2016
DOI: 10.14218/jcth.2016.00034
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Mechanisms of Accelerated Liver Fibrosis Progression during HIV Infection

Abstract: With the introduction of antiretroviral therapy (ART), a dramatic reduction in HIV-related morbidity and mortality has been observed. However, it is now becoming increasingly clear that liver-related complications, particularly rapid fibrosis development from ART as well as from the chronic HIV infection itself, are of serious concern to HIV patients. The pathophysiology of liver fibrosis in patients with HIV is a multifactorial process whereby persistent viral replication, and bacterial translocation lead to … Show more

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Cited by 29 publications
(21 citation statements)
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“…Similar findings have been observed in the US [11]. Several mechanisms underlying the association between HIV and liver fibrosis have been proposed [12]. The strong association between HIV VL and APRI > 0.5 in both HIV and HIV/HBV infected patients that was seen in this study suggests an effect of HIV itself on the liver.…”
Section: Discussionsupporting
confidence: 90%
“…Similar findings have been observed in the US [11]. Several mechanisms underlying the association between HIV and liver fibrosis have been proposed [12]. The strong association between HIV VL and APRI > 0.5 in both HIV and HIV/HBV infected patients that was seen in this study suggests an effect of HIV itself on the liver.…”
Section: Discussionsupporting
confidence: 90%
“…In contrast to HIV/HCV co-infection, liver fibrosis mediated through apoptosis-related receptors do not play a key role in HIV/HBV co-infection. It has been hypothesized that HIV alters HBV-specific immune response by affecting the hepatic cytokine environment, thereby promoting liver fibrosis and disease progression; however, this hypothesis has not been thoroughly tested[69,70]. In HIV/HBV co-infection, it is difficult to determine the stage of liver disease[71].…”
Section: Hiv/hbv Co-infection-induced Liver Injurymentioning
confidence: 99%
“…In HIV-infected individuals, there is dysregulation of the TLR4 response to LPS ex-vivo [161] . As the liver is the first organ to filter blood from the GI tract, the concentrations of LPS in the portal veins is elevated and Kupffer cells have a “tolerised” or reduced response to LPS [162] . We have demonstrated persistently elevated levels of circulating LPS in HIV-HBV co-infected individuals compared to uninfected controls and HBV mono-infected individuals [163] , however, we did not find a direct correlation between elevated circulating LPS and liver fibrosis consistent with similar studies in HIV-HCV co-infection [164166] .…”
Section: Pathogenesismentioning
confidence: 99%