Question:

Hello...
I'm 47, have been positive 17 years this coming June. I finally started meds in 1998 after politely refusing AZT from another doctor shortly after my diagnosis in '86. My only episodes during this long nightmare have been shingles (last outbreak in '94) and fungal infection of the toenails and fingernails, which was completely cleared up by medication.

I'm a non-smoker and drink very little alcohol, once or twice a month. The only meds I've been on are Sustiva and Crixivan. The Crixivan was just replaced with Viread and Videx, even though I've never been resistant yet to any meds I've taken. Because of the "crix-belly" and possibility of kidney stones, I decided after 4 1/2 years (with the blessing of my Doctor) to get off the crix and try something new. It's great to now to be able to take my 3 meds together, only once a day.

My viral load is 105, Tcell count is 577, cholesterol is 254. I'm on Lopid for that, although I'm also concentrating on exericise and lowering my sugar intake to bring down my weight from 175 to 155, mainly to look better and hopefully eliminate the need for the cholestrol drug.

Four and a half years ago, my Tcells were at 71 and viral load over 400,000. My doctor is pleased with my progress.

Based on all this, do you have a feel for how long I can expect to keep HIV at bay and keep my health as good as it has been? And do you feel it was a good idea that I followed my concience and refused the AZT several years ago when that is all we had then?

Answer provided by:

Rodger MacArthur, M.D.
Wayne State University
Division of Infectious Diseases

The data given in the question suggests that HIV infection occurred in or about 1986, and that after 12 ½ years of infection (mid 1998), the CD4+ cell count had fallen to 71 cells/µL in association with a viral load of 400,000 copies/ml. These numbers are about what the average HIV-infected person would be expected to show if followed off therapy for 12 ½ years. In other words, the decline in CD4+ cells over time has been just slightly slower than average, suggesting that this particular individual was always going to require (at some point) antiretroviral therapy for HIV infection. Newer data suggest that it is unwise to wait to initiate therapy until the CD4+ cell count has fallen below 200 cells/µL, because the risk of acquiring an opportunistic infection begins to increase at that point. The risk greatly increases when the CD4+ cell count drops below 50 cells/µL.

It is unknown how long someone with good adherence to the newer, highly active, combinations of antiretrovirals can maintain good health and suppression of HIV RNA. The best guess is that it can be 20 years or more. Many factors, such as toxicity, declining adherence, and selection of drug-limiting mutations due to incomplete suppression of HIV RNA may shorten this time estimate. Data suggest that a person's best chance for a long-term, durable response to therapy is with greater than 95% adherence with the initial highly active antiretroviral combination (HAART). Many such persons are still on their initial HAART regimen 6 years after they started, with HIV RNA maximally suppressed for that entire period and no evidence of drug-related toxicity. For these individuals, immune function approximates that of an uninfected person, and life expectancy also can be expected to approximate that of an uninfected person.

As mentioned, it is risky to delay initiation of therapy when the CD4+ cell count has dropped below 200 cells/µL. Nevertheless, many people who did so have a better chance of success today than those individuals who followed "best medical advice" and began therapy a decade or more ago with AZT, followed by ddI, etc. In other words, the use of "sequential monotherapy" with drugs that, by themselves, had limited potency and poor durability, increased the likelihood of selecting for drug-limiting mutations that decrease the chance that newer HAART regimens used today will work as well as they would normally work in the absence of these mutations.

It should be pointed out, however, that a viral load of 105 copies/ml is not complete viral suppression, and should be monitored closely. In addition, the specific combination of Videx plus Viread plus Sustiva has not been studied adequately for efficacy, and does have the potential disadvantage of having a low barrier to the development of drug-limiting mutations. In other words, just 2 or 3 mutations which could develop at even low levels of viral replication could quickly limit the efficacy of this combination.

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