For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
12
views
87
references
 Top references
cited by
25
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      618
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Histone deacetylases in viral infections

      review-article
      Author(s): 1 , , 2
      Publication date (Electronic):
      Journal: Clinical Epigenetics
      Publisher: Springer-Verlag
      Keywords: HDAC, Viruses, HIV, HCMV, HDAC inhibitors

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Chromatin remodeling and gene expression are regulated by histone deacetylases (HDACs) that condense the chromatin structure by deacetylating histones. HDACs comprise a group of enzymes that are responsible for the regulation of both cellular and viral genes at the transcriptional level. In mammals, a total of 18 HDACs have been identified and grouped into four classes, i.e., class I (HDACs 1, 2, 3, 8), class II (HDACs 4, 5, 6, 7, 9, 10), class III (Sirt1–Sirt7), and class IV (HDAC11). We review here the role of HDACs on viral replication and how HDAC inhibitors could potentially be used as new therapeutic tools in several viral infections.

          Related collections

          Most cited references87

          • Record: found
          • Abstract: found
          • Article: not found

          Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy.

          J. Gallant, R Brookmeyer, J Margolick … (1998)
          The hypothesis that quiescent CD4+ T lymphocytes carrying proviral DNA provide a reservoir for human immunodeficiency virus-type 1 (HIV-1) in patients on highly active antiretroviral therapy (HAART) was examined. In a study of 22 patients successfully treated with HAART for up to 30 months, replication-competent virus was routinely recovered from resting CD4+ T lymphocytes. The frequency of resting CD4+ T cells harboring latent HIV-1 was low, 0.2 to 16.4 per 10(6) cells, and, in cross-sectional analysis, did not decrease with increasing time on therapy. The recovered viruses generally did not show mutations associated with resistance to the relevant antiretroviral drugs. This reservoir of nonevolving latent virus in resting CD4+ T cells should be considered in deciding whether to terminate treatment in patients who respond to HAART.
          Article 0 comments Cited 715 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Selective recognition of methylated lysine 9 on histone H3 by the HP1 chromo domain.

            A Bannister, P Zegerman, J F Partridge … (2001)
            Heterochromatin protein 1 (HP1) is localized at heterochromatin sites where it mediates gene silencing. The chromo domain of HP1 is necessary for both targeting and transcriptional repression. In the fission yeast Schizosaccharomyces pombe, the correct localization of Swi6 (the HP1 equivalent) depends on Clr4, a homologue of the mammalian SUV39H1 histone methylase. Both Clr4 and SUV39H1 methylate specifically lysine 9 of histone H3 (ref. 6). Here we show that HP1 can bind with high affinity to histone H3 methylated at lysine 9 but not at lysine 4. The chromo domain of HP1 is identified as its methyl-lysine-binding domain. A point mutation in the chromo domain, which destroys the gene silencing activity of HP1 in Drosophila, abolishes methyl-lysine-binding activity. Genetic and biochemical analysis in S. pombe shows that the methylase activity of Clr4 is necessary for the correct localization of Swi6 at centromeric heterochromatin and for gene silencing. These results provide a stepwise model for the formation of a transcriptionally silent heterochromatin: SUV39H1 places a 'methyl marker' on histone H3, which is then recognized by HP1 through its chromo domain. This model may also explain the stable inheritance of the heterochromatic state.
            Article 0 comments Cited 621 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              HIV reproducibly establishes a latent infection after acute infection of T cells in vitro.

              Albert Jordan, Dwayne Bisgrove, Eric Verdin (2003)
              The presence of latent reservoirs has prevented the eradication of human immunodeficiency virus (HIV) from infected patients successfully treated with anti-retroviral therapy. The mechanism of postintegration latency is poorly understood, partly because of the lack of an in vitro model. We have used an HIV retroviral vector or a full-length HIV genome expressing green fluorescent protein to infect a T lymphocyte cell line in vitro and highly enrich for latently infected cells. HIV latency occurred reproducibly, albeit with low frequency, during an acute infection. Clonal cell lines derived from latent populations showed no detectable basal expression, but could be transcriptionally activated after treatment with phorbol esters or tumor necrosis factor alpha. Direct sequencing of integration sites demonstrated that latent clones frequently contain HIV integrated in or close to alphoid repeat elements in heterochromatin. This is in contrast to a productive infection where integration in or near heterochromatin is disfavored. These observations demonstrate that HIV can reproducibly establish a latent infection as a consequence of integration in or near heterochromatin.
              Article 0 comments Cited 355 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                : +33-3-81218877 , +33-3-81665695 , gherbein@chu-besancon.fr
                Journal
                Journal ID (nlm-ta): Clin Epigenetics
                Journal ID (iso-abbrev): Clin Epigenetics
                Title: Clinical Epigenetics
                Publisher: Springer-Verlag (Berlin/Heidelberg )
                ISSN (Print): 1868-7075
                ISSN (Electronic): 1868-7083
                Publication date (Electronic): 30 May 2010
                Publication date Collection: September 2010
                Volume: 1
                Issue: 1-2
                Pages: 13-24
                Affiliations
                [1 ]Department of Virology, UPRES EA 4266, IFR 133 INSERM, Franche-Comte University, CHU Besançon, 2 place Saint-Jacques, 25030 Besancon, France
                [2 ]Department of Rheumatology, UPRES EA4266, IFR 133 INSERM, Franche-Comte University, CHU Besançon, 25030 Besancon, France
                Article
                Publisher ID: 3
                DOI: 10.1007/s13148-010-0003-5
                PMC ID: 3365363
                PubMed ID: 22704086
                SO-VID: a4fb5b2a-662a-462b-8d3e-4684081e90fa
                Copyright © © Springer-Verlag 2010
                History
                Date received : 30 December 2009
                Date accepted : 10 May 2010
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer-Verlag 2010

                ScienceOpen disciplines: Genetics
                Keywords: hdac,hdac inhibitors,hiv,viruses,hcmv
                Data availability:
                ScienceOpen disciplines: Genetics
                Keywords: hdac, hdac inhibitors, hiv, viruses, hcmv

                Comments

                Comment on this article

                scite_

                Similar content618

                See all similar

                Cited by25

                See all cited by

                Most referenced authors1,238

                See all reference authors