Elevated Plasma Levels of sCD14 and MCP-1 Are Associated With HIV Associated Neurocognitive Disorders Among Antiretroviral-Naive Individuals in Nigeria.


Journal

Journal of acquired immune deficiency syndromes (1999)
ISSN: 1944-7884
Titre abrégé: J Acquir Immune Defic Syndr
Pays: United States
ID NLM: 100892005

Informations de publication

Date de publication:
01 06 2020
Historique:
pubmed: 23 2 2020
medline: 7 1 2021
entrez: 22 2 2020
Statut: ppublish

Résumé

Mononuclear cells play key roles in the pathogenesis of HIV-associated neurocognitive disorders (HAND). Limited studies have looked at the association of markers of monocyte activation with HAND in Africa. We examined this association among HIV-1-infected patients in Nigeria. A total of 190 HIV-infected treatment-naive participants with immune marker data were included in this cross-sectional study. Plasma levels of soluble CD14 (sCD14), soluble CD163, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and neopterin were measured. Demographically adjusted T scores obtained from a 7-domain neuropsychological test battery were generated, and functional status was assessed using activities of daily living questionnaire. Participants were classified as unimpaired, having asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND), or HIV-associated dementia (HAD) in line with the "Frascati" criteria. Thirty-two participants (16.8%) had ANI, 14 (7.4%) had MND, whereas none had HAD. In multivariable linear regression analyses, after adjusting for age, gender, education, CD4 count, and viral load, mean levels of sCD14 were higher among those with ANI and MND as compared with the unimpaired (P = 0.033 and 0.023, respectively). Similarly, the mean level of MCP-1 was greater among those with HAND as compared with the unimpaired (P = 0.047). There were also trends for higher levels of sCD163 and TNF-α among females with MND in univariable analyses. Levels of monocyte activation markers correlate with the severity of impairment among individuals with HAND. The mechanisms that underlie these effects and the potential role of gender require further study.

Sections du résumé

BACKGROUND
Mononuclear cells play key roles in the pathogenesis of HIV-associated neurocognitive disorders (HAND). Limited studies have looked at the association of markers of monocyte activation with HAND in Africa. We examined this association among HIV-1-infected patients in Nigeria.
METHOD
A total of 190 HIV-infected treatment-naive participants with immune marker data were included in this cross-sectional study. Plasma levels of soluble CD14 (sCD14), soluble CD163, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and neopterin were measured. Demographically adjusted T scores obtained from a 7-domain neuropsychological test battery were generated, and functional status was assessed using activities of daily living questionnaire. Participants were classified as unimpaired, having asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND), or HIV-associated dementia (HAD) in line with the "Frascati" criteria.
RESULTS
Thirty-two participants (16.8%) had ANI, 14 (7.4%) had MND, whereas none had HAD. In multivariable linear regression analyses, after adjusting for age, gender, education, CD4 count, and viral load, mean levels of sCD14 were higher among those with ANI and MND as compared with the unimpaired (P = 0.033 and 0.023, respectively). Similarly, the mean level of MCP-1 was greater among those with HAND as compared with the unimpaired (P = 0.047). There were also trends for higher levels of sCD163 and TNF-α among females with MND in univariable analyses.
CONCLUSIONS
Levels of monocyte activation markers correlate with the severity of impairment among individuals with HAND. The mechanisms that underlie these effects and the potential role of gender require further study.

Identifiants

pubmed: 32084055
doi: 10.1097/QAI.0000000000002320
pii: 00126334-202006010-00009
doi:

Substances chimiques

Anti-Retroviral Agents 0
CCL2 protein, human 0
Chemokine CCL2 0
Lipopolysaccharide Receptors 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

196-202

Subventions

Organisme : BLRD VA
ID : I01 BX003222
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA044908
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH086356
Pays : United States
Organisme : FIC NIH HHS
ID : D43 TW001041
Pays : United States

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Auteurs

Jibreel Jumare (J)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.

Christopher Akolo (C)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.

Nicaise Ndembi (N)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.
Institute of Human Virology Nigeria, Federal Capital Territory, Abuja, Nigeria.

Sunday Bwala (S)

National Hospital Abuja, Federal Capital Territory, Abuja, Nigeria.

Peter Alabi (P)

University of Abuja Teaching Hospital, Federal Capital Territory, Abuja, Nigeria.

Kanayo Okwuasaba (K)

Institute of Human Virology Nigeria, Federal Capital Territory, Abuja, Nigeria.

Ruxton Adebiyi (R)

Institute of Human Virology Nigeria, Federal Capital Territory, Abuja, Nigeria.

Anya Umlauf (A)

University of California San Diego, School of Medicine, San Diego, CA; and.

Mariana Cherner (M)

University of California San Diego, School of Medicine, San Diego, CA; and.

Alash'le Abimiku (A)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.

Man Charurat (M)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.

William A Blattner (WA)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.

Walter Royal (W)

Division of Epidemiology and Prevention, Institute of Human Virology, University of Maryland School of Medicine, University of Maryland School of Medicine, Baltimore, MD.
Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA.

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