Several chronic liver diseases are characterized by a clear gender disparity. Among them, hepatocellular carcinoma (HCC) shows significantly higher incidence rates in men than in women. The different epidemiological distribution of risk factors for liver disease and HCC only partially accounts for these gender differences. In fact, the liver is an organ with recognized sexual dysmorphism and is extremely sensitive to the action of androgens and estrogens. Sex hormones act by modulating the risk of developing HCC and influencing its aggressiveness, response to treatments, and prognosis. Furthermore, androgens and estrogens are able to modulate the action of other factors and cofactors of liver damage (e.g., chronic HBV infection, obesity), significantly influencing their carcinogenic power. The purpose of this review is to examine the factors related to the different gender distribution in the incidence of HCC as well as the pathophysiological mechanisms involved, with particular reference to the central role played by sex hormones.

The outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the related disease (COVID-19) has spread rapidly to pandemic proportions, increasing the demands on healthcare systems for the containment and management of COVID-19. One of the critical issues to be addressed is the improvement in laboratory diagnosis and screening of large portions of the population to stop the virus spreading. Currently, the laboratory diagnosis of SARS-CoV-2 infection and the related disease is based on the research of viral RNA with rt-PCR methods in upper and lower respiratory airways. Serological tests to detect SARS-CoV-2 antibodies could help physicians and healthcare workers to support COVID-19 diagnosis and follow-up and perform population screening. Our review, using MEDLINE and EMBASE, summarizes the current knowledge of direct and serological tests performed to research RNA, antigens, or antibodies for SARS-CoV-2, evaluating the advantages and drawbacks for specific tests.

Background: Health workers (HWs) are at increased risk for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection and a possible source of nosocomial transmission clusters. Despite the increased risk, the best surveillance strategy and management of exposed HWs are not yet well known. The aim of this review was to summarize and critically analyze the existing evidence related to this topic in order to support public health strategies aimed at protecting HWs in the hospital setting. Main text: A comprehensive computerized literature research from 1 January 2020 up to 22 May 2020 was made to identify studies analyzing the burden of infection, risk assessment, surveillance and management of HWs exposed to SARS-CoV-2. Among 1623 citation identified using MEDLINE, Embase, Google Scholar and manual search, we included 43 studies, 14 webpages and 5 ongoing trials. Health workers have a high risk of acquiring infection while caring for coronavirus disease 2019 (COVID-19) patients. In particular, some types exposures and their duration, as well as the inadequate or non-use of personal protective equipment (PPE) are associated with increased infection risk. Strict infection prevention and control procedures (IPC), adequate training programs on the appropriate use of PPE and close monitoring of HWs with symptom surveillance and testing are essential to significantly reduce the risk. At the moment there is not enough evidence to provide precise indications regarding pre-exposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP). Conclusions: During the spread of COVID-19 outbreak, numerous published papers investigated the epidemiology, risk assessment and prevention and control of SARS-CoV-2. However, more high-quality studies are needed to provide valid recommendations for better management and for the clinical and microbiological surveillance of healthcare personnel.

Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.