Search

The 11th International Oncolytic Virus Conference (IOVC) was held from April 9–12, 2018 in Oxford, UK. This is part of the high-profile academic-led series of meetings that was started back in 2002 by Steve Russell and John Bell, with most of the previous meetings being held in North America (often in Banff). The conference brought together many of the major players in oncolytic virotherapy from all over the world, addressing all stages of research and development—from aspects of basic science and cellular immunology all the way through to early- and late-phase clinical trials. The meeting welcomed 352 delegates from 24 countries. The top seven delegate countries, namely, the UK, US, Canada, The Netherlands, Germany, Japan and South Korea, contributed 291 delegates while smaller numbers coming from Australia, Austria, Bulgaria, China, Finland, France, Iraq, Ireland, Israel, Italy, Latvia, Malaysia, Poland, Slovenia, Spain, Sweden and Switzerland. Academics comprised about half of the attendees, industry 30% and students 20%. The next IOVC is scheduled to be held on Vancouver Island in autumn 2019. Here we share brief summaries of the oral presentations from invited speakers and proffered papers in the different subtopics presented at IOVC 2018.

SYNOPSIS. Pigmentary mutants in amphibians provide important vehicles for studying basic problems in development. Some of these mutants exert influences on the tissue environment in which the chromatophores differentiate and others involve the expression of pigment in specific types of pigment cells. Melanophores are the best known of all chromatophores, and albinism has been much studied. Genes controlling its expression may operate at different levels. Some are involved in the production of tyrosinase, whileothers affect the melanosomal matrix. In contrast, melanoid mutants are characterized by an overproduction of eumelanin, usually through the differentiation of an excessive number of melanophores. Melanoid mutants of the axolotl also exhibit a great diminution in xanthophore and iridophore number, and the same seems to be true of some melanoid-like mutants of leopard frogs. The pteridine pigments of xanthophores and purines of iridophores are often products of xanthine dehydrogenase (XDH) activity, and it is suspected that the expression of the melanoid phenotype may result from a genetic defect involving this enzyme. This is supported by experiments involving the administration of an XDH inhibitor, allopurinol, to normal larvae. This inhibitor results in the production of partial phenocopies of the melanoid condition. Blue mutants involving either partial or complete diminution of xanthophore and iridophore pigments may also be based upon deficient XDH activity.