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Cerebrospinal fluid (CSF) neuronal biomarkers across the spectrum of HIV infection: hierarchy of injury and detection.

Journal article
Authors Julia Peterson
Magnus Gisslén
Henrik Zetterberg
Dietmar Fuchs
Barbara L Shacklett
Lars Hagberg
Constantin T Yiannoutsos
Serena S Spudich
Richard W Price
Published in PloS one
Volume 9
Issue 12
Pages e116081
ISSN 1932-6203
Publication year 2014
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Infectious Medicine
Pages e116081
Language en
Links dx.doi.org/10.1371/journal.pone.011...
Keywords Adult, Alzheimer Disease, cerebrospinal fluid, Amyloid beta-Peptides, cerebrospinal fluid, Amyloid beta-Protein Precursor, cerebrospinal fluid, Biomarkers, cerebrospinal fluid, Cross-Sectional Studies, Female, HIV, isolation & purification, HIV Infections, cerebrospinal fluid, complications, diagnosis, Humans, Male, Middle Aged, Nervous System Diseases, cerebrospinal fluid, complications, Neurofilament Proteins, cerebrospinal fluid, Peptide Fragments, cerebrospinal fluid, Phosphorylation, tau Proteins, cerebrospinal fluid
Subject categories Clinical Medicine

Abstract

The character of central nervous system (CNS) HIV infection and its effects on neuronal integrity vary with evolving systemic infection. Using a cross-sectional design and archived samples, we compared concentrations of cerebrospinal fluid (CSF) neuronal biomarkers in 143 samples from 8 HIV-infected subject groups representing a spectrum of untreated systemic HIV progression and viral suppression: primary infection; four groups of chronic HIV infection neuroasymptomatic (NA) subjects defined by blood CD4+ T cells of >350, 200-349, 50-199, and <50 cells/µL; HAD; treatment-induced viral suppression; and 'elite' controllers. Samples from 20 HIV-uninfected controls were also examined. The neuronal biomarkers included neurofilament light chain protein (NFL), total and phosphorylated tau (t-tau, p-tau), soluble amyloid precursor proteins alpha and beta (sAPPα, sAPPβ) and amyloid beta (Aβ) fragments 1-42, 1-40 and 1-38. Comparison of the biomarker changes showed a hierarchy of sensitivity in detection and suggested evolving mechanisms with progressive injury. NFL was the most sensitive neuronal biomarker. Its CSF concentration exceeded age-adjusted norms in all HAD patients, 75% of NA CD4<50, 40% of NA CD4 50-199, and 42% of primary infection, indicating common neuronal injury with untreated systemic HIV disease progression as well as transiently during early infection. By contrast, only 75% of HAD subjects had abnormal CSF t-tau levels, and there were no significant differences in t-tau levels among the remaining groups. sAPPα and β were also abnormal (decreased) in HAD, showed less marked change than NFL with CD4 decline in the absence of HAD, and were not decreased in PHI. The CSF Aβ peptides and p-tau concentrations did not differ among the groups, distinguishing the HIV CNS injury profile from Alzheimer's disease. These CSF biomarkers can serve as useful tools in selected research and clinical settings for patient classification, pathogenetic analysis, diagnosis and management.

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