Factors influencing cerebrospinal fluid and plasma HIV-1 RNA detection rate in patients with and without opportunistic neurological disease during the HAART era

ABSTRACT Human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) is a severe neurological disease that affects a subset of HIV-1-infected individuals. Increased compartmentalization has been reported between blood and cerebrospinal fluid (CSF) HIV-1 populations in subjects with HAD, but it is still not known when compartmentalization arises during the course of infection. To assess HIV-1 genetic compartmentalization early during infection, we compared HIV-1 populations in the peripheral blood and CSF in 11 primary infection subjects, with analysis of longitudinal samples over the first 18 months for a subset of subjects. We used heteroduplex tracking assays targeting the variable regions of env and single-genome amplification and sequence analysis of the full-length env gene to identify CSF-compartmentalized variants and to examine viral genotypes within the compartmentalized populations. For most subjects, HIV-1 populations were equilibrated between the blood and CSF compartments. However, compartmentalized HIV-1 populations were detected in the CSF of three primary infection subjects, and longitudinal analysis of one subject revealed that compartmentalization during primary HIV-1 infection was resolved. Clonal amplification of specific HIV-1 variants was identified in the CSF population of one primary infection subject. Our data show that compartmentalization can occur in the central nervous system (CNS) of subjects in primary HIV-1 infection in part through persistence of the putative transmitted parental variant or via viral genetic adaptation to the CNS environment. The presence of distinct HIV-1 populations in the CSF indicates that independent HIV-1 replication can occur in the CNS, even early after HIV-1 transmission.

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Spectrum of neurological disease in patients with discordant HIV-1 RNA levels in plasma and cerebrospinal fluid

Journal of Infection ◽

10.1016/j.jinf.2009.12.009 ◽

2010 ◽

Vol 60 (3) ◽

pp. 251-252 ◽

Cited By ~ 2

Author(s):

A. Scourfield ◽

L. Waters ◽

M. Nelson

Keyword(s):

Cerebrospinal Fluid ◽

Neurological Disease ◽

Hiv 1 ◽

Rna Levels

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Cerebrospinal fluid (CSF) analyses in HIV-1 primary neurological disease

The Italian Journal of Neurological Sciences ◽

10.1007/bf02334971 ◽

1992 ◽

Vol 13 (8) ◽

pp. 667-683 ◽

Cited By ~ 6

Author(s):

J. Nogales-Gaete ◽

K. Syndulko ◽

W. W. Tourtellotte

Keyword(s):

Cerebrospinal Fluid ◽

Neurological Disease ◽

Hiv 1

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The Relationships between HIV-1 Infection, History of Methamphetamine Use Disorder, and Soluble Biomarkers in Blood and Cerebrospinal Fluid

Viruses ◽

10.3390/v13071287 ◽

2021 ◽

Vol 13 (7) ◽

pp. 1287

Author(s):

T. Walter ◽

Jennifer Iudicello ◽

Debra Cookson ◽

Donald Franklin ◽

Bin Tang ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Immune System ◽

Public Health Problem ◽

Control Group ◽

Csf Biomarkers ◽

Immune System Dysfunction ◽

Immune Biomarkers ◽

Plasma Factor ◽

History Of ◽

Hiv 1

Methamphetamine (METH) use disorder is highly prevalent among people with HIV (PWH) and is a significant public health problem. HIV and METH use are each associated with immune system dysfunction; however, the combined effects on the immune system are poorly understood. This cross-sectional project measured soluble immune biomarkers in plasma and cerebrospinal fluid (CSF) collected from a control group, people with a history of a METH use disorder (METH+), PWH with no history of METH use disorder (HIV+), and PWH with a history of METH use disorder (HIV+/METH+). HIV, METH, and immune dysfunction can also be associated with affective and cognitive deficits, so we characterized mood and cognition in our participants. Two factor analyses were performed for the plasma and CSF biomarkers. Plasma IL-8, Ccl2, VEGF, and 8-isoprostane loaded onto one factor that was highest in the HIV+/METH+ group (p < 0.047) reflecting worse inflammation, vascular injury, and oxidative stress. This plasma factor was also negatively correlated with delayed recall (R = −0.49, p = 0.010), which was worst in the HIV+/METH+ group (p = 0.030 compared to the control group). Overall, these data implicate that combined HIV-1 infection and METH use may exacerbate inflammation, leading to worse cognition.

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