Professor Gregory Atkins

  A7-STRAIN   ALLELE LOSS   ALPHAVIRUS   ALPHAVIRUS ENCEPHALITIS   ALPHAVIRUSES   AMINO-ACID CHANGE   ANTIBODIES   ANTIBODY   ANTI-GALACTOCEREBROSIDE   APOPTOSIS   APOPTOTIC CELLS   BARR VIRUS-DNA   BCL-2   B-CLL   BHK CELLS   BIOSAFETY   BIRNAVIRUS   BORDETELLA-PERTUSSIS   BRAIN   BURSAL DISEASE VIRUS   CANINE-DISTEMPER VIRUS   CARCINOGENESIS   CARCINOMA   CATTLE   CELL-CULTURES   CELLS   CENTRAL-NERVOUS-SYSTEM   CEREBELLUM   CERVICAL-CANCER   CHALLENGE   CULTURES   CUTANEOUS LESIONS   DEFINITIVE DIAGNOSIS   DELETION   DEMYELINATION   DENGUE   DNA   DNA VACCINES   ENVELOPE PROTEIN   EPIDERMODYSPLASIA-VERRUCIFORMIS   EPITHELIAL-CELLS   EPSTEIN-BARR VIRUS   EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS   EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS   EXPRESSION   GALACTOCEREBROSIDE   Gene Therapy   GENE-EXPRESSION   GENE-MUTATIONS   GENOME   GRANULE CELLS   HETEROZYGOSITY   HUMAN ESOPHAGEAL CANCER   HUMAN PAPILLOMAVIRUS   HUMORAL IMMUNE-RESPONSES   IL-12   IL-4   IMMUNE-RESPONSES   IMMUNIZATION   IMMUNOGOLD-SILVER STAINING   IMMUNOHISTOCHEMICAL DETECTION   IMMUNOHISTOCHEMISTRY   IN SITU HYBRIDIZATION   INFECTION   INSITU HYBRIDIZATION   IN-SITU HYBRIDIZATION   INTERFERON-GAMMA   KI-67   LESIONS   LOSS OF HETEROZYGOSITY   LOUPING ILL VIRUS   LOW PH   MATRIX METALLOPROTEINASES   MDM2   MEMBRANE   METASTASIS   MICE   MICROWAVE IN SITU   MOLECULAR ANALYSIS   MOLECULAR PATHOGENESIS   MULTIPLE-SCLEROSIS   MURINE MODEL   MYELIN BASIC-PROTEIN   NEONATAL MICE   NEURONAL DEPLETION   NUCLEOTIDE-SEQUENCE   ORAL HAIRY LEUKOPLAKIA   P21   P53   P53 CODON 72 POLYMORPHISM   PAPILLOMAVIRUS   PLASMID DNA   PROLIFERATION INDEX   PROTECTIVE IMMUNITY   PROTEOLYTIC CLEAVAGE   RECOMBINANT VACCINES   RENAL-TRANSPLANT RECIPIENTS   RETINOBLASTOMA GENE   RISK FACTOR   SEMLIKI FOREST VIRUS   SINDBIS VIRUS   SKIN   SKIN CANCER   SPORADIC BREAST-CANCER   TICK-BORNE ENCEPHALITIS   TISSUE-SECTIONS   VECTOR   Virology

Current research interests 1.Analysis of the molecular basis of alphavirus pathogenicity: We have suggested mechanisms of teratogenesis and neurovirulence of Semliki Forest virus at the cellular level and our current work is aimed at determination of the molecular control of pathogenesis. In this work we utilise infectious clones of SFV. By using chimeric virus construction and site-directed mutagenesis, we have shown that several mutations and sequences can influence viral pathogenesis. Current work involves analysis of the mechanisms of virus-induced death in neural cells and the involvement of virus proteins in this process. 2. Analysis of the mechanism of virus-induced demyelination and its relevance to multiple sclerosis: Present work is aimed at elucidating the role of cytokines, virus persistence and apoptosis in the process of demyelination. This work has been extended to include human rubella virus (a togavirus like SFV), and we have shown that rubella virus has similar tropism in neural cell culture to SFV. 3. Use of Semliki Forest virus as a vector in the construction of viral vaccines ,as a tumour therapy agent and as a CNS vector: Virus vaccines in current use have many disadvantages and in rare cases can cause disease. We are using a vector system, developed by workers at the Karolinska Institute in Stockholm with our help, to construct new virus vaccines. This is a collaborative project with the Karolinska Institute and the Department of Veterinary Pathology at UCD, and part of our work is concerned with improvement of the biosafety of the system. This work has recently been extended to the use of SFV as a cytotoxic cancer therapy agent, and to the development of SFV as a vector for the central nervous system. New virus vectors are currently being constructed and patented.