Role of retroviral restriction factors in the interferon-α-mediated suppression of HIV-1 in vivo.

The antiviral potency of the cytokine IFN-α has been long appreciated but remains poorly understood. A number of studies have suggested that induction of the apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3 (APOBEC3) and bone marrow stromal cell antigen 2 (BST-2/tetherin/CD317) retroviral restriction factors underlies the IFN-α-mediated suppression of HIV-1 replication in vitro. We sought to characterize the as-yet-undefined relationship between IFN-α treatment, retroviral restriction factors, and HIV-1 in vivo.

Hepatitis E Virus seroprevalence and chronic infections in patients with HIV, Switzerland.

We screened 735 HIV-infected patients in Switzerland with unexplained alanine aminotransferase elevation for hepatitis E virus (HEV) immunoglobulin G. Although HEV seroprevalence in this population is low (2.6%), HEV RNA can persist in patients with low CD4 cell counts.

MRSA admission screening in a low prevalence setting - much ado about nothing?

Objective: To prospectively evaluate new guidelines for MRSA admission screening and pre-emptive isolation implemented in response to a doubling of newly diagnosed MRSA patients in 2007.

Design: One-year surveillance (04/2008-03/2009).

Setting: Patients admitted to the tertiary-care hospital in St.

Management of hepatitis C virus (HCV) infection in drug substitution programs.

Background: In Switzerland, intravenous drug use (IDU) accounts for 80% of newly acquired hepatitis C virus (HCV) infections. Early HCV treatment has the potential to interrupt the transmission chain and reduce morbidity/mortality due to decompensated liver cirrhosis and hepatocellular carcinoma. Nevertheless, patients in drug substitution programs are often insufficiently screened and treated.

Genetic variation in IL28B is associated with chronic hepatitis C and treatment failure: a genome-wide association study.

Background & Aims: Hepatitis C virus (HCV) induces chronic infection in 50% to 80% of infected persons; approximately 50% of these do not respond to therapy. We performed a genome-wide association study to screen for host genetic determinants of HCV persistence and response to therapy.

Methods: The analysis included 1362 individuals: 1015 with chronic hepatitis C and 347 who spontaneously cleared the virus (448 were coinfected with human immunodeficiency virus [HIV]).

Contribution of genome-wide significant single-nucleotide polymorphisms and antiretroviral therapy to dyslipidemia in HIV-infected individuals: a longitudinal study.

Background: HIV-infected individuals have an increased risk of myocardial infarction. Antiretroviral therapy (ART) is regarded as a major determinant of dyslipidemia in HIV-infected individuals. Previous genetic studies have been limited by the validity of the single-nucleotide polymorphisms (SNPs) interrogated and by cross-sectional design.

Unusually high HIV infectiousness in an HIV-, HCV- and HSV-2-coinfected heterosexual man.

We report an HIV-HCV-HSV-2-coinfected man, who infected all of five sequential female sexual partners within seven years. HIV-RNA in semen was unusually high and exceeded that in plasma by one log10. Screening for sexually transmitted diseases remained negative with the exception of HSV-2-seropositivity.

Delayed diagnosis of atypical mycobacterial skin and soft tissue infections in non-immunocompromized hosts.

Relapsing or persisting skin and soft tissue infections after injury with biological materials should prompt consideration of atypical mycobacteria, even in non-immunocompromized hosts. We report 3 cases where diagnosis was delayed for 3-10 months. Insidiously, Mycobacterium marinum infection can occur without any contact to fish tank or swimming pool.

Rho protein-mediated changes in the structure of the actin cytoskeleton regulate human inducible NO synthase gene expression.

Rho proteins (Rho, Rac, Cdc 42) are known to control the organization of the actin cytoskeleton as well as gene expression. Inhibition of Rho proteins by Clostridium difficile toxin B disrupted the F-actin cytoskeleton and enhanced cytokine-induced inducible nitric oxide synthase (iNOS) expression in human epithelial cells. Also specific inhibition by Y-27632 of p160ROCK, which mediates Rho effects on actin fibers, caused a disruption of the actin cytoskeleton and a superinduction of cytokine-induced iNOS expression.