Several aspects are revised on the subject hepatocellular carcinoma related to its incidence/prevalence, risk and prognostic factors, cellular proliferation, pathological aspects, progression of chronic hepatitis B and C to cirrhosis and hepatocellular carcinoma, natural course of hepatocellular carcinoma, some clinical data, morphological diagnosis with special emphasis on radiological findings as ultrasound, dynamic computed tomography and magnetic resonance imaging, color-power Doppler, tissue and contrast harmonic.

Hepatitis C virus was identified in 1989 as the main causative agent of non-A, non-B and was followed by the recognition of a high prevalence of hepatitis C virus infection after transfusion of infected blood or blood products and in association with intravenous drug abuse. The availability of sensitive and reliable techniques to screen blood for hepatitis C virus has reduced the incidence of post-transfusion hepatitis. True healthy carriers of hepatitis C virus did not exist. Approximately 95% of hepatitis C virus infected individuals can be identified by third generation anti-hepatitis C virus testing. Retrospective studies of iatrogenic hepatitis C virus infection are the main source of the natural history of the disease. The distribution of different hepatitis C virus genotypes varies according to the geographic region. In South America, Europe, The United States and Japan hepatitis C virus genotypes 1, 2 and 3 account for the majority of the infections, being (sub)type 1b the most prevalent. Epidemiological parameters (age, risk factors and duration of infection) may be associated with hepatitis C virus genotypes (intravenous drug abuse with types 1-a and 3-a and 1-b with post-transfusion hepatitic C). Subtype 1-b, lead to a more severe course of viral infection, with ultrastructural alterations of the mitochondria, and greater impairment of the process of oxidative phosphorylation. No increased production of free radicals may influence the evolution of the liver disease by an enhancement of the cytopathic effect of hepatitis C virus. The clinical significance of intrahepatic hepatitis C virus level in patients with chronic hepatitis C virus infection is not determined by host factors (age of patient, mode or duration of infection) or by virus factors (hepatitis C virus genotypes) and, repeatedly negative RT-PCR for hepatitis C virus RNA in serum does not indicate absence of hepatitis C virus from the liver. The association between autoimmunity and hepatitis C virus is questioned. Markers of its does occur with high frequency in these patients. Modulation of immune responses to hepatitis C virus envelope E2 protein following injection of plasmid DNA, has been used for induction of specific response to hepatitis C virus. The spectrum of such responses could likely be broadened by combining plasmids, delivery routes, and other forms of encoded immunogens (peptide vaccines). These may be important to the development of a vaccine against the high mutable hepatitis C virus. The pathogenic role of novel DNA virus (TTV) is under spotlight. As with hepatitis G, however, the association of TTV with disease is far from clear.

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Objectives HIV‐coinfected patients experience higher incidences of non‐liver‐related cancers than HCV‐monoinfected patients. Chronic inflammation, immunosuppression, but also higher tobacco or alcohol consumption and metabolic dysregulation could explain this higher risk. We aimed to estimate the direct, indirect and total effects of HIV coinfection on the risk of non‐liver‐related cancers in HCV participants treated with direct‐acting antivirals (DAAs). Methods Up to four HCV‐monoinfected participants from the ANRS CO22 HEPATHER cohort were matched by age and sex to HIV/HCV‐coinfected participants from the ANRS CO13 HEPAVIH cohort. Participants were followed from DAA initiation until the occurrence of a non‐liver‐related cancer. Counterfactual mediation analysis was carried out to estimate the direct (chronic inflammation and immunosuppression), indirect (tobacco and alcohol consumption and metabolic syndrome) and total effect of HIV coinfection on the risk of non‐liver‐related cancers. Results 548 HIV/HCV‐coinfected and 2016 monoinfected participants were included. Overall, HIV coinfection was associated with a 3.7‐fold [95% confidence interval (CI): 1.7–7.0] higher risk of non‐liver‐related cancers in HCV participants. This increased risk was explained by significant direct effect [hazard ratio (HR) = 3.4, 95% CI: 1.7–6.6] but not indirect effect (HR = 1.1, 95% CI: 0.8–1.5) of HIV coinfection. Conclusions In HCV participants treated with DAAs, the direct effect of HIV coinfection, reflecting chronic inflammation and immunosuppression, was associated with a 3.7‐fold higher risk of non‐liver‐related cancer. By contrast, the indirect effect of HIV coinfection, reflecting higher tobacco and alcohol consumption and metabolic dysregulation, was not significantly associated with the risk of non‐liver‐related cancers.