Journal of NeuroVirology | 2019

Monocyte activation, HIV, and cognitive performance in East Africa

 
 
 
 
 
 
 
 
 
 
 
 
 
 

Abstract


Chronic inflammation associated with monocyte activation has been linked to HIV-related cognitive outcomes in resource-rich settings. Few studies have investigated this relationship in the African context where endemic non-HIV infections may modulate effects. We characterized immune activation biomarkers in Kenyan and Ugandan participants in relation to neuropsychological testing performance (NTP) from the African Cohort Study (AFRICOS). We focused on activation markers associated with monocytes (sCD14, sCD163, neopterin), T cells (HLA-DR + CD38 + on CD4 + and CD8 + T lymphocytes), and microbial translocation (intestinal fatty acid-binding protein, I-FABP). The HIV-infected ( n \u2009=\u2009290) vs. HIV-uninfected ( n \u2009=\u2009104) groups were similar in age with mean (SD) of 41 (9.5) vs. 39 (9.9) years, respectively ( p \u2009=\u20090.072). Among HIV-infected participants, the mean (SD) current CD4 + count was 402 (232); 217 (75%) were on combination antiretroviral therapy (cART) and 199 (69%) had suppressed plasma HIV RNA. sCD14 was inversely correlated to NTP ( r \u2009=\u2009−\u20090.14, p \u2009=\u20090.037) in models that included both HIV-infected and uninfected individuals, adjusted for HIV status and research site, whereas sCD163 was not ( r \u2009=\u20090.041, p \u2009=\u20090.938). Neither of the T cell activation markers correlated with NTP. In the HIV-infected group, I-FABP was inversely associated with NTP ( r \u2009=\u2009−\u20090.147, p \u2009=\u20090.049), even among those with suppressed plasma virus ( r \u2009=\u2009−\u20090.0004, p \u2009=\u20090.025). Among the full group, HIV status did not appear to modulate the effects observed. In this cohort from East Africa, sCD14, but not sCD163, is associated with cognitive performance regardless of HIV status. Findings among both HIV-infected and HIV-uninfected groups is supportive that HIV and non-HIV-related inflammatory sources contribute to cognitive performance in this setting.

Volume 26
Pages 52-59
DOI 10.1007/s13365-019-00794-3
Language English
Journal Journal of NeuroVirology

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