Molecular Mechanisms of Liver Fibrosis in HIV/HCV Coinfection

Mastroianni, Claudio Maria; Lichtner, Miriam; Mascia, Claudia; Zuccalà, Paola; Vullo, Vincenzo

doi:10.3390/ijms15069184

Cited by 91 publications

(104 citation statements)

References 169 publications

(206 reference statements)

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“…Also, HALS can lead to insulin resistance, with an increase in plasma glucose 20. High levels of insulin and glucose eventually stimulate HSC proliferation and increase expression of connective tissue growth factor (CTGF) which promotes liver fibrosis progression 21,22. Although the mechanisms are not entirely clear, it seems evident that HIV patients present higher degrees of fat infiltration in the liver in a BMI-related or -unrelated manner, which worsens the direct and immune-related effects of the virus in liver fibrosis.…”

Section: Metabolic Dysfunction During Hiv Infectionmentioning

confidence: 99%

Mechanisms of Accelerated Liver Fibrosis Progression during HIV Infection

Debes

Bohjanen

Boonstra

2016

JCTH

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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 chronic immune activation and inflammation, which ART is unable to fully suppress, promoting production of fibrinogenic mediators and fibrosis. In addition, mitochondrial toxicity, triggered by both ART and HIV, contributes to intrahepatic damage, which is even more severe in patients co-infected with viral hepatitis. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV has been obtained, and these are detailed and discussed in this review.

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Section: Metabolic Dysfunction During Hiv Infectionmentioning

confidence: 99%

Mechanisms of Accelerated Liver Fibrosis Progression during HIV Infection

Debes

Bohjanen

Boonstra

2016

JCTH

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“…Acute HCV infection is more likely to become persistent in the presence of HIV, and liver fibrosis progression in chronic HCV infection is more rapid even in patients with undetectable HIV viral loads [3]. The evidence points to blood as the medium of sexual HCV exposure in these cases [4–9].…”

Section: Introductionmentioning

confidence: 99%

Incidence of sexually transmitted hepatitis C virus infection in HIV-positive men who have sex with men

Hagan

Jordan

Neurer

et al. 2015

Aids

203

176

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Objectives The epidemiology of the incidence of sexually-transmitted hepatitis C virus (HCV) infection in HIV-positive men who have sex with men (HIV+MSM) is only partially understood. In the presence of HIV, HCV infection is more likely to become chronic and liver fibrosis progression is accelerated. Design A systematic review and meta-analysis was used to synthesize data characterizing sexually transmitted HCV in HIV+MSM. Methods Electronic and other searches of medical literature (including unpublished reports) were conducted. Eligible studies reported on HCV seroconversion or on reinfection post-successful HCV treatment in HIV+MSM who were not injecting drugs. Pooled incidence rates were calculated using random-effects meta-analysis, and meta-regression was used to assess study-level moderators. Attributable risk measures were calculated from statistically significant associations between exposures and HCV seroconversion. Results More than 13,000 HIV+MSM in 17 studies were followed >91,000 person-years (PY) between 1984–2012; the pooled seroconversion rate was 0.53/100PY. Calendar time was a significant moderator of HCV seroconversion, increasing from an estimated rate of 0.42/100PY in 1991 to 1.09/100PY in 2010, and 1.34/100PY in 2012. Reinfection post-successful HCV treatment (n=2 studies) was 20 times higher than initial seroconversion rates. Among the seroconverters, a large proportion of infections were attributable to high risk behaviors including mucosally-traumatic sex and sex while high on methamphetamine. Conclusions The high reinfection rates and the attributable risk analysis suggest the existence of a subset of HIV+MSM with recurring sexual exposure to HCV. Approaches to HCV control in this population will need to consider the changing epidemiology of HCV infection in MSM.

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“…2 The imbalance between CD4 and CD8 cells seen in HIV infection can lead to alterations in the cytokine profiles with the reduction in anti-fibrotic cytokines mediated by a decrease of the interferon (IFN)-gamma from Th1 cells and an increase in the profibrotic cytokines (IL-4, IL-5, IL-10 and IL-13) due to a relative increase in the TH2 signal. 17,18 In addition to the infectious process, other factors may also alter the levels of cytokines in the genital fluids, such as oral contraceptive use, pregnancy, age and the use of vaginal antiseptics. 19 However, studies show that in chronic HIV infection, the epithelial cells, fibroblasts and the immune cells that reside in the female reproductive tract tissues contribute to the pool of cytokines, chemokines and growth factors present in the sexual hormones tissue environment, estradiol and progesterone.…”

Section: Discussionmentioning

confidence: 99%