Human immunodeficiency virus and cerebrovascular diseases – review

Abstract

Human immunodeficiency virus (HIV) is thought to increase the risk of cerebrovascular disease, although few data exist linking these two disease entities. The aetiology of vasculopathy in both adults and children with HIV remains unknown. However, it has been postulated that direct infection by HIV, immune complex deposition, and impaired regulation of the immune response are the likely causes. HIVassociated vasculopathy in the cerebral circulation encompasses several forms of arterial disease occurring in the absence of any cause other than HIV infection. It includes disease of extra cranial large arteries, intracranial medium sized arteries with or without aneurysm formation and small vessel disease. The pathology appears to differ across vessel types, and the exact mechanism by which HIV induces vessel wall damage in each case remains uncertain. Furthermore, immuno suppression secondary to HIV can predispose to opportunistic infections of the central nervous sys tem. These acquired immune deficiency syndrome (AIDS)defining infections include toxoplasmosis, cryptococcal meningitis, tuberculosis, cytomegalovirus, and progressive multifocal leukoencephalop athy secondary to JC virus reactivation, which can also present as cerebrovascularlike manifestation in patients with HIV. Although several causative mechanisms have been proposed for the relationship between HIV infection and cerebrovascular diseases, including HIVassociated dyslipidaemia, endo thelial dysfunction, inflammation, and hypercoagulability, the pathogenesis of HIVvasculopathy is not completely understood. Beside the above pathological entities, HIV itself has been implicated in the pathogenesis of cerebrovascular diseases, either through direct invasion and vessel wall destruc tion or cytokinemediated vascular remodelling.

Obstructive ureteric calculus with superimposed infections causing reversible posterior leukoencephalopathy syndrome

“…[ 7 , 18 ] It is wealth noting that, HIV maybe an independent risk factor for endothelial dysfunction as well as vascular disease. [ 7 , 18 , 19 ] Azotemia may trigger interstitial brain edema via augmentation of capillary permeability as well as cytotoxic edema resulting in direct injury to the brain parenchyma in patients with renal failure. [ 20 ] RPLS has also been reported in dialysis-dependent patients as a result of uremia and not dialysis disequilibrium syndrome that often occurs few hours after treatment.…”

The Therapeutic Potential of Resveratrol in Gliomas

“…Pokemon is trigger protein that binds precisely to short transcripts constituent of HIV-1 facilitator gene (88,164). It is now clear that Pokemon can also trigger Tat action on HIV, augment NF-κB-facilitated transcription as well as block human ADH5/FDH gene release (88,110,164). Research has demonstrated that Over-secretion of the Pokemon gene dwindles the release ARF gene, which also trigger the mortification of p53 as well as oncogenic alteration.…”