Hepatitis C Virus and Hepatocellular Carcinoma: Pathogenetic Mechanisms and Impact of Direct-Acting Antivirals

Schietroma, Ivan; Scheri, Giuseppe Corano; Pinacchio, Claudia; Statzu, Maura; Petruzziello, Arnolfo; Vullo, Vincenzo

doi:10.2174/1874357901812010016

Cited by 28 publications

(22 citation statements)

References 57 publications

(71 reference statements)

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“…Thus, it is clear that a better survey of HCV epidemiology, especially focused on the knowledge of different genotypes distribution worldwide, could essentially help to reduce the effects of this severe pandemic disease …”

Section: Introductionmentioning

confidence: 99%

Prevalence of Hepatitis C virus genotypes in nine selected European countries: A systematic review

Petruzziello

Loquercio

Sabatino

et al. 2019

Clinical Laboratory Analysis

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BackgroundHepatitis C virus (HCV) infection is a global health problem especially for its increasing level of mortality. Detailed knowledge of HCV genotypes prevalence has clinical relevance since the efficacy of therapies is impacted by genotypes and subtypes distribution. Moreover, HCV exhibits a great genetic variability regionally.To date, there are no published studies assessing HCV genotypes distribution in specific countries of the Mediterranean basin. The aim of this study was to review data published from 2000 to 2017 with the purpose to estimate genotypes distribution of HCV infection in nine European countries all located in the Mediterranean basin.MethodsA systematic research of peer‐reviewed journals indexed in PubMed, Scopus, and EMBASE databases selected if containing data regarding distribution of HCV genotypes in nine selected European countries (Albania, Bosnia, Croatia, France, Greece, Italy, Montenegro, Slovenia, and Spain) was performed.ResultsGenotype 1 is the most common (61.0%), ranging from 80.0% in Croatia to 46.0% in Greece, followed by genotype 3 (20.0%), varying from 38.0% in Slovenia to 7.0% and 8.0%, respectively, in Italy and in Albania and by genotype 4 (10.0%) that shows an increase of 1.1% with respect to data obtained till 2014 probably due to the increasing migrants arrivals to Southern Europe. G2, the fourth most frequent genotype (8.5%), particularly common in Italy (27.0%) and Albania (18.0%) might be probably introduced in Southern Italy as a result of Albanian campaign during Second World War and more and more increased by the migration flows from Albania to Italy in the 90s.ConclusionEpidemiology of HCV infection shows a high variability across the European countries that border the Mediterranean Sea. HCV genotyping is a relevant tool to monitor the dynamic process influenced by both evolving transmission trends and new migration flows on HCV scenario.

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Section: Introductionmentioning

confidence: 99%

Prevalence of Hepatitis C virus genotypes in nine selected European countries: A systematic review

Petruzziello

Loquercio

Sabatino

et al. 2019

Clinical Laboratory Analysis

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“…Globally, over 70 million people are infected with HCV . An estimated 400 000 people die annually due to HCV‐related disease …”

Section: Introductionmentioning

confidence: 99%

Modelling the potential prevention benefits of a treat‐all hepatitis C treatment strategy at global, regional and country levels: A modelling study

Trickey

Fraser

Lim

et al. 2019

Journal of Viral Hepatitis

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The World Health Organization (WHO) recently produced guidelines advising a treatall policy for HCV to encourage widespread treatment scale-up for achieving HCV elimination. We modelled the prevention impact achieved (HCV infections averted [IA]) from initiating this policy compared with treating different subgroups at country, regional and global levels. We assessed what country-level factors affect impact. A dynamic, deterministic HCV transmission model was calibrated to data from global systematic reviews and UN data sets to simulate country-level HCV epidemics with ongoing levels of treatment. For each country, the model projected the prevention impact (in HCV IA per treatment undertaken) of initiating four treatment strategies; either selected randomly (treat-all) or targeted among people who inject drugs (PWID), people aged ≥35, or those with cirrhosis. The IA was assessed over 20 years.Linear regression was used to identify associations between IA per treatment and demographic factors. Eighty-eight countries (85% of the global population) were modelled. Globally, the model estimated 0.35 (95% credibility interval [95%CrI]: 0.16-0.61) IA over 20 years for every randomly allocated treatment, 0.30 (95%CrI: 0.12-0.53) from treating those aged ≥35 and 0.28 (95%CrI: 0.12-0.49) for those with cirrhosis.

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“…Interestingly, the incidence of high grade tumors in p53ser246 transgenic mice that are HBsAg-positive is 100% [31]. The common molecular mechanisms by which HBV and HCV infection stimulates AFB1-associated genetic instability phenotypes are still not completely understood; HBV is a DNA virus that replicates by reverse transcription while HCC is a RNA virus that replicates by RNA replication and encodes a single polycistronic message [34,35]. While 257 million individuals are estimated to be infected with HBV, 140 million individuals are estimated to be infected with HCV; and chronic HBV and HCV infection is the leading cause for 60-70% of HCC [35,36].…”

Section: Associated Risk Factors That Accelerate Afb1-associated Livementioning

confidence: 99%

Cellular Responses to Aflatoxin-Associated DNA Adducts

Fasullo¹

2019

DNA Repair- An Update

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Aflatoxin B1 (AFB1) is the most potent known hepatocarcinogen. The signature p53 mutation (p53 249 ser) that is found in AFB1-associated liver cancer suggests that AFB1 is a potent genotoxin. AFB1 is not genotoxic per se but is metabolically activated by cytochrome P450 enzymes that convert the promutagen into a highly reactive epoxide, which primarily reacts with the N 7 group of guanine, forming 8,9-dihydro-8-(N 7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N 7-dG). While this primary adduct is unstable, the subsequent trans-8,9-dihydro-8-(2,6-diamino-4-oxo-3,4-dihydropyrimid-5-yl-formamido)-9-hydroxy aflatoxin B1 (AFB1-Fapy)derived adducts are stable and are mutagenic. Studies have revealed that nucleotide excision repair (NER), base excision repair (BER), recombinational repair, and DNA replication bypass are all involved in conferring AFB1 resistance. To minimize the genotoxicity of AFB1, pathways function to detoxify the metabolically active intermediate, excise resulting DNA adducts, bypass unrepaired adducts, and repair secondary DNA breaks. How these repair pathways functionally cooperate to minimize AFB1-associated genetic instability phenotypes is not well understood. Insights can be gained from epidemiological research and model organisms. Gene profiling and next-generation sequencing are facilitating how pathways and tissuespecific differences are induced. This review will encompass studies concerning human genetic susceptibility to AFB1 and pathways that repair and tolerate AFB1associated DNA damage.

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Hepatitis C Virus and Hepatocellular Carcinoma: Pathogenetic Mechanisms and Impact of Direct-Acting Antivirals

Cited by 28 publications

References 57 publications

Prevalence of Hepatitis C virus genotypes in nine selected European countries: A systematic review

Prevalence of Hepatitis C virus genotypes in nine selected European countries: A systematic review

Modelling the potential prevention benefits of a treat‐all hepatitis C treatment strategy at global, regional and country levels: A modelling study

Cellular Responses to Aflatoxin-Associated DNA Adducts

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