Varicella-Zoster Virus Gene Expression in Latently Infected and Explanted Human Ganglia
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Published in | Journal of Virology Vol. 74; no. 24; pp. 11893 - 11898 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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American Society for Microbiology
01.12.2000
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ISSN | 0022-538X 1098-5514 |
DOI | 10.1128/JVI.74.24.11893-11898.2000 |
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AbstractList | A consistent feature of varicella-zoster virus (VZV) latency is the restricted pattern of viral gene expression in human ganglionic tissues. To understand further the significance of this gene restriction, we used in situ hybridization (ISH) to detect the frequency of RNA expression for nine VZV genes in trigeminal ganglia (TG) from 35 human subjects, including 18 who were human immunodeficiency virus (HIV) positive. RNA for VZV gene 21 was detected in 7 of 11 normal and 6 of 10 HIV-positive subjects, RNA for gene 29 was detected in 5 of 14 normal and 11 of 11 HIV-positive subjects, RNA for gene 62 was detected in 4 of 10 normal and 6 of 9 HIV-positive subjects, and RNA for gene 63 was detected in 8 of 17 normal and 12 of 15 HIV-positive subjects. RNA for VZV gene 4 was detected in 2 of 13 normal and 4 of 9 HIV-positive subjects, and RNA for gene 18 was detected in 4 of 15 normal and 5 of 15 HIV-positive subjects. By contrast, RNAs for VZV genes 28, 40, and 61 were rarely or never detected. In addition, immunocytochemical analysis detected the presence of VZV gene 63-encoded protein in five normal and four HIV-positive subjects. VZV RNA was also analyzed in explanted fresh human TG and dorsal root ganglia from five normal human subjects over a period of up to 11 days in culture. We found a very different pattern of gene expression in these explants, with transcripts for VZV genes 18, 28, 29, 40, and 63 all frequently detected, presumably as a result of viral reactivation. Taken together, these data provide further support for the notion of significant and restricted viral gene expression in VZV latency. A consistent feature of varicella-zoster virus (VZV) latency is the restricted pattern of viral gene expression in human ganglionic tissues. To understand further the significance of this gene restriction, we used in situ hybridization (ISH) to detect the frequency of RNA expression for nine VZV genes in trigeminal ganglia (TG) from 35 human subjects, including 18 who were human immunodeficiency virus (HIV) positive. RNA for VZV gene 21 was detected in 7 of 11 normal and 6 of 10 HIV-positive subjects, RNA for gene 29 was detected in 5 of 14 normal and 11 of 11 HIV-positive subjects, RNA for gene 62 was detected in 4 of 10 normal and 6 of 9 HIV-positive subjects, and RNA for gene 63 was detected in 8 of 17 normal and 12 of 15 HIV-positive subjects. RNA for VZV gene 4 was detected in 2 of 13 normal and 4 of 9 HIV-positive subjects, and RNA for gene 18 was detected in 4 of 15 normal and 5 of 15 HIV-positive subjects. By contrast, RNAs for VZV genes 28, 40, and 61 were rarely or never detected. In addition, immunocytochemical analysis detected the presence of VZV gene 63-encoded protein in five normal and four HIV-positive subjects. VZV RNA was also analyzed in explanted fresh human TG and dorsal root ganglia from five normal human subjects over a period of up to 11 days in culture. We found a very different pattern of gene expression in these explants, with transcripts for VZV genes 18, 28, 29, 40, and 63 all frequently detected, presumably as a result of viral reactivation. Taken together, these data provide further support for the notion of significant and restricted viral gene expression in VZV latency.A consistent feature of varicella-zoster virus (VZV) latency is the restricted pattern of viral gene expression in human ganglionic tissues. To understand further the significance of this gene restriction, we used in situ hybridization (ISH) to detect the frequency of RNA expression for nine VZV genes in trigeminal ganglia (TG) from 35 human subjects, including 18 who were human immunodeficiency virus (HIV) positive. RNA for VZV gene 21 was detected in 7 of 11 normal and 6 of 10 HIV-positive subjects, RNA for gene 29 was detected in 5 of 14 normal and 11 of 11 HIV-positive subjects, RNA for gene 62 was detected in 4 of 10 normal and 6 of 9 HIV-positive subjects, and RNA for gene 63 was detected in 8 of 17 normal and 12 of 15 HIV-positive subjects. RNA for VZV gene 4 was detected in 2 of 13 normal and 4 of 9 HIV-positive subjects, and RNA for gene 18 was detected in 4 of 15 normal and 5 of 15 HIV-positive subjects. By contrast, RNAs for VZV genes 28, 40, and 61 were rarely or never detected. In addition, immunocytochemical analysis detected the presence of VZV gene 63-encoded protein in five normal and four HIV-positive subjects. VZV RNA was also analyzed in explanted fresh human TG and dorsal root ganglia from five normal human subjects over a period of up to 11 days in culture. We found a very different pattern of gene expression in these explants, with transcripts for VZV genes 18, 28, 29, 40, and 63 all frequently detected, presumably as a result of viral reactivation. Taken together, these data provide further support for the notion of significant and restricted viral gene expression in VZV latency. Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI |
Author | Jeanne E. Bell Esther Grinfeld Peter G. E. Kennedy |
AuthorAffiliation | Glasgow University Department of Neurology, Southern General Hospital, Glasgow, 1 and Edinburgh University Department of Neuropathology, Western General Hospital, Edinburgh, 2 United Kingdom |
AuthorAffiliation_xml | – name: Glasgow University Department of Neurology, Southern General Hospital, Glasgow, 1 and Edinburgh University Department of Neuropathology, Western General Hospital, Edinburgh, 2 United Kingdom |
Author_xml | – sequence: 1 givenname: Peter G. E. surname: Kennedy fullname: Kennedy, Peter G. E. organization: <!--label omitted: 1-->Glasgow University Department of Neurology, Southern General Hospital, Glasgow,1 and – sequence: 2 givenname: Esther surname: Grinfeld fullname: Grinfeld, Esther organization: <!--label omitted: 1-->Glasgow University Department of Neurology, Southern General Hospital, Glasgow,1 and – sequence: 3 givenname: Jeanne E. surname: Bell fullname: Bell, Jeanne E. organization: <!--label omitted: 2-->Edinburgh University Department of Neuropathology, Western General Hospital, Edinburgh,2 United Kingdom |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11090189$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1128/jvi.70.5.2789-2796.1996 10.1073/pnas.92.24.10980 10.1016/B978-0-407-02293-5.50015-5 10.1128/jvi.66.6.3899-3903.1992 10.1007/BF02935640 10.1128/jvi.68.12.7900-7908.1994 10.1016/S0065-3527(08)60859-3 10.1128/jvi.69.4.2674-2678.1995 10.1016/S0140-6736(83)90736-5 10.1073/pnas.95.8.4658 10.1006/viro.1993.1115 10.1073/pnas.85.7.2362 10.1073/pnas.95.12.7080 10.3109/13550289909045372 10.1056/NEJM200003023420906 10.1073/pnas.85.24.9773 10.1002/ana.410220315 10.1093/infdis/166.Supplement_1.S24 10.1006/viro.1999.9745 10.1073/pnas.93.5.2122 10.1128/jvi.69.5.3240-3245.1995 10.1128/JVI.73.10.8571-8577.1999 |
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Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 Corresponding author. Mailing address: Glasgow University Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, Scotland, United Kingdom. Phone: 44-141-201-2474. Fax: 44-141-201-2993. E-mail: P.G.Kennedy@clinmed.gla.ac.uk. |
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Mendeley... A consistent feature of varicella-zoster virus (VZV) latency is the restricted pattern of viral gene expression in human ganglionic tissues. To understand... |
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SubjectTerms | Adult Female Ganglia - virology Gene Expression Regulation, Viral Herpes Zoster - genetics Herpes Zoster - virology Herpesvirus 3, Human - genetics Herpesvirus 3, Human - isolation & purification Human immunodeficiency virus Humans Male Middle Aged Pathogenesis and Immunity Polymerase Chain Reaction RNA, Viral - analysis Varicella-zoster virus |
Title | Varicella-Zoster Virus Gene Expression in Latently Infected and Explanted Human Ganglia |
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