by As Told to Lark Lands
Is the grass greener after Sean Strub’s second drug holiday? Whether it revved up his immune system is too soon to tell.
The last time POZ founder Sean O. Strub dipped his toe into the choppy waters of Strategic Treatment Interruptions (STIs), the results were so bad that Virginia Cafaro, MD, warned him, “Never do this again”. But two years ago is ancient history in HIV land. With all the new talk about possible benefits of STIs (see “Gimme a Break), Sean decided to step into the same river twice. POZ Science Editor Lark Lands asked him to describe his three-week swim.
I had been reading about the potential of STIs to both stimulate the immune system’s control of HIV and offer a vacation from side effects. Luckily, I wasn’t having many problems with my HAART meds—indinavir (Crixivan), d4T (Zerit) and delavirdine (Rescriptor)—other than persistent post-dosing anxiety (caused by the Crixivan, I think). But I was curious to see whether my viral load might come back slower this time than with my first STI, possibly indicating some return of anti-HIV immune response.
I wondered whether immune response might be like starting a lawnmower in the spring after it’s sat in the garage all winter: You pull it the first time and it does nothing. The second time it sputters. The third time it runs for a moment and then stops. The fourth time, it starts going.
During my previous two-week STI, the virus came back like a freight train. In just 10 days, my viral load jumped from undetectable to over a million, and my CD4s plummeted from 357 to 154—and it took three months for my lab numbers to recover. While I was off drugs, I had severe fatigue, painfully swollen lymph glands and headaches. I felt so severely ill that I couldn’t work.
This time my viral load glided up a bit slower. After months of undetectable viral loads, I went off my meds on March 22. Within two weeks my count had crept up to 505. By three weeks it was only at 105,760. The CD4s dropped from 483 pre-STI to 306, which many consider a significant falloff, although smaller than last time.
My symptoms during this STI were greatly reduced. For the first two weeks, I felt great and my anxiety began waning. At about three weeks, I felt my lymph glands swell—most visibly in my groin—and began feeling some fatigue. I also experienced an instinctive, hard-to-describe “active virus” feeling. Interestingly, I expected viral activity slower and later than during the first STI, and that’s exactly what I got. (I don’t know how much my expectations affected the outcome.) When I resumed therapy on April 13, I was feeling the viral rebound, but nothing like the first time.
I expect to try another STI at some point. Meanwhile, I’ll keep reading up on these interesting and risky experiments. I’ve been urging PWAs to carefully document and share their experiences. As has happened before, we may point the way to promising new research.
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