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MRS suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal HIV infection.

ABSTRACT: The neurological changes in children living with perinatal HIV (PHIV) on antiretroviral therapy (ART) can be studied at a metabolic level through proton magnetic resonance spectroscopy. While previous studies in children have largely focused on individual metabolite changes, investigating patterns within and across regions of interest can aid in identifying metabolic markers of HIV infection. In this study 76 children with PHIV from the Children with HIV Early AntiRetroviral (CHER) trial, 30 children who were HIV-exposed-uninfected (HEU) and 30 children who were HIV-unexposed (HU), were scanned at the age of 11.6 (sd = 0.3) years using a 3 T Skyra scanner. Metabolite concentrations were quantified within the basal ganglia (BG), midfrontal gray matter (MFGM) and peritrigonal white matter (PWM), comparing levels between HIV status groups using linear regression. Factor analysis and logistic regression were performed to identify metabolic patterns characteristic of HIV infection within and across the regions of interest. In the BG region we observed restored metabolic activity in children with PHIV and children who were HEU, despite differences being previously observed at younger ages, suggesting that treatment may effectively reduce the effects of HIV infection and exposure. Elevated MFGM choline levels in children with PHIV are indicative of inflammation. Further, we observed reduced N-acetyl-aspartate (NAA) in the PWM of children with PHIV and children who were HEU, indicating possible axonal damage. Lower levels of PWM creatine in children with PHIV suggest that this may not be a valid reference metabolite in HIV studies. Finally, factor scores for a cross-regional inflammatory factor and a PWM axonal factor, driven by PWM NAA and creatine levels, distinguished children with PHIV from children without HIV (HEU and HU) at 11 years. Therefore, the effects of perinatal HIV infection and exposure continue to be seen at 11 years despite early treatment.

SUBMITTER: Graham AS

PROVIDER: S-EPMC7721646 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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MRS suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal HIV infection.

Graham Amy S AS Holmes Martha J MJ Little Francesca F Dobbels Els E Cotton Mark F MF Laughton Barbara B van der Kouwe Andre A Meintjes Ernesta M EM Robertson Frances C FC

NeuroImage. Clinical 20201119

The neurological changes in children living with perinatal HIV (PHIV) on antiretroviral therapy (ART) can be studied at a metabolic level through proton magnetic resonance spectroscopy. While previous studies in children have largely focused on individual metabolite changes, investigating patterns within and across regions of interest can aid in identifying metabolic markers of HIV infection. In this study 76 children with PHIV from the Children with HIV Early AntiRetroviral (CHER) trial, 30 chi ...[more]

PMID: 33395994

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Project description:New techniques for individualized assessment of white matter integrity are needed to detect traumatic axonal injury (TAI) and predict outcomes in critically ill patients with acute severe traumatic brain injury (TBI). Diffusion MRI tractography has the potential to quantify white matter microstructure in vivo and has been used to characterize tract-specific changes following TBI. However, tractography is not routinely used in the clinical setting to assess the extent of TAI, in part because focal lesions reduce the robustness of automated methods. Here, we propose a pipeline that combines automated tractography reconstructions of 40 white matter tracts with multivariate analysis of along-tract diffusion metrics to assess the presence of TAI in individual patients with acute severe TBI. We used the Mahalanobis distance to identify abnormal white matter tracts in each of 18 patients with acute severe TBI as compared to 33 healthy subjects. In all patients for which a FreeSurfer anatomical segmentation could be obtained (17 of 18 patients), including 13 with focal lesions, the automated pipeline successfully reconstructed a mean of 37.5 ± 2.1 white matter tracts without the need for manual intervention. A mean of 2.5 ± 2.1 tracts resulted in partial or failed reconstructions and needed to be reinitialized upon visual inspection. The pipeline detected at least one abnormal tract in all patients (mean: 9.1 ± 7.9) and accurately discriminated between patients and controls (AUC: 0.91). The number and neuroanatomic location of abnormal tracts varied across patients and levels of consciousness. The premotor, temporal, and parietal sections of the corpus callosum were the most commonly damaged tracts (in 10, 9, and 8 patients, respectively), consistent with prior histopathological studies of TAI. TAI measures were not associated with concurrent behavioral measures of consciousness. In summary, we provide proof-of-principle evidence that an automated tractography pipeline has translational potential to detect and quantify TAI in individual patients with acute severe TBI.

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MRS suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal HIV infection.

Publications

MRS suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal HIV infection.

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