Paul S. Frenette (1965–2021)
Teresa V. BowmanCatriona JamiesonUlrich SteidlE. Richard StanleyKira GritsmanDenisa D. WagnerDeepa ManwaniAndreas TrumppToshio SudaKeisuke ItoMeelad M. DawlatyDaniel LucasSandra Pinho
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ABSTRACT Recent DNA sequence analysis indicates that rhesus rhadinovirus (RRV) is a member of the lymphotropic gamma-2 herpesvirus family. To determine if RRV is lymphotropic, peripheral blood mononuclear cells from naturally infected monkeys were separated by immunomagnetic bead depletion and analyzed for the presence of RRV by virus isolation and nested PCR. The recovery and consistent detection of RRV in the CD20 + -enriched fraction clearly demonstrates that B lymphocytes are a major site of virus persistence.
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Rhesus monkey rhadinovirus (RRV) is one of the closest phylogenetic relatives to the human pathogen Kaposi's sarcoma-associated herpesvirus (KSHV), yet it has the distinct experimental advantage of entering efficiently into lytic replication and growing to high titers in culture. RRV therefore holds promise as a potentially attractive model with which to study gammaherpesvirus structure and assembly. We have isolated RRV capsids, determined their molecular composition, and identified the genes encoding five of the main capsid structural proteins. Our data indicate that, as with other herpesviruses, lytic infection with RRV leads to the synthesis of three distinct intranuclear capsid species. However, in contrast to the inefficiency of KSHV maturation following reactivation from latently infected B-cell lines (K. Nealon, W. W. Newcomb, T. R. Pray, C. S. Craik, J. C. Brown, and D. H. Kedes, J. Virol. 75:2866-2878, 2001), de novo infection of immortalized rhesus fibroblasts with RRV results in the release of high levels of infectious virions with genome-containing C capsids at their center. Together, our findings argue for the use of RRV as a powerful model with which to study the structure and assembly of gammaherpesviruses and, specifically, the human rhadinovirus,KSHV.
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Journal Article Dinucleotide repeat polymorphisms at the D5S257 and D5S268 loci on chromosome 5p Get access L.E. Bernard, L.E. Bernard Department of Medical Genetics, 6174 University Boulevard, University of British ColumbiaVancouver, BCV6T1Z3, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar C.N. Kreklywich, C.N. Kreklywich Department of Medical Genetics, 6174 University Boulevard, University of British ColumbiaVancouver, BCV6T1Z3, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Wood S. Wood Department of Medical Genetics, 6174 University Boulevard, University of British ColumbiaVancouver, BCV6T1Z3, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 19, Issue 20, 25 October 1991, Page 5794, https://doi.org/10.1093/nar/19.20.5794 Published: 25 October 1991
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Arabidopsis DNA hypomethylation mutation, ddm1 , results in a variety of developmental abnormalities by slowly inducing heritable lesions at unlinked loci. Here, late‐flowering traits observed at high frequencies in independently‐established ddm1 lines were genetically characterized. In all of the four late‐flowering lines examined the traits were dominant and mapped to the same chromosomal region, which is close or possibly identical to the FWA locus. The ddm1 ‐induced phenotypic onsets are apparently not random mutation events, but specific to a group of genes, suggesting the underlying epigenetic mechanism. The DNA methylation mutant provide useful system for identifying epigenetically‐regulated genes important for plant development.
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The ganglia of rabbits infected with a relatively benign strain of herpesvirus (E-43) and challenged with either of two virulent neurotrophic strains (MP or McKrae) were found to be colonized only by the initial benign infecting strain. Primary infection with the E-43 strain resulted in milder disease when the animals were infected with MP or McKrae strains and also prevented colonization of the ganglion by these strains. Neutralization with anti-glycoprotein C, plaque morphology, cytopathic effects, reconstruction experiments, and restriction endonuclease analysis indicated that the virus recovered from the ganglion was the initial infecting E-43 strain; no traces of the challenging MP and McKrae strains were found. The challenging McKrae strain was shed for several weeks in a few animals, but the virus isolated from the trigeminal ganglia of these animals was the primary infecting E-43 strain. These results suggest that initial infection with a relatively benign strain of herpesvirus may prevent superinfection of the ganglion (but not necessarily the end organ) by highly virulent herpes simplex virus strains and could have significant implications in the consideration of immunization against this disease in humans.
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