Hepatitis B virus infection and metabolic syndrome: Fact or fiction?

Although hepatitis C virus infection is known to be linked with insulin resistance, dyslipidemia, and hepatic steatosis, the relationship between hepatitis B virus (HBV) infection and metabolic factors remains unclear. HBV infection is a health problem worldwide, especially in endemic regions such as Asia and Africa. It induces liver decompensation, cirrhosis, hepatocellualr carcinoma, and premature mortality. The prevalence of metabolic syndrome continues to increase in parallel with the epidemic of obesity, which is closely associated with the development of diabetes, cardiovascular disease, or even cancer. The systemic review shows that chronic HBV infection protects against instead of promotes fatty liver. The mechanism is possibly due to a lower frequency of dyslipidemia profile in patients with chronic HBV infection. The association of HBV with metabolic syndrome, insulin resistance, and the risk of arteriosclerosis is still inconclusive. In addition, obesity, diabetes, and metabolic syndrome may accelerate the progression of liver disease in patients with chronic HBV infection and synergistically induce cirrhosis or even hepatocellualr carcinoma development.     

Psychotropic substance‐seeking: evolutionary pathology or adaptation?

According to a conventional evolutionary perspective, the human propensity for substance use is the product of a 'mismatch' between emotional mechanisms that evolved in a past without pure drugs or direct routes of drug administration, and the occurrence of these phenomena in the contemporary environment. The primary purpose of this review is to assert that, contrary to the conventional view, humans have shared a coevolutionary relationship with psychotropic plant substances that is millions of years old. We argue that this 'deep time' relationship is self-evident both in the extant chemical-ecological adaptations that have evolved in mammals to metabolize psychotropic plant substances and in the structure of plant defensive chemicals that have evolved to mimic the structure, and interfere with the function, of mammalian neurotransmitters. Given this evidence, we question how emotional mechanisms easily triggered by plant toxins can have evolved. Our argument is also supported with archeological and historical evidence of substance use in antiquity suggesting that, for people in the past, psychotropic plant substances were as much a mundane everyday item as they are for many people today. Our second, and more speculative objective is to suggest provisional hypotheses of human substance-using phenomena that can incorporate the evolutionary implications of a deep time relationship between psychotropic substances and people. We discuss hypotheses of selective benefits of substance use, including the idea that neurotransmitter-analog plant chemicals were exploited as substitutes for costly, nutritionally constrained endogenous neurotransmitters. However, even if substance seeking was adaptive in the environment of our hominid ancestors, it may not still be so in the contemporary environment. Thus, the implications of our argument are not that the mismatch concept does not apply to human substance-using phenomena, but that it must be reconsidered and extended to incorporate the implications of a substance-rich, rather than substance-free, evolutionary past.     

Hepatitis C virus and Sjögren's syndrome: trigger or mimic?

Patients who have chronic hepatitis C virus infection present some extrahepatic manifestations that may mimic the clinical, immunologic, and histologic manifestations of primary Sj?gren's syndrome (SS). Various demographic, clinical, and immunologic features may aid differentiation between the two processes. Chronic hepatitis C virus infection should be considered an exclusion criterion for the classification of primary SS, not because it mimics primary SS, but because the virus may be implicated in the development of SS in a specific subset of patients.     

Hepatitis C – contamination of toothbrushes: myth or reality?

Chronic hepatitis C patients are advised not to share toothbrushes, razors, nail-scissors or other personal articles that potentially may have been in contact with blood, with others. This study examines the contamination of toothbrushes in patients with chronic hepatitis C as a model for a possible unconventional way of transmission. In 30 patients with chronic hepatitis C, 2 mL of saliva (before and after toothbrushing) and the toothbrush rinsing water after toothbrushing were tested for HCV-RNA. Saliva before and after toothbrushing was positive for HCV-RNA in nine (30%) and 11 patients (36.7%), respectively. Twelve of the toothbrush rinsing water specimens (40%) tested HCV-RNA-positive. In six of these 12 patients, the 'native' saliva had been negative for HCV-RNA. Patients with HCV-RNA-positive toothbrush rinsing water showed no significant differences from those with negative rinsing water with respect to certain clinical, biochemical and virological parameters. In conclusion, our study demonstrates a contamination with HCV-RNA of a considerable portion of toothbrushes used by hepatitis C patients, suggesting at least a theoretical risk of infection by sharing these objects and strengthening the recommendations to take care of a clear separation of these personal care objects between patients and their household members.     

Hepatitis C virus infection during pregnancy and the newborn period – are they opportunities for treatment?

The worldwide prevalence of hepatitis C virus (HCV) infection in pregnant women is estimated to be between 1 and 8% and in children between 0.05% and 5%. While parenteral transmission is still common in children living in developing countries, perinatal transmission is now the leading cause of HCV transmission in developed countries. The absence of an HCV vaccine or approved therapy during pregnancy means that prevention of vertical transmission is still not possible. However, a low vertical transmission rate of 3-5%, a high rate of spontaneous clearance (25-50%) and delayed morbidity have resulted in HCV being overlooked in pregnant women and their infants. Yet a study of the natural history in mothers and children demonstrates that the prognosis of HCV can vary greatly and should be taken seriously. Factors known to increase the risk of perinatal transmission include HIV coinfection and higher maternal viral loads, while elective C-section and withholding breastfeeding have not been demonstrated to reduce vertical transmission. Current guidelines for the diagnosis of persistent perinatal infection require a positive anti-HCV test in infants born to infected mothers after 12 months or two positive HCV RNA tests at least 6 months apart. Current HCV treatment options using pegylated interferon and ribavirin are both unsuitable for use in pregnancy and infancy. However, new agents currently in preclinical phases of development, along with the recently identified association between single-nucleotide polymorphisms within the IL28 gene and treatment response, may serve to create a therapeutic window for these patients.     

Hepatitis C virus infection: Are there still specific problems with genotype 3?

Hepatitis C virus(HCV) infection is one of the most common causes of chronic liver disease and the main indication for liver transplantation worldwide. As promising specific treatments have been introduced for genotype 1, clinicians and researchers are now focusing on patients infected by non-genotype 1 HCV, particularly genotype 3. Indeed, in the golden era of direct-acting antiviral drugs, genotype 3 infections are no longer considered as easy to treat and are associated with higher risk of developing severe liver injuries, such as cirrhosis and hepatocellular carcinoma. Moreover, HCV genotype 3 accounts for 40% of all HCV infections in Asia and is the most frequent genotype among HCV-positive injecting drug users in several countries. Here, we review recent data on HCV genotype 3 infection/treatment, including clinical aspects and the underlying genotype-specific molecular mechanisms.     

Hepatitis E virus in professionally exposed: A reason for concern?

The zoonotic risk of hepatitis E virus(HEV) is well established. The HEV seroprevalence rates vary according to geographical region, assays used, and study cohorts. HEV infection is still underdiagnosed, implying the need to evaluate the disease's burden in the general population and specific risk groups, such as professionally exposed. Close contact with various animal reservoirs such as pigs, rabbits, sheep, dogs, wild boars, and deer has been associated with higher anti-HEV seroprevalence as a part of occupational exposure. While exact transmission routes remain to be determined, some general preventive measures such as proper hand hygiene, the usage of personal protective equipment, and the thermal processing of food before consumption should be followed. A "OneHealth" multisectoral approach should be implemented to achieve optimal health and well-being outcomes, recognizing the interconnections between humans, animals, plants, and their shared environment, in which a vaccine against the zoonotic genotypes 3 and 4 and swine vaccination should be considered as a possible public health measure. This opinion review comprehensively addresses the HEV burden of professional exposure for butchers, slaughterhouse workers, veterinarians, farmers, hunters, and forestry workers delineates the current limits of protective work measures, and tackles future directions.     

Hepatitis C virus and human immunodeficiency virus coinfection: where do we stand?

Both human immunodeficiency virus (HIV) and hepatitis C (HCV) are globally infecting millions of people. Since these viruses are both transmitted through blood-blood contact the rate of coinfection is as high as 30% and among i.v. drug users in the Western world 70%. In The Netherlands, 8% of HCV-infected patients are coinfected with HIV. After the successful introduction of antiretroviral therapy (HAART) the survival of patients with HIV has increased considerably. Coinfection leads to accelerated progression of liver cirrhosis and liver failure but conflicting evidence exists about the effect of HCV on the natural course of HIV. Four randomised controlled trials have shown that treatment with pegylated interferon plus ribavirin leads to an overall sustained viral response (SVR) rate between 27 and 44%. Divided by genotype the SVR is between 14 and 38% in genotype 1 (and 4) while between 53 and 73% for genotype 2 and 3. These percentages are calculated based on an intention-to-treat analysis. Although lower than in HCV-monoinfected patients this is much higher than achieved with conventional interferon. However, coinfected patients with genotypes 2 and 3 also need to be treated for 48 weeks in contrast to monoinfected patients. As the number and severity of side effects is low, coinfected patients now have a substantially better option for treatment.