Chronic brain damage in HIV-infected individuals under antiretroviral therapy is associated with viral reservoirs, sulfatide release, and compromised cell-to-cell communication.
Daniela D'AmicoRosario BaroneValentina Di FeliceBeau AncesBrendan PrideauxEliseo A EugeninPublished in: Cellular and molecular life sciences : CMLS (2023)
HIV infection has become a chronic and manageable disease due to the effective use of antiretroviral therapies (ART); however, several chronic aging-related comorbidities, including cognitive impairment, remain a major public health issue. However, these mechanisms are unknown. Here, we identified that glial and myeloid viral reservoirs are associated with local myelin damage and the release of several myelin components, including the lipid sulfatide. Soluble sulfatide compromised gap junctional communication and calcium wave coordination, essential for proper cognition. We propose that soluble sulfatide could be a potential biomarker and contributor to white matter compromise observed in HIV-infected individuals even in the current ART era.
Keyphrases
- hiv infected
- antiretroviral therapy
- white matter
- human immunodeficiency virus
- hiv infected patients
- hiv positive
- hiv aids
- public health
- single cell
- cognitive impairment
- multiple sclerosis
- sars cov
- cell therapy
- oxidative stress
- stem cells
- drug induced
- spinal cord injury
- bone marrow
- spinal cord
- dendritic cells
- mild cognitive impairment
- blood brain barrier