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Abstract
<p class="first" id="P2">While the severe cognitive effects of HIV-associated dementia
have been reduced by
combined antiretroviral therapy (cART), nearly half of HIV-positive (HIV+) patients
still suffer from some form of HIV-Associated Neurocognitive Disorders (HAND). While
frank neuronal loss has been dramatically reduced in HAND patients, white matter loss,
including dramatic thinning of the corpus callosum, and loss of volume and structural
integrity of myelin persists despite viral control by cART. It remains unclear whether
changes in white matter underlie the clinical manifestation seen in patients or whether
they are the result of persistent viral reservoirs, remnant damage from the acute
infection, the antiretroviral compounds used to treat HIV, secondary effects due to
peripheral toxicities or other associated comorbid conditions. Both HIV infection
itself and its treatment with antiretroviral drugs can induce metabolic syndrome,
lipodystrophy, atherosclerosis and peripheral neuropathies by increased oxidative
stress, induction of the unfolded protein response and dysregulation of lipid metabolism.
These virally and/or cART-induced processes can also cause myelin loss in the CNS.
This review aims to highlight existing data on the contribution of white matter damage
to HAND and explore the mechanisms by which HIV infection and its treatment contribute
to persistence of white matter changes in people living with HIV currently on cART.
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