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Antiretroviral therapy for the prevention of HIV-1 transmission
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Adjunctive Dexamethasone in HIV-Associated Cryptococcal Meningitis
Outcomes of HIV-associated Hodgkin lymphoma in the era of antiretroviral therapy
CD8 T-Cell Expansion and Inflammation Linked to CMV Coinfection in ART-treated HIV Infection
Ongoing HIV Replication Replenishes Viral Reservoirs During Therapy
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Levels of intracellular HIV-DNA in patients with suppressive antiretroviral therapy
Course and Clinical Significance of CD8+ T-Cell Counts in a Large Cohort of HIV-Infected Individuals
Impact of low-level viremia on clinical and virological outcomes in treated HIV-1-infected patients
Predicting the outcomes of treatment to eradicate the latent reservoir for HIV-1
CMV+ Serostatus Associates Negatively with CD4:CD8 Ratio Normalization in Controlled HIV-Infected Patients on cART
Published by Pedro CAHN
Updated: 15 January, 2017
Cytomegalovirus (CMV) infection is common among HIV-infected patients but its repercussion on the course of CD4+ and CD8+ T cells after cART initiation remains elusive. The French Dat'AIDS cohort enrolled 5,688 patients on first-line cART, from which we selected patients who achieved HIV suppression for at least 12 months without modification of cART, and for whom CMV serostatus was available. Five hundred and three patients fulfilled the selection criteria (74% male, median age 43 yrs, 15.5% CDC stage C), of whom 444 (88.3%) were seropositive for CMV (CMV+).
Multivariate analyses using mixed-linear models adjusted for the time from HIV suppression, sex, age, transmission risk group, duration of HIV follow-up, the interaction between time from HIV suppression and CMV+ serology, and the nadir CD4 count revealed a negative correlation between CMV+ and CD4:CD8 ratio (coeff. = -0.16; p = 0.001). This correlation was also observed among patients displaying optimal CD4 recovery (≥ 500 cells/mm 3 at M12; coeff. = -0.24; p = 0.002).
Hence, CMV+ serostatus antagonizes normalization of the CD4:CD8 ratio, although further analyses of the impact of co-morbidities that associate with CMV serostatus, like HCV infection, are needed to elucidate this antagonism formally. However, this might reflect a premature T cell senescence, thus advocating for a close monitoring of T cells in CMV coinfected patients. In addition, our results raise the question of the benefit of treatment for asymptomatic CMV co-infection in HIV-infected patients.