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Low CD4 cells with undetectable viral loads
Dec 29, 2007

Dr. DAAR I happen to be reading one of your forums on strategies of treatment. You mentioned what to do when you have a patient with an undetectable viral load but low CD4 CELLS. My question is what to do, I am in a facility where we se about 300 HIV PATIENTS , I'm an infectious disease specialist and we have many patients that have undetectable HIV VIRAL LOADS but have CD4 AS LOW AS 40, WE EVEN HAD TWO PATIENTS WITH 0 CD4S obviously I rapidly sent him back to get another exam done because I thought it was a lab mistake but when he came back he only had about 20 cd4s. Can it be that we measure quantities of CD4s and not functionality,could it be by any chance even though they have very poor quantities they function ok, I am very interested in doing investigation on this respect because as I MENTIONED WE HAVE MANY PATIENTS WITH THESE CHARACTERISTICS. DR. ALMA MINERVA PEREZ RIOS MD PhD

Response from Dr. Daar

Hi Dr. Rios, Thank you for your posting. Many of us taking care of patients struggle with this issue, as do our clients. You raise several very good points. First of all, you are absolutely right that we do measure the number of CD4 cells and not their function. In fact, there is every reason to believe that those with undetectable viral loads do indeed have improved CD4 function. This is at least in part related to the effect reducing viral load has on cellular activation. It is further supported in the clinic by our experience that some untreatable opportunistic infections, such as cryptosporidium clinically improve with the initiation of antiretroviral therapy before we see much in the way of increased CD4 cell counts. I believe it is in part because of improved function that most of our patients with good viral suppression with minimal CD4 responses, including those that remain less than 200 or even 100 cells/uL for prolonged periods of time do not seem to be at much risk for developing opportunistic infection.

With regards to the "what to do" question, this is less clear. It is obviously important to make sure that the viral load assay is able to quantitate the particular patients virus. This has become less of a problem with the development of assays that detect diverse subtypes of HIV-1, but still can occur. In addition, if the epidemiology fits it is worth at least considering HIV-2 and/or HTLV co-infection. Other factors associated with reduced CD4 response include other co-infections, such as HCV, older age and delayed initiation of therapy. Strategically, other than considering these other issues some have tried switching NNRTI-based treatment to PIs, or ZDV-based regimens to non-ZDV-based regimens since there is growing evidence that immunologic responses are greater in those treated with select PIs versus select NNRTIs, and abacavir and tenofovir DF than with ZDV. That said, the clinical relevance of all of these differences is not known. Finally, some have considered IL-2, although there is no data showing it changes clinical outcomes, and other novel therapeutics are being studied, including a study with palifermin (recombinant human keratinocyte growth factor) being performed through the ACTG.

Thank you for your comments.

Best, Eric


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