that after just 18 months in wide use, these drug cocktails, in isolated cases, are already proving ineffective in treating certain strains of HIV. So while there is a certain amount of promise in the latest treatments, HIV is still winning the battle. If you're going to play, play safe.


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