Presence of Hepatitis E Virus in a RED Deer (Cervus elaphus) Population in Central Italy

Hepatitis E is an acute human disease caused by the hepatitis E virus (HEV). In addition to humans, HEV has been detected in several animal species and is recognized as a zoonotic pathogen. Pigs, wild boar and deer can be reservoir. In this study, we evaluated HEV prevalence in a free‐living red deer (Cervus elaphus) population in central Italy by detecting virus‐specific antibodies and RNA in sera. A total of 35 of 251 red deer sera were positive for anti‐HEV IgG. HEV RNA was detected in 10 of 91 sera examined. Two genomic fragments targeted by diagnostic PCRs in the capsid region were sequenced, both matching with genotype 3 HEV. Overall results confirmed the occurrence of HEV infection in deer also in Italy.     

The effect of rituximab on anti‐platelet autoantibody levels in patients with immune thrombocytopenia

Rituximab is an effective therapy resulting in a platelet count improvement in 60% of patients with immune thrombocytopenia (ITP). Rituximab depletes B cells; thus, a reduction in platelet autoantibody levels would be anticipated in patients who achieve a clinical response to this treatment. The objectives of this study were to determine whether rituximab was associated with a reduction in platelet autoantibody levels, and to correlate the loss of autoantibodies with the achievement of a treatment response. We performed a case‐control study nested within a previous randomized controlled trial of standard therapy plus adjuvant rituximab or placebo. We measured platelet‐bound anti‐glycoprotein (GP) IIbIIIa and anti‐GPIbIX using the antigen capture test. Of 55 evaluable patients, 25 (45%) had a detectable platelet autoantibody at baseline. Rituximab was associated with a significant reduction in anti‐GPIIbIIIa levels (P = 0·02) but not anti‐GPIbIX levels (P = 0·51) compared with placebo. Neither the presence of an autoantibody at baseline nor the loss of the autoantibody after treatment was associated with a response to rituximab. The subset of patients with persistent autoantibodies after treatment failed to achieve a platelet count response, suggesting that persistence of platelet autoantibodies can be a marker of disease severity.     

Exacerbation of oxidative stress during sickle vaso‐occlusive crisis is associated with decreased anti‐band 3 autoantibodies rate and increased red blood cell‐derived microparticle level: a prospective study

Painful vaso‐occlusive crisis, a hallmark of sickle cell anaemia, results from complex, incompletely understood mechanisms. Red blood cell (RBC ) damage caused by continuous endogenous and exogenous oxidative stress may precipitate the occurrence of vaso‐occlusive crises. In order to gain insight into the relevance of oxidative stress in vaso‐occlusive crisis occurrence, we prospectively compared the expression levels of various oxidative markers in 32 adults with sickle cell anaemia during vaso‐occlusive crisis and steady‐state conditions. Compared to steady‐state condition, plasma levels of free haem, advanced oxidation protein products and myeloperoxidase, RBC caspase‐3 activity, as well as the concentrations of total, neutrophil‐ and RBC ‐derived microparticles were increased during vaso‐occlusive crises, whereas the reduced glutathione content was decreased in RBC s. In addition, natural anti‐band 3 autoantibodies levels decreased during crisis and were negatively correlated with the rise in plasma advanced oxidation protein products and RBC caspase‐3 activity. These data showed an exacerbation of the oxidative stress during vaso‐occlusive crises in sickle cell anaemia patients and strongly suggest that the higher concentration of harmful circulating RBC ‐derived microparticles and the reduced anti‐band 3 autoantibodies levels may be both related to the recruitment of oxidized band 3 into membrane aggregates.