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September  2020

de Almeida SM, Ribeiro CE, Rotta I, Letendre S, Potter M, Tang B, Batistela M, Vaida F, Ellis RJ, and the HIV Neurobehavioral Research Center Group. Blood amyloid-beta protein isoforms are affected by HIV-1 in a subtype-dependent patternJ Neurovirol. 2019;26(1):3-13. PMID: 31281948. PMCID: 6944779

About This Paper

This study aimed to compare serum amyloid processing biomarkers among HIV subtype B (n?=?25), HIV subtype C (n?=?26), healthy HIV-negative controls (n?=?18), and patients with Alzheimer's disease (AD; n?=?24). Immunoassays were used to measure main soluble A? isoforms A?38, A?40, A?42, and A?-total in serum and cerebrospinal fluid (CSF). People living with HIV (PLWH) and HIV(-) samples, including AD samples, were compared for gender and age, while HIV subtypes were compared for nadir CD4 and plasma viral load suppression. CSF/serum ratios of A?40, A?42, and A?-total were lower in HIV-1C group than in HIV-1B group (p?=?0.020, 0.025, and 0.050, respectively). In serum, these biomarkers were comparable. Serum A? isoforms were significantly lower in PLWH than in AD. Serum A?42 levels in PLWH were decreased compared to those in control group, thus similar to A?42 alterations in CSF; these results were different from those observed in AD. Impaired cellular immunity, low CD4 cell count (nadir or current) influences serum A? metabolism in HIV-1B but not HIV-1C. However, in PLWH overall, but not in individual HIV subtype groups, greater CD4 recovery, calculated as the difference between current and nadir CD4, correlated with A?42/A?40 ratio in serum (rs 0.246; p?=?0.0479). No significant correlation was found with global deficit score (GDS), an index of neurocognitive performance, age, or duration of infection. These findings are consistent with those of subtype-dependent amyloid processing in blood in chronic HIV disease.

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