This study describes changes in oxidative stress (OS) parameters in mice experimentally infected with Angiostrongylus costaricensis, which causes abdominal angiostrongyliasis. For this, 28 Swiss mice were used, divided into two groups (G1 and G2), with 14 animals each. Of these, eight were infected with ten infective larvae each, by gavage, and six were used as a control group. Mice from G1 and G2 were euthanized at 14 days and 24 days post-infection, respectively. Tissue samples were used for histopathological analysis and blood (serum) samples were taken to assess the levels of proteins, non-protein thiols (NPTs) and nitric oxide (NO), from centrifugation and subsequent collection of aliquots of the supernatant. Among OS parameters, infected mice in both groups had higher NO levels than the control group, due to the presence of: eosinophil infiltrate in the liver and intestine; pancreatitis; and intestinal granuloma. However, the infected mice of both groups showed a reduction in the levels of NPTs, in relation to the control group, due to the presence of: eosinophilic infiltrate in the liver and intestine; and intestinal granuloma. Our results suggest that A. costaricensis infection has important effects on the intestine, liver and pancreas, and the analyses were performed from the tissue of these organs. The mechanisms for these changes are related to the decrease in the body's main antioxidant defences, as demonstrated by the reduction of NPTs, thus contributing to the development of more severe tissue damage. Thus, the objective of the present study was to evaluate the relationship between histopathological lesions and markers for OS.

Some European countries recently reported an increase in hepatitis E virus genotype 3 (HEV-3) of the subtype 3c. No link between HEV-3 subtypes and severity is established to date. Here, we report that patients infected with HEV-3c were at lower risk of hospitalisation, compared to those infected with HEV-3f, the other main subtype circulating in Belgium.

Accumulating evidence suggests that orally ingested lactoferrin protects against inflammation. To assess the efficacy of orally administered bovine lactoferrin (bLF) against hepatitis and to identify the underlying mechanism, in the present study, we used four mouse models of hepatitis induced by d-galactosamine (GalN), carbon tetrachloride (CCl4), GalN plus lipopolysaccharide (LPS) and zymosan plus LPS. Intraperitoneal (i.p.) injection of GalN (500 mg/kg body weight) in mice treated with bovine serum albumin (BSA) for 14 d significantly increased serum aspartate aminotransferase (AST) concentrations compared with the untreated mice. However, orally administered bLF reduced AST concentrations compared with BSA treatment. In mice that received a single injection (0·4 ml/kg) and twice-weekly injections (0·08 ml/kg) of CCl4 for 24 weeks and pretreated with bLF for 14 d and 24 weeks, respectively, significantly suppressed alanine aminotransferase and AST concentrations were observed compared with the BSA-treated control. Oral administration of bLF for 14 d before i.p. injection of LPS (5 mg/kg) plus GalN (1 g/kg) significantly improved the survival rate. In mice that received intravenous injection of zymosan (25 mg/kg) and LPS (15 μg/kg) at 7 d intervals, bLF reduced the elevation of AST concentrations and enhanced the production of IL-11 and bone morphogenetic protein 2 in the small intestine compared with the BSA-treated control. To evaluate the effects of IL-11, we used IL-11 receptor α-null mice treated with GalN, CCl4 and zymosan plus LPS. In this group, the activity of bLF was not significantly different from that of BSA. These data indicate that orally ingested bLF enhances the expression of IL-11 in the small intestine and up-regulates protective activity in mice with hepatitis.

We sought to estimate mortality and associated factors in HIV-hepatitis co-infected individuals in Michigan using a retrospective cohort study. For the study period of 1 January 2006 to 31 December 2009, all HIV-infected individuals were matched to hepatitis B and C cases. In the final Cox proportional hazards regression model, individuals of other [hazard ratio (HR) 2·2, 95% confidence interval (CI) 1·4–3·2] and black (HR 1·3, 95% CI 1·1–1·6) race had decreased survival compared to white race. Similarly, injecting drug users (IDUs) (HR 2·1, 95% CI 1·6–2·6), men who have sex with men (MSM)/IDUs (HR 1·5, 95% CI 1·1–2·2), individuals with undetermined risk (HR 1·5, 95% CI 1·2–1·9) and heterosexual practices (HR 1·4, 95% CI 1·1–1·8) had decreased survival compared to MSM. Additionally, an interaction was found between current HIV status and co-infection. Mortality in HIV-hepatitis co-infected individuals remains a continuing problem. Our study can help in planning interventions to reduce mortality in HIV-infected individuals.

A retrospective cohort study was conducted from 1 January 2006 to 31 December 2009 in Michigan to estimate the prevalence of HIV and hepatitis co-infection and identify associated factors. The prevalence of co-infection was 4·1% [95% confidence interval (CI) 3·8–4·5]. Multivariable logistic regression analysis revealed a significant association between co-infection and being male and: of Black race [odds ratio (OR) 2·0, 95% CI 1·2–3·6] and of Other race (OR 3·5, 95% CI 1·7–7·0) compared to Hispanic race. A significant association was found between co-infection and risk categories of blood products (OR 11·1, 95% CI 6·2–20·2), injecting drug user (IDU) (OR 3·6, 95% CI 2·7–4·8) and men who have sex with men/IDU (OR 3·4, 95% CI 2·4–4·9) in addition to two interactions; one between sex and current HIV status and the other between current HIV status and age at HIV diagnosis. Our results document the changing epidemiology of HIV–hepatitis co-infection which can guide preventive measures and interventions to reduce the prevalence of hepatitis co-infection.

Viral hepatitis is recognized as one of the most frequently reported diseases, and especially in China, acute and chronic liver disease due to viral hepatitis has been a major public health problem. The present study aimed to analyse and predict surveillance data of infections of hepatitis A, B, C and E in Wuhan, China, by the method of time-series analysis (MemCalc, Suwa-Trast, Japan). On the basis of spectral analysis, fundamental modes explaining the underlying variation of the data for the years 2004–2008 were assigned. The model was calculated using the fundamental modes and the underlying variation of the data reproduced well. An extension of the model to the year 2009 could predict the data quantitatively. Our study suggests that the present method will allow us to model the temporal pattern of epidemics of viral hepatitis much more effectively than using the artificial neural network, which has been used previously.

This study aimed to determine the prevalence of serological markers for HIV-1/2, HBV, HCV, Treponema cruzi and T. pallidum infections. The association of these infections with risk factors in a population from Salvador, Bahia, Brazil was also analysed. Of the 780 enrolled individuals, 545 (70%) were female and 235 (30%) were male. Seroprevalence of 0·8% (6/702), 1·3% (9/678), 1·5% (10/684), 3·5% (23/663) and 11·5% (77/668) for HIV-1/2, HBV, HCV, T. cruzi and T. pallidum infections, respectively, was observed. The seroprevalence of T. pallidum was higher in males 20% (43/210) than in females 7% (34/458) (P < 0·01). An association between age and seroprevalence for T. cruzi (P = 0·02) and T. pallidum (P < 0·01) was observed. HBsAg was associated with having tattoos (3/37 vs. 6/623, P = 0·01) and not having a steady sexual partner (5/141 vs. 4/473, P = 0·04), while anti-HIV-1/2 was associated with having tattoos (2/39 vs. 4/647, P = 0·04); however, larger studies are needed to categorically state the relationship of these risk factors with infectious agents. The prevalence of serological markers for HIV-1/2, HBV, HCV and T. cruzi was consistent with other studies.

Aims — Patients with chronic viral hepatitis suffer from a high prevalence of psychiatric problems. Furthermore, the treatment for chronic viral hepatitis, with interferon (IFN) alpha, induces the occurrence of further psychopathological symptoms. The autors examined whether patients with a pre-existing psychiatric diagnosis had more severe IFN alpha-induced psychiatric adverse effects, and whether they were more likely to interrupt the IFN alpha therapy, compared with control patients with no pre-existing psychiatric diagnosis. They also examined the psychopharmacological management of the interferon-alpha-induced psychiatric side effects. Methods — The authors studied prospectively 60 patients with chronic hepatitis B or C in Cagliari, Italy. Patients underwent psychiatric assessment before starting interferon alpha and monthly throughout the therapy. Results — After adjusting for the baseline psychopathology, there was no statistically significant difference in interferon-alpha-induced psychiatric adverse effects between patients with a pre-existing psychiatric diagnosis and controls. There was also no evidence that psychiatric cases were more likely than controls to interrupt the IFN alpha therapy because of psychiatric side effects. Moreover, there was no difference in the psychiatric adverse effects severe enough to require psychopharmacological treatment. Finally, psychopharmaco-logical management successfully treated psychiatric symptoms induced by the IFN alpha. Conclusions — Patients with a pre-existing psychiatric diagnosis do not have a specific vulnerability to interferon-alpha-induced psychiatric adverse effects.

Declaration of Interest: none of the authors have conflict of interests in writing this paper; CM. Pariante is funded by the UK Medical Research Council and by the NARSAD and the Guy's and St Thomas Charity

The worldwide obesity epidemic over the last 20 years has led to a dramatic increase in the prevalence of non-alcoholic fatty liver disease, the hepatic manifestation of the metabolic syndrome. Estimates of prevalence vary depending on the population studied and the methods used to assess hepatic fat content, but are commonly quoted as between 10 and 30% of the adults in the Western hemisphere. Fatty liver develops when fatty acid uptake and synthesis in the liver exceeds fatty acid oxidation and export as TAG. Studies of pathogenesis point to insulin resistance, lipotoxicity, oxidative stress and chronic inflammation being central to the development and progression of the disease. A proportion of individuals with fatty liver develop progressive disease, though large prospective longitudinal studies are lacking. Nevertheless, fatty liver is associated with increased all-cause and liver-related mortality compared with the general population. Management of fatty liver centres around lifestyle and dietary measures to induce controlled and sustained weight loss. Management of cardiovascular risk factors aims to reduce mortality, while certain dietary interventions have been shown to reduce steatosis and inflammation. Specific pharmacological treatments also show promise, but their use is not widespread. A multi-system and multi-disciplinary approach to the management of this disorder is proposed.