Increased diagnosis and treatment of hepatitis C in prison by universal offer of testing and use of telemedicine

With recent advances in anti‐viral therapy there is an opportunity to eliminate HCV from the UK population. HCV is common in incarcerated individuals, with previous estimates suggesting ~7% of the UK prison population is anti‐HCV antibody positive. Increasing diagnosis and treatment of HCV in prison is a priority in seeking to eliminate transmission in the general population. Thus the study aimed, to assess the impact implementation of: 1. A universal offer of blood borne virus testing (UOBBVT) using dry blood spot testing for prisoners at reception to increase diagnosis; 2. Telemedicine clinics (TC) within North East England (NEE) prisons to increase HCV treatment rates. UOBBVT was initially implemented at Her Majesty's Prison (HMP) Durham, commencing March 2016. From March 2016 to February 2017, 2,831 of 4,280 (66%) new receptions were offered BBV testing. Of these, 1,495 (53% of offered) accepted BBV testing, of whom 95 (6.4%) were HCV antibody positive, with 47 of those 95 (49.5%) HCV RNA positive, suggesting a prevalence of active infection in the tested population of 3.1% (95% CI 2.4% to 4.2%). Between August 2015 and October 2017, 80 individuals were seen in the TC and 57 (71%) commenced antiviral therapy. Of those with known outcome (n=29), 100% achieved sustained virological response. In the year prior to implementation, only 4 patients received HCV treatment. In conclusion, a universal offer of BBV testing to inmates presenting at HMP reception coupled with linkage into specialist care via TC can substantially increase rates of testing, diagnosis and treatment of HCV in this high prevalence population

STAT2 deficiency and susceptibility to viral illness in humans

Severe infectious disease in children may be a manifestation of primary immunodeficiency. These genetic disorders represent important experiments of nature with the capacity to elucidate nonredundant mechanisms of human immunity. We hypothesized that a primary defect of innate antiviral immunity was responsible for unusually severe viral illness in two siblings; the proband developed disseminated vaccine strain measles following routine immunization, whereas an infant brother died after a 2-d febrile illness from an unknown viral infection. Patient fibroblasts were indeed abnormally permissive for viral replication in vitro, associated with profound failure of type I IFN signaling and absence of STAT2 protein. Sequencing of genomic DNA and RNA revealed a homozygous mutation in intron 4 of STAT2 that prevented correct splicing in patient cells. Subsequently, other family members were identified with the same genetic lesion. Despite documented infection by known viral pathogens, some of which have been more severe than normal, surviving STAT2-deficient individuals have remained generally healthy, with no obvious defects in their adaptive immunity or developmental abnormalities. These findings imply that type I IFN signaling [through interferon-stimulated gene factor 3 (ISGF3)] is surprisingly not essential for host defense against the majority of common childhood viral infections

Q Fever Outbreak in Industrial Setting

An outbreak of Q fever was likely caused by renovation work that aerosolized contaminated straw board

Human IFNAR2 deficiency : lessons for antiviral immunity

C.J.A.D. was supported by the Academy of Medical Sciences (AMS-SGCL11), the British Infection Association, and the UK NIH Research (NIHR); S.M.B.M. was supported by the Universiti Sains Malaysia Fellowship; K.R.E. and S.H. were supported by the Sir Jules Thorn Trust (12/JTA); D.F.Y., D.C.M., and R.E.R. were supported by the Wellcome Trust (101788/Z/13/Z); and A.J.S. was supported by the Medical Research Council–Arthritis Research UK Centre for Integrated Research into Musculoskeletal Ageing and NIHR Newcastle Biomedical Research Centre. J.B. receives funding from the UCLH/UCL NIHR Biomedical Research Centre. S.M. is supported by the FP7 PATHSEEK grant. J.R.B. is supported by an NIHR fellowship.Type I interferon (IFN-α/β) is a fundamental antiviral defense mechanism. Mouse models have been pivotal to understanding the role of IFN-α/β in immunity, although validation of these findings in humans has been limited. We investigated a previously healthy child with fatal encephalitis after inoculation of the live attenuated measles, mumps, and rubella (MMR) vaccine. By targeted resequencing, we identified a homozygous mutation in the high-affinity IFN-α/β receptor (IFNAR2) in the proband, as well as a newborn sibling, that rendered cells unresponsive to IFN-α/β. Reconstitution of the proband's cells with wild-type IFNAR2 restored IFN-α/β responsiveness and control of IFN-attenuated viruses. Despite the severe outcome of systemic live vaccine challenge, the proband had previously shown no evidence of heightened susceptibility to respiratory viral pathogens. The phenotype of IFNAR2 deficiency, together with similar findings in STAT2-deficient patients, supports an essential but narrow role for IFN-α/β in human antiviral immunity.PostprintPeer reviewe