Skip Navigation LinksHome > December 15, 2011 - Volume 58 - Issue 5 > Longitudinal Assessment of Interleukin 7 Plasma Levels in HI...
JAIDS Journal of Acquired Immune Deficiency Syndromes:
doi: 10.1097/QAI.0b013e318231de37
Basic and Translational Science

Longitudinal Assessment of Interleukin 7 Plasma Levels in HIV-Infected Patients in the Absence of and Under Antiretroviral Therapy

Rallón, Norma I. PhD*; López, Mariola PhD*; Lozano, Sara*; Sempere-Ortells, José M. MD, PhD; Soriano, Vincent MD, PhD*; Benito, José M. PhD, MD*

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Background: Cross-sectional studies in HIV-positive patients have suggested that interleukin 7 (IL-7) may increase in parallel to CD4 decline during the natural course of HIV infection. We tested this hypothesis in a longitudinal study examining the evolution of IL-7 and CD4 counts in 2 different scenarios.

Methods: IL-7 and CD4 counts were regularly monitored in 30 drug-naive patients during a follow-up period of 46 ± 14 months in the absence of therapy and in 42 patients who started highly active antiretroviral therapy and maintained undetectable viremia for 2 years. Multivariate linear regression analysis was used to ascertain what factors were associated with IL-7 variations during follow-up.

Results: In antiretroviral therapy–naive patients, CD4 counts significantly decreased (P < 0.0001), whereas plasma HIV-RNA and IL-7 levels remained fairly stable. In patients on highly active antiretroviral therapy, CD4 counts significantly increased (P < 0.0001) and IL-7 tended to decrease (P = 0.1). There was no correlation between CD4 and IL-7 variations either in the naive or in the treated population. The only parameter significantly associated with IL-7 variation during follow-up was its baseline level that showed a negative correlation.

Conclusions: In HIV patients with low or moderate degree of immunodeficiency, CD4 counts and plasma IL-7 levels do not evolve in parallel, suggesting that other factors different from CD4 counts must be involved in the upregulation of IL-7 observed in HIV infection.

© 2011 Lippincott Williams & Wilkins, Inc.


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