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long-term and future success?

Oct 23, 2000

I have been spending a lot of time lately reading the questions and responses here. When I first started to learn about the disease and treatment options, I felt optimistic - obviously things have come a long way in the last few years and will hopefully continue along that path in the future. However, as I continue reading, I seem to be losing the optimism. And maybe that is because of the nature of the column - people may not tend to have questions if they are having success and are happy with their current treatments.

I guess what I am asking is, are there are a number of people out there that have been successful at controlling the virus for years (since the new therapies have come out) without really having to change their treatment much? Any statistics? Does resistance inevitably happen no matter how faithful someone is about taking their meds? When I read about people saying that they are changing things so frequently - either because the meds aren't working properly or they can't tolerate the side effects, it scares me to think about how quickly the options may be running out. Will the new classes and kinds of drugs coming out be able to keep up?

Thank you for your response.

Response from Dr. Cohen

Well -- this is a great point to bring up as it is the other side of the coin. You are right on target with your concern -- with all of the postings about problems of resistance and treatment problems -- just how good are these combos anyway?

Well -- here is what it takes to make a long term successful combo. It appears that there are three key ingredients -- first is that the drugs must be active against the strains of HIV that someone has. Second, the regimen must be potent enough for this person's level of virus. And third, the blood levels of each of the drugs must be there most if not all of the time to control HIV. A bit more detail on each --

First -- activity of the meds. All of the antivirals are developed to be active against the original "wild type" HIV that was identified about 15 years ago. It is the most common HIV strain, and the one that grows in the absence of our meds. However -- after exposure to our meds, HIV develops mutations in its genetic structure that allow it to become resistant to the meds. And this newer resistant strain can also be transmitted -- so we now see some who have never taken meds, but whose HIV is resistant to at least some of our meds. Even all of the meds on rare occasion. So for these people, HIV is much less treatable -although research continues to find meds that might work in these cases. But this issue is one that leads us to work harder to better control HIV when we do treat, as well as our work to minimize risk taking behaviors that lead someone to acquire HIV, since starting out with a resistant HIV strain does rapidly decrease the number of treatment options.

Second -- potency. We know from many studies that while our triple combos work well against most viral loads (measured before treatment), there are some whose viral load is higher, and they appear to have a lower chance of responding to many of the triple combos. There is no specific line above which this drop off happens, although many studies have explored the likelihood of response both above and below 100,000 copies on the viral load test to explore this issue. There are some combinations that do work equally well both above and below this line -- ones that stand out on this issue include the combination of two nucleoside antivirals plus Sustiva/efavirenz, as well as the newest PI Kaletra plus two nucleosides. When other combos are used, some would monitor carefully since they can often work well, and consider the use of a fourth med is the viral load is not fully controlled. This concern is also true for those whose CD4 counts are on the low side when starting meds -- low defined as somewhere below 100 cells.

Note that by potency I am referring to the ability of a combo of meds to drive the viral load to as low a level as possible -- like below 50 copies. The reason this is the goal is because when the viral load is this low, the regimen appears to work for a very long time and HIV has much more trouble developing resistance to any of the meds when it is stopped or slowed to this degree. How long is a long time? Well -- one more point to discuss.

Third -- adherence. A combination may be active, and potent enough. But then we must keep the blood level of the meds present -- all the time preferably. And this is probably the hardest part because it involves taking meds each day each dose. And while that is easy to write and even plan on, it is just plain hard to do. We forget. We make a mistake. That is common and normal -- but HIV will take advantage of a missed dose, and lower blood levels of the meds, to grow and develop resistance to a medication that is now working. Fortunately, we are working on many ways to make meds easier to do -- fewer pills, and fewer times per day. That makes it easier -- but for some, this is still not easy to do.

When all three ingredients are there -- active meds, potent enough, and someone takes them -- these combos work -- perhaps for as long as we need them to. There is a chance that resistance can still happen -- there are surprises. But we are learning about some -- such as unexpected drug interactions like how St Johns Wort, a commonly used herb, can lower blood levels of the protease inhibitors. The more we can keep these three ingredients present -- the more we can expect that HIV can be suppressed for as long as we need it to be.

The last barrier is the side effects showing up in those on some of these combos. Here we are working hard to understand the cause and the best ways to avoid them and reverse them. But if we maintain the activity of the meds, and keep them fully active by avoiding resistance to them, we can keep the immune system strong and then focus our energy on how to avoid these side effects, rather than on how to compensate for resistant HIV and avoid side effects as well.

A long answer, but hope it clarifies where we are.


Cal Cohen, M.D., M.S.

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