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HIV-1 RNA Detected in the CNS after Years of Suppressive Antiretroviral Therapy Can Originate from a Replicating CNS Reservoir or Clonally Expanded Cells.

Journal article
Authors Sarah B Joseph
Laura P Kincer
Natalie M Bowman
Chris Evans
Michael J Vinikoor
Christopher K Lippincott
Magnus Gisslén
Serena Spudich
Prema Menezes
Kevin Robertson
Nancie Archin
Angela Kashuba
Joseph J Eron
Richard W Price
Ronald Swanstrom
Published in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
Volume 69
Issue 8
Pages 1345-1352
ISSN 1537-6591
Publication year 2019
Published at Institute of Biomedicine, Department of Infectious Medicine
Pages 1345-1352
Language en
Keywords CNS, CSF escape, HIV reservoirs, drug resistance, persistence
Subject categories Infectious Medicine


HIV-1 populations are detected in cerebrospinal fluid (CSF) of some people on suppressive antiretroviral therapy (ART). Detailed analysis of these populations may reveal whether they are produced by central nervous system (CNS) reservoirs.We performed a study of 101 asymptomatic participants on stable ART. HIV-1 RNA concentrations were cross-sectionally measured in CSF and plasma. In participants with CSF HIV-1 RNA concentrations sufficiently high to permit analysis, viral populations were genetically and phenotypically characterized over multiple time points.For 6% of participants (6 of 101), the concentration of HIV-1 RNA in their CSF was ≥ 0.5 log copies/mL above that of plasma (i.e. CSF escape). We generated viral envelope sequences from CSF of three participants. One had a persistent CSF escape population that was macrophage-tropic, partially drug resistant, genetically diverse and closely related to a minor macrophage-tropic viral lineage present in the blood prior to viral suppression and enriched for after ART. Two participants (one suppressed and one not) had transient CSF escape populations that were R5 T cell-tropic with little genetic diversity.Extensive analysis of viral populations in one participant revealed that CSF escape was from a persistently replicating population, likely in macrophages/microglia, present in the CNS over 3 years of ART. CSF escape in two other participants was likely produced by trafficking and transient expansion of infected T cells in the CNS. Our results show that CNS reservoirs can persist during ART, but that CSF escape is not exclusively produced by a replicating CNS reservoir.

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