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.
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.
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.
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.
*Infectious Diseases Department, Hospital Carlos III, Madrid, Spain
†Biotechnology Department, Alicante University, Alicante, Spain
Supported in part by grants from Fundación para la Investigación y la Prevención del SIDA (Síndrome de Inmunodeficiencia Adquirida) en España (grant number 36617/06), Fundación Investigacion y Educacion en SIDA, Red de Investigacion en SIDA (grant reference FIS-RD06/0006), and the European Union 6th Framework Programme (European AIDS Treatment Network, LSHP-CT-2006-037570).
The authors have no conflicts of interest to disclose.
Correspondence to: José M. Benito, PhD, MD, Infectious Diseases Department, Hospital Carlos III, Calle Sinesio Delgado 10, 28029 Madrid, Spain (e-mail: firstname.lastname@example.org)
Received March 15, 2011
Accepted August 4, 2011