HIV Associated Eye Diseases: Existing Cognitive and Possible Mechanisms


HIV-1-related eye diseases have become a great challenge for patients of HAART treatment all over the world. Approximately 70% of HIV-1 infected patients acquire ocular opportunistic infections and manifest eye disorders during the course of their illness [1]. A single-center, retrospective study in Tokyo, of the 1,515 study patients, HIV retinopathy (HIV-R) was diagnosed in 127 (8%) patients [2]. Severe retinopathy and uveitis are the main unon treatable causes of ablepsia in these patients, since the molecular mechanism has remained unclear until now. In this Review, we present an overview of the existing cognitive and possible mechanisms for retinopathy and uveitis in HIV-1-related eye diseases [3-6].

At present, existing knowledge has believed that disruption of the structure and function of the blood-retina barrier (BRB) is the major contributor of HIV-1-related eye diseases. The BRB include the neurons, pigment epithelium, vascular cells and microglia or resident macrophages that are organized into distinct layers [7,8]. Both the vascular endothelium and retinal pigment epithelial possess a well-developed tight junction complex to form the BRB, which give a stringent control of solute and fluid permeability and maintains the autologous microenvironment for a functional retina.

Pathways by which HIV-1 enters various tissues across the epithelium have been covered, containing transcytosis, direct infection, diffusive percolation and sequestration. Some studies revealed that direct interaction of HIV-1 with the endothelium, which share tight junction structures in common with the epithelium, could lead to the disruption of endothelial integrity and subsequent increased HIV' leakage across the endothelium [9]. It has been confirmed that gp120 has many functions, for example, apoptosis, HIV-associated B cell dysfunction, inflammation and so on. HIV-1 envelope glycoprotein gp120 mediates viral entry by binding to receptors-CD4 glycoprotein on host cells [10]. Gp120 and Tat protein have been associated with the disruption of tight junctions in the endothelium. Notably, gp120 can induce the degradation of tight junction proteins in endothelial cells and has been associated with increased permeability of the BRB during progressive HIV-1- associated retinopathy and uveitis. The enhanced BRB permeability induced by HIV-1 gp120 has also been observed in transgenic mice. Treatment with HIV-1 gp120 down-regulated the expression of tight junction proteins in human RPE cells and led to increased monolayer permeability and consequent translocation of HIV-1 and bacteria across the epithelium. However, the molecular mechanism of gp120 down regulating tight junction protein is still elusive.

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