It has been found that human immunodeficiency virus (HIV)-1 RNA or antigens can be
detected in the intraocular tissues of HIV-1 patients even under effective highly active anti-retroviral
therapy (HAART). In vivo, blood-retinal barrier (BRB) establishes a critical, physiological guardian
against microbial invasion of the eye, but may be compromised in the presence of HIV-1. The envelope
glycoprotein gp120 is exposed on the surface of the HIV envelope, essential for virus entry into
cells by the attachment to specific cell surface receptors. The BRB disruption by glycoprotein gp120
has been widely recognized, which is toxic to human retinal epithelial cells (RPE) and umbilical
vein endothelial cells (HUVEC). The present review elaborates on various mechanisms of BRB disruption
induced by HIV gp120, which may represent potential targets for the prevention of ocular
HIV complications in the future.
Keywords: Blood-retinal barrier, HIV gp120, tight junction proteins, inflammatory cytokines, oxidative stress, MMPs.
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