Inhibition of the Super Elongation Complex Suppresses Herpes Simplex Virus Immediate Early Gene Expression, Lytic Infection, and Reactivation from Latency
HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at...
Saved in:
| Published in | mBio Vol. 11; no. 3 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
09.06.2020
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 2161-2129 2150-7511 2150-7511 |
| DOI | 10.1128/mBio.01216-20 |
Cover
Loading…
| Abstract | HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals.
Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active
s
uper
e
longation
c
omplex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes.
IMPORTANCE
HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. |
|---|---|
| AbstractList | Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active
uper
longation
omplex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes.
HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active s uper e longation c omplex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes. IMPORTANCE HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active super elongation complex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes.IMPORTANCE HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals.Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active super elongation complex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes.IMPORTANCE HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active s uper e longation c omplex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes. ABSTRACT Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in sensory neurons. IE genes are transcribed by the cellular RNA polymerase II (RNAPII) and regulated by multiple transcription factors and coactivators. The HCF-1 cellular coactivator plays a central role in driving IE expression at multiple stages through interactions with transcription factors, chromatin modulation complexes, and transcription elongation components, including the active super elongation complex/P-TEFb (SEC-P-TEFb). Here, we demonstrate that the SEC occupies the promoters of HSV IE genes during the initiation of lytic infection and during reactivation from latency. Specific inhibitors of the SEC suppress viral IE expression and block the spread of HSV infection. Significantly, these inhibitors also block the initiation of viral reactivation from latency in sensory ganglia. The potent suppression of IE gene expression by SEC inhibitors indicates that transcriptional elongation represents a determining rate-limiting stage in HSV IE gene transcription and that the SEC plays a critical role in driving productive elongation during both phases of the viral life cycle. Most importantly, this supports the model that signal-mediated induction of SEC-P-TEFb levels can promote reactivation of a population of poised latent genomes. IMPORTANCE HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency in sensory neurons are dependent on the induced expression of the viral immediate early genes. Transcription of these genes is controlled at multiple levels, including modulation of the chromatin state of the viral genome and appropriate recruitment of transcription factors and coactivators. Following initiation of transcription, IE genes are subject to a key regulatory stage in which transcriptional elongation rates are controlled by the activity of the super elongation complex. Inhibition of the SEC blocks both lytic infection and reactivation from latency in sensory neurons. In addition to providing insights into the mechanisms controlling viral infection and reactivation, inhibitors of critical components such as the SEC may represent novel antivirals. |
| Author | Arbuckle, Jesse H. Alfonso-Dunn, Roberto Vogel, Jodi L. Kristie, Thomas M. |
| Author_xml | – sequence: 1 givenname: Roberto surname: Alfonso-Dunn fullname: Alfonso-Dunn, Roberto organization: Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA – sequence: 2 givenname: Jesse H. surname: Arbuckle fullname: Arbuckle, Jesse H. organization: Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA – sequence: 3 givenname: Jodi L. surname: Vogel fullname: Vogel, Jodi L. organization: Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA – sequence: 4 givenname: Thomas M. surname: Kristie fullname: Kristie, Thomas M. organization: Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32518191$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1UsFu1DAQjVARLaVHrshHDqR47NhJLkiwWtqVVkKiwNVynMmuq8QOdrbq_gpfizdbKoqELzOeefPeeDwvsxPnHWbZa6CXAKx6P3yy_pICA5kz-iw7YyBoXgqAk4MvIWfA6tPsIsZbmg7nUHH6IjvlTEAFNZxlv1Zuaxs7We-I78i0RXKzGzGQZe_dRs_xhR_GHu8PiTFgjBjJNYYxmRt7zPywYRfJahiwtXpCstSh35MrdMm9n2sSzzuy3k_WkJXr0ExzQLuWfEWdbndHqS74gawThTP7V9nzTvcRLx7sefb98_Lb4jpff7laLT6uc1MIPuXAkaPRMj1XStmiAdFqIUuoJNY0JSpthG4M0LopDFatrFGnOenDQGgr-Xm2OvK2Xt-qMdhBh73y2qo54MNG6ZAa71EZKKuuMUmxlAXVIk2TsgabUooCeMkS14cj17hr0jAMuino_gnp04yzW7Xxd6rkJYe6TARvHwiC_7nDOKnBRoN9rx36XVSsABCFkCAS9M3fWo8ifz43AfIjwAQfY8DuEQJUHfZHHfZHzfujGE14_g_e2Gn-l9Sq7f9T9RuIdMt- |
| CitedBy_id | crossref_primary_10_1128_jvi_01392_23 crossref_primary_10_1128_jvi_02015_23 crossref_primary_10_1128_mbio_03542_22 crossref_primary_10_3390_cancers13092181 crossref_primary_10_1371_journal_ppat_1012621 crossref_primary_10_1073_pnas_2023025118 crossref_primary_10_1007_s13365_022_01064_5 crossref_primary_10_1016_j_antiviral_2021_105103 crossref_primary_10_1126_sciadv_adi4565 crossref_primary_10_3390_v15051032 crossref_primary_10_3390_microorganisms12020262 |
| Cites_doi | 10.1101/gad.252103 10.7554/eLife.06535 10.1128/mBio.02047-18 10.1126/scitranslmed.aan5861 10.1128/mBio.00590-12 10.1126/scitranslmed.3005145 10.1017/CBO9780511545313.033 10.1016/j.chom.2017.03.007 10.1038/ng.2007.21 10.1371/journal.ppat.1002540 10.1128/JVI.00686-09 10.1016/j.molcel.2010.04.013 10.1016/j.chom.2011.11.002 10.1101/gad.2059211 10.1016/j.molcel.2015.02.003 10.1016/j.cell.2018.09.027 10.1128/JVI.01115-09 10.1371/journal.pone.0201880 10.1038/nrm3417 10.1128/JVI.03052-14 10.1371/journal.ppat.1005950 10.1016/j.chom.2015.11.007 10.1128/JVI.79.11.6757-6762.2005 10.1128/JVI.00712-09 10.3390/v5051272 10.1128/JVI.02035-19 10.1128/JVI.75.7.3240-3249.2001 10.1146/annurev-biochem-052610-095910 10.1016/j.molcel.2005.06.027 10.1371/journal.ppat.0030146 10.1172/JCI80565 10.1074/jbc.M410178200 10.1080/21541264.2018.1523668 10.1073/pnas.0704351104 10.1016/j.bbagrm.2009.12.001 10.1101/gad.1643208 10.1093/nar/gkw585 10.1016/j.celrep.2018.05.084 10.1128/JVI.75.13.6143-6153.2001 10.1128/JVI.63.2.759-768.1989 10.1038/nature09504 10.1128/mBio.00732-19 10.1016/j.molcel.2005.06.029 10.1101/gad.325142.119 10.1128/mBio.00745-17 10.1128/jvi.78.4.1763-1774.2004 10.1073/pnas.1912375117 10.1038/35104581 10.1128/jvi.77.6.3680-3689.2003 10.1038/nrm3953 10.1128/mBio.00558-12 10.3390/molecules23040933 10.1021/cr400105n 10.1097/QCO.0000000000000288 10.1038/nm.2051 10.1074/jbc.M112.410746 10.1101/gad.335679.119 10.1371/journal.pone.0107654 10.1128/mBio.01141-17 10.1016/j.virol.2015.01.026 10.1126/scitranslmed.3010643 10.1016/j.virol.2014.02.008 10.1038/nrmicro1794 10.1073/pnas.96.4.1229 10.1093/nar/gkw571 10.1128/JVI.01012-12 10.1016/j.molcel.2012.03.007 10.1128/JVI.03046-12 10.1139/bcb-2015-0045 10.1021/cr400120z 10.1093/infdis/jit350 10.1002/bies.201670912 10.1158/0008-5472.CAN-15-2721 10.1128/MCB.00040-17 10.1128/JVI.02207-10 10.1371/journal.pone.0045749 10.1371/journal.ppat.1004350 10.1128/JVI.00943-10 10.1038/ng.3229 10.1038/35104575 |
| ContentType | Journal Article |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1128/mBio.01216-20 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE CrossRef MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| DocumentTitleAlternate | SEC Inhibitors Block HSV Infection and Reactivation |
| EISSN | 2150-7511 |
| ExternalDocumentID | oai_doaj_org_article_c178fbc3e37640a583002beb76541372 PMC7373197 32518191 10_1128_mBio_01216_20 |
| Genre | Journal Article Research Support, N.I.H., Intramural |
| GrantInformation_xml | – fundername: ; |
| GroupedDBID | --- 0R~ 53G 5VS AAFWJ AAGFI AAUOK AAYXX ADBBV AENEX AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV BTFSW CITATION DIK E3Z EBS FRP GROUPED_DOAJ GX1 H13 HYE HZ~ KQ8 M48 O5R O5S O9- OK1 P2P PGMZT RHI RNS RPM RSF CGR CUY CVF ECM EIF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-c453t-13e3eca6161666dec15da567186e90ca68ac5abc109b4ce8d69ea150a00030d63 |
| IEDL.DBID | DOA |
| ISSN | 2161-2129 2150-7511 |
| IngestDate | Wed Aug 27 01:17:11 EDT 2025 Thu Aug 21 14:08:16 EDT 2025 Fri Jul 11 15:33:09 EDT 2025 Thu Apr 03 06:53:06 EDT 2025 Tue Jul 01 01:52:44 EDT 2025 Thu Apr 24 22:50:32 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 3 |
| Keywords | herpes simplex virus transcription elongation HSV reactivation transcription super elongation complex latency HCF-1 AFF4 |
| Language | English |
| License | This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c453t-13e3eca6161666dec15da567186e90ca68ac5abc109b4ce8d69ea150a00030d63 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Present address: Roberto Alfonso-Dunn, Tisch MS Research Center of New York, New York, New York, USA. |
| OpenAccessLink | https://doaj.org/article/c178fbc3e37640a583002beb76541372 |
| PMID | 32518191 |
| PQID | 2411545615 |
| PQPubID | 23479 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_c178fbc3e37640a583002beb76541372 pubmedcentral_primary_oai_pubmedcentral_nih_gov_7373197 proquest_miscellaneous_2411545615 pubmed_primary_32518191 crossref_primary_10_1128_mBio_01216_20 crossref_citationtrail_10_1128_mBio_01216_20 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 20200609 |
| PublicationDateYYYYMMDD | 2020-06-09 |
| PublicationDate_xml | – month: 6 year: 2020 text: 20200609 day: 9 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: 1752 N St., N.W., Washington, DC |
| PublicationTitle | mBio |
| PublicationTitleAlternate | mBio |
| PublicationYear | 2020 |
| Publisher | American Society for Microbiology |
| Publisher_xml | – name: American Society for Microbiology |
| References | e_1_3_3_50_2 e_1_3_3_75_2 e_1_3_3_71_2 e_1_3_3_77_2 e_1_3_3_79_2 e_1_3_3_16_2 e_1_3_3_18_2 e_1_3_3_39_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_58_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_56_2 e_1_3_3_33_2 e_1_3_3_54_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_52_2 e_1_3_3_73_2 e_1_3_3_40_2 e_1_3_3_61_2 e_1_3_3_5_2 e_1_3_3_7_2 e_1_3_3_9_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_23_2 e_1_3_3_48_2 e_1_3_3_69_2 e_1_3_3_25_2 e_1_3_3_46_2 e_1_3_3_67_2 e_1_3_3_80_2 e_1_3_3_44_2 e_1_3_3_65_2 e_1_3_3_82_2 e_1_3_3_3_2 e_1_3_3_21_2 e_1_3_3_42_2 e_1_3_3_63_2 e_1_3_3_51_2 e_1_3_3_74_2 e_1_3_3_76_2 e_1_3_3_70_2 e_1_3_3_78_2 e_1_3_3_17_2 e_1_3_3_19_2 e_1_3_3_38_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_59_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_57_2 e_1_3_3_32_2 e_1_3_3_55_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_53_2 e_1_3_3_72_2 e_1_3_3_62_2 e_1_3_3_60_2 e_1_3_3_6_2 e_1_3_3_8_2 e_1_3_3_28_2 e_1_3_3_49_2 e_1_3_3_24_2 e_1_3_3_47_2 e_1_3_3_26_2 e_1_3_3_45_2 e_1_3_3_68_2 Roizman B (e_1_3_3_2_2) 2013 e_1_3_3_20_2 e_1_3_3_43_2 e_1_3_3_66_2 e_1_3_3_81_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_41_2 e_1_3_3_64_2 |
| References_xml | – ident: e_1_3_3_10_2 doi: 10.1101/gad.252103 – ident: e_1_3_3_52_2 doi: 10.7554/eLife.06535 – ident: e_1_3_3_43_2 doi: 10.1128/mBio.02047-18 – ident: e_1_3_3_75_2 doi: 10.1126/scitranslmed.aan5861 – ident: e_1_3_3_79_2 doi: 10.1128/mBio.00590-12 – ident: e_1_3_3_7_2 doi: 10.1126/scitranslmed.3005145 – ident: e_1_3_3_3_2 doi: 10.1017/CBO9780511545313.033 – ident: e_1_3_3_16_2 doi: 10.1016/j.chom.2017.03.007 – ident: e_1_3_3_19_2 doi: 10.1038/ng.2007.21 – ident: e_1_3_3_11_2 doi: 10.1371/journal.ppat.1002540 – ident: e_1_3_3_82_2 doi: 10.1128/JVI.00686-09 – ident: e_1_3_3_62_2 doi: 10.1016/j.molcel.2010.04.013 – ident: e_1_3_3_42_2 doi: 10.1016/j.chom.2011.11.002 – ident: e_1_3_3_30_2 doi: 10.1101/gad.2059211 – ident: e_1_3_3_21_2 doi: 10.1016/j.molcel.2015.02.003 – ident: e_1_3_3_48_2 doi: 10.1016/j.cell.2018.09.027 – ident: e_1_3_3_13_2 doi: 10.1128/JVI.01115-09 – ident: e_1_3_3_57_2 doi: 10.1371/journal.pone.0201880 – ident: e_1_3_3_32_2 doi: 10.1038/nrm3417 – ident: e_1_3_3_73_2 doi: 10.1128/JVI.03052-14 – ident: e_1_3_3_69_2 doi: 10.1371/journal.ppat.1005950 – ident: e_1_3_3_74_2 doi: 10.1016/j.chom.2015.11.007 – ident: e_1_3_3_65_2 doi: 10.1128/JVI.79.11.6757-6762.2005 – ident: e_1_3_3_80_2 doi: 10.1128/JVI.00712-09 – ident: e_1_3_3_4_2 doi: 10.3390/v5051272 – ident: e_1_3_3_63_2 doi: 10.1128/JVI.02035-19 – ident: e_1_3_3_71_2 doi: 10.1128/JVI.75.7.3240-3249.2001 – ident: e_1_3_3_25_2 doi: 10.1146/annurev-biochem-052610-095910 – ident: e_1_3_3_29_2 doi: 10.1016/j.molcel.2005.06.027 – ident: e_1_3_3_28_2 doi: 10.1371/journal.ppat.0030146 – ident: e_1_3_3_37_2 doi: 10.1172/JCI80565 – ident: e_1_3_3_5_2 doi: 10.1074/jbc.M410178200 – ident: e_1_3_3_26_2 doi: 10.1080/21541264.2018.1523668 – ident: e_1_3_3_9_2 doi: 10.1073/pnas.0704351104 – ident: e_1_3_3_78_2 doi: 10.1016/j.bbagrm.2009.12.001 – ident: e_1_3_3_18_2 doi: 10.1101/gad.1643208 – start-page: 2501 volume-title: Fields virology year: 2013 ident: e_1_3_3_2_2 – ident: e_1_3_3_34_2 doi: 10.1093/nar/gkw585 – ident: e_1_3_3_56_2 doi: 10.1016/j.celrep.2018.05.084 – ident: e_1_3_3_70_2 doi: 10.1128/JVI.75.13.6143-6153.2001 – ident: e_1_3_3_72_2 doi: 10.1128/JVI.63.2.759-768.1989 – ident: e_1_3_3_51_2 doi: 10.1038/nature09504 – ident: e_1_3_3_76_2 doi: 10.1128/mBio.00732-19 – ident: e_1_3_3_35_2 doi: 10.1016/j.molcel.2005.06.029 – ident: e_1_3_3_17_2 doi: 10.1101/gad.325142.119 – ident: e_1_3_3_66_2 doi: 10.1128/mBio.00745-17 – ident: e_1_3_3_60_2 doi: 10.1128/jvi.78.4.1763-1774.2004 – ident: e_1_3_3_53_2 doi: 10.1073/pnas.1912375117 – ident: e_1_3_3_33_2 doi: 10.1038/35104581 – ident: e_1_3_3_59_2 doi: 10.1128/jvi.77.6.3680-3689.2003 – ident: e_1_3_3_23_2 doi: 10.1038/nrm3953 – ident: e_1_3_3_15_2 doi: 10.1128/mBio.00558-12 – ident: e_1_3_3_61_2 doi: 10.3390/molecules23040933 – ident: e_1_3_3_22_2 doi: 10.1021/cr400105n – ident: e_1_3_3_49_2 doi: 10.1097/QCO.0000000000000288 – ident: e_1_3_3_8_2 doi: 10.1038/nm.2051 – ident: e_1_3_3_27_2 doi: 10.1074/jbc.M112.410746 – ident: e_1_3_3_24_2 doi: 10.1101/gad.335679.119 – ident: e_1_3_3_68_2 doi: 10.1371/journal.pone.0107654 – ident: e_1_3_3_77_2 doi: 10.1128/mBio.01141-17 – ident: e_1_3_3_6_2 doi: 10.1016/j.virol.2015.01.026 – ident: e_1_3_3_14_2 doi: 10.1126/scitranslmed.3010643 – ident: e_1_3_3_41_2 doi: 10.1016/j.virol.2014.02.008 – ident: e_1_3_3_81_2 doi: 10.1038/nrmicro1794 – ident: e_1_3_3_12_2 doi: 10.1073/pnas.96.4.1229 – ident: e_1_3_3_31_2 doi: 10.1093/nar/gkw571 – ident: e_1_3_3_45_2 doi: 10.1128/JVI.01012-12 – ident: e_1_3_3_55_2 doi: 10.1016/j.molcel.2012.03.007 – ident: e_1_3_3_46_2 doi: 10.1128/JVI.03046-12 – ident: e_1_3_3_20_2 doi: 10.1139/bcb-2015-0045 – ident: e_1_3_3_40_2 doi: 10.1021/cr400120z – ident: e_1_3_3_50_2 doi: 10.1093/infdis/jit350 – ident: e_1_3_3_47_2 doi: 10.1002/bies.201670912 – ident: e_1_3_3_64_2 doi: 10.1158/0008-5472.CAN-15-2721 – ident: e_1_3_3_39_2 doi: 10.1128/MCB.00040-17 – ident: e_1_3_3_58_2 doi: 10.1128/JVI.02207-10 – ident: e_1_3_3_67_2 doi: 10.1371/journal.pone.0045749 – ident: e_1_3_3_44_2 doi: 10.1371/journal.ppat.1004350 – ident: e_1_3_3_38_2 doi: 10.1128/JVI.00943-10 – ident: e_1_3_3_54_2 doi: 10.1038/ng.3229 – ident: e_1_3_3_36_2 doi: 10.1038/35104575 |
| SSID | ssj0000331830 |
| Score | 2.31804 |
| Snippet | HSV infections can cause pathologies ranging from recurrent lesions to significant ocular disease. Initiation of lytic infection and reactivation from latency... Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from latency in... ABSTRACT Induction of herpes simplex virus (HSV) immediate early (IE) gene transcription promotes the initiation of lytic infection and reactivation from... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| SubjectTerms | AFF4 Animals Antiviral Agents - pharmacology Cell Line Chlorocebus aethiops Fibroblasts - virology Gene Expression Genes, Immediate-Early HCF-1 herpes simplex virus Herpesvirus 1, Human - drug effects Herpesvirus 1, Human - genetics Herpesvirus 1, Human - physiology Host-Microbe Biology HSV reactivation Humans Immediate-Early Proteins - genetics latency Lung - cytology transcription elongation Transcriptional Elongation Factors - antagonists & inhibitors Transcriptional Elongation Factors - genetics Vero Cells Virus Latency - drug effects Virus Latency - genetics Virus Replication - drug effects |
| SummonAdditionalLinks | – databaseName: Scholars Portal Journals: Open Access dbid: M48 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3db9MwELdgCIkXxPfCl4yEeFqH8-E4eUCIoU4t2nhgFO0tsp3zFqlLStpK7b_CX8udkxY6jTeeItmO4uTOvt85d79j7K12NokE6IEuFToo1hncB50YuNKFThqXCEPJyadf09Ek-XIuz_9QCvUfcH6ja0f1pCbt9HD1c_0RF_yHLgEme391VDWHxE2WosxvsztolBRVcTjtkb7flGNSXrFh2bx-145V8uT9NyHO64GTf1mi4wfsfg8h-adO5g_ZLagfsbtdUcn1Y_ZrXF9Wxkdi8cZxBHj8bDmDlg-nTX3hBcFpF5jCijp8ICzM-QjaGV7Oqq7nR9Uu53x85TNLFsA9ETInkmo-XPXBs_UBP1njJPi4j-jCBl2X_BtQtkR31sspf4WfaILm6ydscjz8_nk06CswDGwiY6pTDzFYnSIsRDenBBvKUssU7VkKucCOTFupjQ1FbhILWZnmoBFiau9qlWn8lO3VTQ37jBvIQysVKoyJ0SAKk4lIJxIcEZalSRawg40ECtvTk1OVjGnh3ZQoK0hghRdYEYmAvdsOn3W8HP8aeETi3A4iOm3f0LQXRb86CxuqzBmLb6vSRGiJmiIiA0ZRlfRYRQF7s1GGApcf_VPRNTTLeYG61oFQGbBnnXJsHxUjdiR_OGBqR2125rLbU1eXnuJbxQr3RvX8f0z-BbsX0SEBHR3lL9neol3CK0RSC_Par5Hflcwg7g priority: 102 providerName: Scholars Portal |
| Title | Inhibition of the Super Elongation Complex Suppresses Herpes Simplex Virus Immediate Early Gene Expression, Lytic Infection, and Reactivation from Latency |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/32518191 https://www.proquest.com/docview/2411545615 https://pubmed.ncbi.nlm.nih.gov/PMC7373197 https://doaj.org/article/c178fbc3e37640a583002beb76541372 |
| Volume | 11 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlUOil9F23TVCh9BQ3smX5cUzCprsl6aFpyt6MJI8Sw8Ze9gHZv5JfmxnZu-yWll56sUEjsJBmNN_Io28Y-6SdTWIBOtRVhgGKdQb3QSdCV7nIKeMSYehy8sX3dHiVfBur8VapL8oJ6-iBu4k7slGWO2MloCUkQqtcog0bMBkVsJaZ333R520FU34PlqSrYk2qGedHtyd1-4UIzNKQantvOSHP1f8ngPl7nuSW4zl7xp72iJEfdyN9zh5B84I97mpIrl6y-1FzUxufeMVbxxHP8cvlFGZ8MGmbaz_vnIx-Anck8HmvMOdDmE3xdVl3kl_1bDnno1t_kWQB3PMec-Kk5oO7Ple2OeTnKxwEH_UJXNigm4r_ALoc0R3tcrquws81IfHVK3Z1Nvh5Ogz7gguhTZSksvQgweoUUSBGNRXYSFVapei-UigECnJtlTY2EoVJLORVWoBGRKl9ZFWl8jXba9oG3jJuoIisylA_jET_J0wuYp0ocMRPliZ5wA7XK1Dano2cimJMSh-VxHlJC1b6BStjEbDPm-7Tjobjbx1PaDk3nYg92zegTpW9TpX_0qmAfVwrQ4nWRr9QdAPtcl4i3ukwpwrYm045Np-SCBUp_A1YtqM2O2PZlTT1jWf0zmSGW2H27n8M_j17EtOZAJ0UFR_Y3mK2hH0ETgtz4G0En1_HET4vkvwBPEwbEw |
| linkProvider | Directory of Open Access Journals |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Inhibition+of+the+Super+Elongation+Complex+Suppresses+Herpes+Simplex+Virus+Immediate+Early+Gene+Expression%2C+Lytic+Infection%2C+and+Reactivation+from+Latency&rft.jtitle=mBio&rft.au=Roberto+Alfonso-Dunn&rft.au=Jesse+H.+Arbuckle&rft.au=Jodi+L.+Vogel&rft.au=Thomas+M.+Kristie&rft.date=2020-06-09&rft.pub=American+Society+for+Microbiology&rft.eissn=2150-7511&rft.volume=11&rft.issue=3&rft_id=info:doi/10.1128%2FmBio.01216-20&rft.externalDBID=DOA&rft.externalDocID=oai_doaj_org_article_c178fbc3e37640a583002beb76541372 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2161-2129&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2161-2129&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2161-2129&client=summon |