Recognizing the importance of timely guidance regarding the rapidly evolving field of hepatitis C management, the American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) developed a web-based process for the expeditious formulation and dissemination of evidence-based recommendations. Launched in 2014, the hepatitis C virus (HCV) guidance website undergoes periodic updates as necessitated by availability of new therapeutic agents and/or research data. A major update was released electronically in September 2017, prompted primarily by approval of new direct-acting antiviral agents and expansion of the guidance's scope. This update summarizes the latest release of the HCV guidance and focuses on new or amended recommendations since the previous September 2015 print publication. The recommendations herein were developed by volunteer hepatology and infectious disease experts representing AASLD and IDSA and have been peer reviewed and approved by each society's governing board.

Hepatitis C Guidance 2018 Update: AASLD-IDSA Recommendations for Testing, Managing, and Treating Hepatitis C Virus Infection

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.27222

Epidemiology of hepatocellular carcinoma in the United States: Where are we? Where do we go?

Background. Infection with human immunodeficiency virus type 1 (HIV) is associated with clinical symptoms of accelerated aging, as evidenced by the increased incidence and diversity of age-related illnesses at relatively young ages and supporting findings of organ and cellular pathologic analyses. But it has been difficult to detect an accelerated aging effect at a molecular level. Methods. Here, we used an epigenetic biomarker of aging based on host DNA methylation levels to study accelerated aging effects due to HIV infection. DNA from brain and blood tissue was assayed via the Illumina Infinium Methylation 450 K platform. Results. Using 6 novel DNA methylation data sets, we show that HIV infection leads to an increase in epigenetic age both in brain tissue (7.4 years) and blood (5.2 years). While the observed accelerated aging effects in blood may reflect changes in blood cell composition (notably exhausted cytotoxic T cells), it is less clear what explains the observed accelerated aging effects in brain tissue. Conclusions. Overall, our results demonstrate that the epigenetic clock is a useful biomarker for detecting accelerated aging effects due to HIV infection. This tool can be used to accurately determine the extent of age acceleration in individual tissues and cells.

HIV-1 Infection Accelerates Age According to the Epigenetic Clock

BackgroundEffective treatment for hepatitis C virus (HCV) in patients coinfected with human immunodeficiency virus type 1 (HIV-1) remains an unmet medical need. MethodsWe conducted a multicenter, single-group, open-label study involving patients coinfected with HIV-1 and genotype 1 or 4 HCV receiving an antiretroviral regimen of tenofovir and emtricitabine with efavirenz, rilpivirine, or raltegravir. All patients received ledipasvir, an NS5A inhibitor, and sofosbuvir, a nucleotide polymerase inhibitor, as a single fixed-dose combination for 12 weeks. The primary end point was a sustained virologic response at 12 weeks after the end of therapy. ResultsOf the 335 patients enrolled, 34% were black, 55% had been previously treated for HCV, and 20% had cirrhosis. Overall, 322 patients (96%) had a sustained virologic response at 12 weeks after the end of therapy (95% confidence interval [CI], 93 to 98), including rates of 96% (95% CI, 93 to 98) in patients with HCV genotype 1a, 96% (95% CI, 89 to 99) in those w...

/pdf/ledipasvir-and-sofosbuvir-for-hcv-in-patients-coinfected-2antsxbwep.pdf

Ledipasvir and Sofosbuvir for HCV in Patients Coinfected with HIV-1

Guidelines for the care and treatment of persons diagnosed with chronic hepatitis C virus infection

Even when treated with antiretroviral therapy (ART), persons with HIV are more likely to develop or die of cardiovascular disease, liver disease, and some forms of cancer than are those without HIV of similar age and sex (1–3). Because the incidence rates of these conditions increase with age, an explanation of these findings is that HIV accelerates the biological effects of aging. The observations that both HIV infection and aging are associated with accelerated thymic atrophy, immunosenescence, and increased susceptibility to infections support this hypothesis (4–6). On the other hand, the increased risk for such conditions as cardiovascular and liver disease associated with HIV may merely reflect greater exposure to tobacco, alcohol, viral hepatitis, or illicit drugs, which themselves could be responsible for the observed elevated disease risk (3, 7, 8). Differences in the underlying age structure between younger populations with HIV infection and the general population at risk for these chronic diseases could also explain the age disparity (3). Because studies have lacked appropriate control participants without HIV; data on confounding exposures; or structured, valid disease assessments, it has not been possible to answer this question conclusively.

To investigate whether HIV reduces the age at which liver disease occurs and understand other correlates of liver fibrosis in this setting, we studied a cohort of persons with hepatitis C virus (HCV) in whom liver fibrosis, HIV disease, and other key exposures have been systematically monitored since 2006.

/pdf/hiv-age-and-the-severity-of-hepatitis-c-virus-related-liver-4imbzegvfz.pdf

HIV, Age, and the Severity of Hepatitis C Virus–Related Liver Disease: A Cohort Study

It has been postulated that HIV infection accelerates hepatitis C virus (HCV)–related liver disease. This cohort study followed persons with HCV infection prospectively to compare the progression o...

HIV, Age, and the Severity of Hepatitis C Virus–Related Liver Disease

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HIV, Age, and the Severity of Hepatitis C Virus–Related Liver Disease: A Cohort Study

HIV, Age, and the Severity of Hepatitis C Virus–Related Liver Disease