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Analysis of 179 new Ebola virus sequences from patient samples collected in Guinea between March 2014 and January 2015 shows how different lineages evolved and spread in West Africa. Ebola virus lineage evolution Miles Carroll and colleagues report describe the genetic evolution of Ebola virus circulating in West Africa, based on 179 new virus sequences from patient samples collected in Guinea between March 2014 and January 2015. Their analysis shows how different lineages evolved and spread in West Africa between Sierra Leone, Guinea and Liberia. West Africa is currently witnessing the most extensive Ebola virus (EBOV) outbreak so far recorded 1 , 2 , 3 . Until now, there have been 27,013 reported cases and 11,134 deaths. The origin of the virus is thought to have been a zoonotic transmission from a bat to a two-year-old boy in December 2013 (ref. 2 ). From this index case the virus was spread by human-to-human contact throughout Guinea, Sierra Leone and Liberia. However, the origin of the particular virus in each country and time of transmission is not known and currently relies on epidemiological analysis, which may be unreliable owing to the difficulties of obtaining patient information. Here we trace the genetic evolution of EBOV in the current outbreak that has resulted in multiple lineages. Deep sequencing of 179 patient samples processed by the European Mobile Laboratory, the first diagnostics unit to be deployed to the epicentre of the outbreak in Guinea, reveals an epidemiological and evolutionary history of the epidemic from March 2014 to January 2015. Analysis of EBOV genome evolution has also benefited from a similar sequencing effort of patient samples from Sierra Leone. Our results confirm that the EBOV from Guinea moved into Sierra Leone, most likely in April or early May. The viruses of the Guinea/Sierra Leone lineage mixed around June/July 2014. Viral sequences covering August, September and October 2014 indicate that this lineage evolved independently within Guinea. These data can be used in conjunction with epidemiological information to test retrospectively the effectiveness of control measures, and provides an unprecedented window into the evolution of an ongoing viral haemorrhagic fever outbreak.

Objectives: We compared outcomes of the hepatitis C virus (HCV) cure cascade (ie, the path a patient follows from diagnosis to cure), including antiviral treatment outcomes, from 2 HCV screening programs. Our objective was to assess whether treatment uptake and HCV cure rates improved in the cohort screened after the release of all-oral HCV direct-acting antiviral therapies. Methods: We retrospectively compared outcomes of the HCV cure cascade from a cohort of newly diagnosed patients screened during 2012-2014 (period 1) with outcomes from a cohort of newly diagnosed patients screened during 2015-2016 (period 2) at Grady Health System in Atlanta, Georgia. Cure cascade outcomes included HCV antibody (anti-HCV) and RNA testing, linkage to care, antiviral treatment, and sustained virologic response. Results: During period 1, 412 of 5274 (7.8%) persons screened were anti-HCV positive, and 264 (69.3%) of those tested were RNA positive. During period 2, 462 of 7137 (6.5%) persons screened were anti-HCV positive, and 240 (59.3%) of those tested were RNA positive (P = .003). The percentage of newly diagnosed patients who were treated during period 2 (64.0%) was 3 times that of newly diagnosed patients treated during period 1 (21.2%; P < .001). Both cohorts had similarly high levels of linkage to care (95.8% during period 1, 95.4% during period 2) and cure (92.6% during period 1, 95.5% during period 2). Conclusions: Over time, the prevalence of anti-HCV and HCV RNA positivity declined substantially, and linkage-to-care and cure rates remained high. Treatment uptake increased significantly after the introduction of all-oral direct-acting antiviral therapy. These findings suggest that combining large-scale screening initiatives with treatment programs can speed progress toward HCV elimination.

This book is an up to date compendium on the biology and molecular pathogenesis of lymphomas, which represent malignant cancers of the lymphoid system. With its focus on the biology and genetic basis of these diseases, the book is of interest to basic scientists, biologists, clinical hematologists and pathologists as well as medical students. Different chapters will cover all major lymphoma subtypes, as well as chronic lymphocytic leukemia and selected less common lymphoma entities such as T-cell lymphomas and central nervous system lymphomas.