Endothelial Dysfunction
Endothelial dysfunction and injury have been described in HIV infection [45]. Circulating markers of endothelial activation such as soluble adhesion molecules and procoagulant proteins are elaborated in HIV infection.
HIV may enter the endothelium via CD4 or galactosylceramide receptors [45]. Other possible mechanisms of entry include chemokine receptors [46]. Endothelium isolated from the brain of HIV-infected subjects strongly expresses both CCR3 and CXCR4 HIV-1 coreceptors, whereas coronary endothelium strongly expresses CXCR4 and CCCR2A coreceptors [46]. CCR5 is expressed at a lower level in both types of endothelium. The fact that CCR3 is more common in brain endothelium than in coronary endothelium could be significant in light of the different susceptibilities of the heart and brain to HIV-1 invasion. Endothelial activation in HIV infection may also be caused by cytokines (e.g., TNF-α) secreted in response to mononuclear or adventitial cell activation by the virus, or it may be a direct effect of the secreted HIV- associated proteins gp 120 (envelope glycoprotein) and tat (transactivator of viral replication) on endothelium with the possible induction of an apoptosis process [47]. Opportunistic agents such as cytomegalovirus, frequently coinfect HIV-infected patients and may contribute to the development of endothelial damage. It has also been hypothesized that human herpes virus-8 (a virus that is found in all forms of Kaposi’s sarcoma) may trigger or accelerate the development of atheroma in the presence of HAART-related hyperlipidemia [48]. In spite of all these observations, the clinical consequences of HIV-1 and opportunistic agents on endothelial function have not been elucidated yet.
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