scholarly journals HIV/HCV Co-infection, Liver Disease Progression, and Age-Related IGF-1 Decline

2017 ◽  
Vol 2 (1) ◽  
pp. 50 ◽  
Author(s):  
Jeffrey Quinn ◽  
Jacquie Astemborski ◽  
Shruti H. Mehta ◽  
Gregory D. Kirk ◽  
David L. Thomas ◽  
...  

Background: We have previously reported that persons co-infected with HIV and hepatitis C virus (HCV) had liver disease stages similar to HIV-uninfected individuals who were approximately 10 years older. Insulin-like growth factor 1(IGF-1) levels have long been known to decline with advancing age in humans and non-humans alike. We examined whether HIV infection affects the expected decline in IGF-1 in persons with chronic hepatitis C virus (HCV) infection and if that alteration in IGF-1 decline contributes to the link between HIV, aging, and liver disease progression.Methods: A total of 553 individuals with HCV infection were studied from the AIDS Linked to the Intravenous Experience (ALIVE) cohort for whom more than 10 years of follow-up was available. Serum IGF-1 levels were determined by ELISA and evaluated according to baseline characteristics and over time by HIV status and liver disease progression. Linear regression with generalized estimating equations was used to determine whether IGF-1 decline over time was independently associated with liver disease progression.Results: Baseline IGF-1 levels were strongly associated with age (P < 0.0001) but not with gender or HIV infection. Levels of IGF-1 declined at a rate of -1.75 ng/mL each year in HCV mono-infected individuals and at a rate of -1.23 ng/mL each year in HIV/HCV co-infected individuals (P < 0.05). In a multivariable linear regression model, progression of liver fibrosis was associated with HIV infection and age, as well as with a slower rate of IGF-1 decline (P = 0.001); however, the rate of IGF-1 decline did not alter the strength of the associations between HIV, liver disease, and age.Conclusions: The normal decline in IGF-1 levels with age was attenuated in HIV/HCV co-infected individuals compared to those with HCV mono-infection, and slower IGF-1 decline was independently associated with liver disease progression. Keywords: IGF-1, HIV-1, Hepatitis C, Fibrosis, Liver

2013 ◽  
Vol 208 (4) ◽  
pp. 679-689 ◽  
Author(s):  
A. L. French ◽  
C. T. Evans ◽  
D. M. Agniel ◽  
M. H. Cohen ◽  
M. Peters ◽  
...  

Hepatology ◽  
2014 ◽  
Vol 60 (4) ◽  
pp. 1448-1449 ◽  
Author(s):  
Claudio Puoti ◽  
Lia Bellis ◽  
Olga Mitidieri Costanza ◽  
Maria Giuseppa Elmo

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Mashael R. Al-Anazi ◽  
Sabine Matou-Nasri ◽  
Ayman A. Abdo ◽  
Faisal M. Sanai ◽  
Saad Alkahtani ◽  
...  

Toll-like receptor 3 (TLR3) plays a key role in innate immunity by recognizing pathogenic, double-stranded RNAs. Thus, activation of TLR3 is a major factor in antiviral defense and tumor eradication. Although downregulation of TLR3 gene expression has been mainly reported in patients infected with hepatitis C virus (HCV), the influence of TLR3 genotype on the risk of HCV infection, HCV-related cirrhosis, and/or hepatocellular carcinoma (HCC) remains to be determined. Single-nucleotide polymorphisms (SNPs) within the TLR3 gene and their associations with HCV-related disease risk were investigated in a Saudi Arabian population in this study. Eight TLR3 SNPs were analyzed in 563 patients with HCV, which consisted of 437 patients with chronic HCV infections, 88 with HCV-induced liver cirrhosis, and 38 with HCC. A total of 599 healthy control subjects were recruited to the study. Among the eight TLR3 SNPs studied, the rs78726532 SNP was strongly associated with HCV infection when compared to that in healthy control subjects. The rs5743314 was also strongly associated with HCV-related liver disease progression (cirrhosis and HCC). In summary, these results indicate that distinct genetic variants of TLR3 SNPs are associated with HCV infection and HCV-mediated liver disease progression in the Saudi Arabian population.


2020 ◽  
Vol 133 (3) ◽  
pp. 253-261
Author(s):  
Nan Wu ◽  
Hui-Ying Rao ◽  
Wei-Bo Yang ◽  
Zhi-Liang Gao ◽  
Rui-Feng Yang ◽  
...  

2020 ◽  
Author(s):  
Satoko Ohfuji ◽  
Tomoka Matsuura ◽  
Akihiro Tamori ◽  
Shoji Kubo ◽  
Satoshi Sasaki ◽  
...  

Abstract Background Hepatocellular carcinoma develops in some patients with hepatitis C virus (HCV), even after achieving sustained virological response (SVR). This prospective cohort study of SVR patients examined factors associated with liver disease progression. Methods Participants were patients who had visited a hospital for clinical follow-up of chronic HCV infection in 2005 and had reached SVR as a result of subsequent antiviral treatment. Baseline information including lifestyle and dietary habits before SVR were collected in 2005 using self-administered questionnaires, and clinical information before SVR was collected from medical records in 2005. Study outcome was liver disease progression such as liver cirrhosis, hepatocellular carcinoma, and/or liver disease-related death after SVR. Logistic regression models were employed to calculate odds ratios (ORs) and 95% confidence intervals for each variable. Results Of 180 SVR patients, 27 patients (15%) showed liver disease progression after SVR: 26 (14%) were diagnosed with liver cirrhosis, two (1%) with hepatocellular carcinoma, and/or one (0.6%) with liver-disease related death. Besides older age at SVR (OR=6.65, P=0.01) and aspartate aminotransferase-to-platelet ratio index score ≥ 1.0 before SVR (OR=5.22, P<0.01), alcohol drinkers before SVR (OR=2.83, P=0.09) appeared to be associated with liver disease progression after SVR, whereas higher consumption of vitamin B12 before SVR showed a decreased OR for liver disease progression (OR=0.35, P=0.09). Conclusions Alcohol drinking was associated with liver disease progression, whereas vitamin B12 intake had protective effects for liver disease progression after eradication of HCV. Further studies are needed to confirm these findings.


2013 ◽  
Vol 5 (1S) ◽  
pp. 7 ◽  
Author(s):  
Priyanka Gupta

Around 33 million people worldwide are living with Human Immunodeficiency Virus (HIV) infection, and approximately 20-30% of HIV-infected individuals are also infected with Hepatitis C virus (HCV). The main form of HCV transmission is via the blood borne route; high rates of co-infection are found in intravenous drug users with HCV prevalence rates as high as 90%. Introduction of effective anti-retroviral therapy (ART) has led to a significant decline in HIV-related morbidity, but at the same time the incidence of HCV related liver disease is increasing in the co-infected population. Meta analysis has revealed that individuals who are co-infected with HIV/HCV harbor three times greater risk of progression to liver disease than those infected with HCV alone. Increased risk of progression to Acquired Immunodeficiency Syndrome (AIDS) and AIDS-related deaths is shown among the co-infected patients by some studies, suggesting that HCV infection may accelerate the clinical course of HIV infection. HCV may also affect the incidence of liver toxicity associated with ART, affecting the management of HIV infection. There is a lack of optimal therapeutic approaches to treat HCV infection in HIV co-infected patients. This review discusses recent literature pertaining HIV/HCV co-infection, in addition to providing a snapshot of impact of co-infection on human genome at the level of gene expression and its regulation by microRNAs (miRNAs).


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