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Progressive increase in central nervous system immune activation in untreated primary HIV-1 infection

Journal article
Authors J. Suh
E. Sinclair
J. Peterson
E. Lee
T. C. Kyriakides
F. Y. Li
Lars Hagberg
D. Fuchs
R. W. Price
Magnus Gisslén
S. Spudich
Published in Journal of Neuroinflammation
Volume 11
ISSN 1742-2094
Publication year 2014
Published at Institute of Biomedicine, Department of Infectious Medicine
Language en
Links dx.doi.org/10.1186/s12974-014-0199-...
Keywords HIV, Central Nervous System Viral Infections, Inflammation, Neopterin, Activated T-cells, Immune, IMMUNODEFICIENCY-VIRUS-INFECTION, CEREBROSPINAL-FLUID NEOPTERIN, ACTIVE, ANTIRETROVIRAL THERAPY, T-CELLS, NEUROCOGNITIVE IMPAIRMENT, VIRAL LOAD, FOLLOW-UP, REPLICATION, IMMUNOACTIVATION, INDIVIDUALS, Immunology, Neurosciences
Subject categories Immunology in the medical area, Neurosciences

Abstract

Background: Central nervous system (CNS) inflammation is a mediator of brain injury in HIV infection. To study the natural course of CNS inflammation in the early phase of infection, we analyzed longitudinal levels of soluble and cellular markers of inflammation in cerebrospinal fluid (CSF) and blood, beginning with primary HIV-1 infection (PHI). Methods: Antiretroviral-naive subjects identified as having PHI (less than one year since HIV transmission) participated in phlebotomy and lumbar puncture at baseline and at variable intervals thereafter. Mixed-effects models were used to analyze longitudinal levels of CSF neopterin and percentages of activated cluster of differentiation (CD) 4+ and CD8+ T-cells (co-expressing CD38 and human leukocyte antigen-D-related (HLA-DR)) in blood and CSF. Results: A total of 81 subjects were enrolled at an average of 100 days after HIV transmission and had an average follow-up period of 321 days, with the number of visits ranging from one to 13. At baseline, the majority of subjects had CSF neopterin concentrations above the upper limit of normal. The baseline concentration was associated with the longitudinal trajectory of CSF neopterin. In subjects with baseline levels of less than 21 nmol/L, a cutoff value obtained from a mixed-effects model, CSF neopterin increased by 2.9% per 10 weeks (n = 33; P < 0.001), whereas it decreased by 6.7% in subjects with baseline levels of more than 21 nmol/L (n = 11; P = 0.001). In a subset with available flow cytometry data (n = 42), the percentages of activated CD4+ and CD8+ T-cells in CSF increased by 0.8 (P < 0.001) and 0.73 (P = 0.02) per 10 weeks, respectively. Conclusions: Neopterin levels and the percentages of activated CD4+ and CD8+ T-cells in CSF progressively increase in most subjects without treatment during early HIV-1 infection, suggesting an accrual of intrathecal inflammation, a major contributor to neuropathology in HIV infection.

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