"One hypothesis is that HIV persists in these sanctuaries during antiretroviral treatment and may cause the generation and dissemination of drug-resistant viruses (8). Another hypothesis is that the breakdown of the blood-retinal barrier (BRB), which is associated with the changes in the tight junctions, contributes to the trafficking of HIV into the eye (9,10). Therefore, the present review focused on the key breakdown mechanisms of tight junctions. "
[Show abstract][Hide abstract] ABSTRACT: Human immunodeficiency virus (HIV)-1 has been detected in ocular tissues; however, the mechanism of entry has not been established. It has been hypothesized that the blood-retinal barrier (BRB), a critical guardian against microbial invasion of the eye, may be compromised in the presence of HIV-1 in the eye. In vivo and in vitro model systems have shown that the breach of tight junctions induced by HIV-1-associated factors contributes to the breakdown of the BRB. The present study reviews the mechanism of tight junction disruption, focusing on signaling pathways, the expression of enzymes, including metalloproteinases, and cytokines that affect inflammation. The studied pathways may be potential targets for the prevention of ocular HIV complications.
Experimental and therapeutic medicine 04/2014; 7(4):768-772. DOI:10.3892/etm.2014.1521 · 1.27 Impact Factor
"Crucial to many of the antithrombotic activities of endothelium are the synthesis of prostacyclin (PGI2) and of nitric oxide (NO). In the context of VTE, a dysfunctional venous endothelium may express increased amounts of P-selectin, von Willebrand factor (vWF), tissue factor (TF), plasminogen activator inhibitor-1 (PAI-1), and factor V, all of which may promote blood clotting and participate in the development of a thrombus.61 It is now well estabilished that the endothelium could be activated directly by HIV virus. "
[Show abstract][Hide abstract] ABSTRACT: HIV infection has been recognized as a prothrombotic condition and this association has now been proven by a large number of studies with a reported VTE frequency among HIV-infected patients ranging from 0.19% to 7,63 %/year. HIV infection is associated with a two to tenfold increased risk of venous thrombosis in comparison with a general population of the same age. Some risk factors demonstrated a strongest association with VTE such as, low CD4(+) cell count especially in the presence of clinical AIDS, protein S deficiency, and protein C deficiency. Whereas other risk factors are still controversial like protease inhibitor therapy, presence of active opportunistic infections and presence of antiphospholipid antibodies, including anticardiolipin antibodies and lupus anticoagulant. Physicians caring for HIV positive patients should be able to recognize and treat not only the well-known opportunistic infections and malignancies associated with this chronic disease, but also be alert to the less well-known complications such as thromboses. Pulmonary embolism should be included in the differential diagnosis when patients with HIV/AIDS have unexplained dyspnea or hypoxemia. In younger individuals with VTE, especially men, without other identifiable risk factors for VTE, HIV should be considered. Because interactions between warfarin and antiretrovirals is possible, health care providers should also be alert to the potential of dangerously high or low INRs when they are giving anticoagulants to patients with HIV infection who are undergoing antiretroviral therapy.
Mediterranean Journal of Hematology and Infectious Diseases 07/2011; 3(1):e2011030. DOI:10.4084/MJHID.2011.030
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