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The Body Covers: The 7th Conference on Retroviruses and Opportunistic Infections
Session 40
Pathogenesis and Treatment of CMV Disease in the Era of HAART

January 31, 2000

  • Poster 267: Long-Term Effects of HAART on Morbidity and Mortality in HIV-1-Infected Patients at Risk for CMV Disease (Authored by E. Martinez, E. Buira, J. Mallolas, M.A. Garcia, J.L. Blanco, F. Garcia, J.M. Miro, T. Pumarola, and J.M. Gatell. Hosp. Clin. Univ., Barcelona, Spain)
    Click here to view the original abstract

  • Poster 273: Multicenter Evaluation of CMV Reactivation in HIV-infected Women at Potential Risk for CMV Disease (Authored by C.E. Bush, R.S. Klein, R.M. Donovan, D.J. Ing, D. Jabs, K. Mayer, P. Schuman, and K. Tashima’ for the HER Study Group. Henry Ford Hosp., Detroit, MI; Montefiore Med. Ctr., Bronx, NY; CDC, Atlanta, GA; Johns Hopkins Univ., Baltimore, MD; Brown Univ., Providence, RI; Wayne State Univ., Detroit, MI; and Miriam Hosp., Providence RI)
    Click here to view the original abstract


Poster 267: Long-Term Effects of HAART on Morbidity and Mortality in HIV-1-Infected Patients at Risk for CMV Disease

How common is CMV disease since the introduction of potent antiretroviral therapy? This study reports on the incidence of CMV in a cohort of patients with advanced disease prior to starting protease inhibitor-based antiretroviral therapy.

One hundred twenty consecutive patients were included. Prior to beginning therapy with a protease inhibitor, this group had a mean CD4 cell count of 16 and a viral load of >100,000; all were CMV antibody positive. After a mean follow-up of 159 weeks, CMV disease (mostly retinitis) developed in 13 patients, for a rate of 3.6 cases/100 patient-years. While more than half of the cases occurred in the first three months after starting the protease-inhibitor-based regimen, there were still cases of CMV that occurred more than three years after starting therapy. They conclude that CMV remains a significant problem despite the availability of potent antiretroviral therapy, especially for patients with persistently low CD4 cell counts.


Poster 273: Multicenter Evaluation of CMV Reactivation in HIV-infected Women at Potential Risk for CMV Disease

Bush and colleagues report on their experience using three different CMV viral load assays in 121 HIV-infected women followed in the HER Study Group. The study took place between January 1996 and March 1998, and enrolled CMV antibody positive women with a CD4 cell count <100. During the study, CMV viral load testing was done every three months with the Chiron bDNA assay, the Digene Hybrid Capture assay, and the Biotest CMV pp65 antigen test.

Nearly all of the women were on antiretroviral therapy; still, 108 (89%) of the women had a detectable HIV viral load at baseline, with a median plasma HIV RNA of 55,000 copies/mL. Furthermore, at some point during the study, 78 (64%) of the women were viremic with CMV, at least transiently, demonstrating CMV reactivation. Two cases of CMV retinitis developed; both were positive by the CMV antigen test, but the bDNA test was negative in one and the hybrid capture assay negative in the other. Overall, the investigators found the antigen testing to be more sensitive than either of the two other methods.

The important finding in this study is that CMV reactivation continues to occur despite the administration of antiretroviral therapy. It remains to be seen whether this reactivation will lead to CMV disease or have other adverse consequences in these patients.



  
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