{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T13:07:50Z","timestamp":1753880870220,"version":"3.41.2"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"23","license":[{"start":{"date-parts":[[2018,12,1]],"date-time":"2018-12-01T00:00:00Z","timestamp":1543622400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["SC1AI112785"],"award-info":[{"award-number":["SC1AI112785"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81701999"],"award-info":[{"award-number":["81701999"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:p>\n            Our finding that HCMV IE1 protected hPML from degradation by HSV ICP0 is important, because the PML body (aka ND10) is believed to be the first line of host intrinsic defense against herpesviral infection. How the infected viruses overcome the nuclear defensive structure (PML body) has not been fully understood. Herpesviral proteins, ICP0 of HSV and IE1 of CMV, have been identified to interact with PML. Here, we report that HCMV IE1 incompletely deSUMOylated PML, resulting in the mono-SUMOylated PML, which is consistent with the report of Schilling et al. (J Virol 91:e02049-16, 2017,\n            <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1128\/JVI.02049-16\">https:\/\/doi.org\/10.1128\/JVI.02049-16<\/jats:ext-link>\n            ). The mono-SUMOylated PML was subjected to degradation by HSV ICP0. However, it was protected by IE1 from degradation by ICP0 or HSV-1 infection. In contrast, IE1 with L174P mutation lost the function of deSUMOylating PML and failed to protect the degradation of the mono-SUMOylated PML. Whether the mono-SUMOylated PML has any defensive function against viral infection will be further investigated.\n          <\/jats:p>","DOI":"10.1128\/jvi.01452-18","type":"journal-article","created":{"date-parts":[[2018,9,26]],"date-time":"2018-09-26T16:54:53Z","timestamp":1537980893000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["Expression of Human Cytomegalovirus IE1 Leads to Accumulation of Mono-SUMOylated PML That Is Protected from Degradation by Herpes Simplex Virus 1 ICP0"],"prefix":"10.1128","volume":"92","author":[{"given":"Wangheng","family":"Hou","sequence":"first","affiliation":[{"name":"Department of Microbiology, Howard University College of Medicine, Washington, DC, USA"},{"name":"State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Public Health, Xiamen University, Xiamen, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ruth","family":"Cruz-Cosme","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Howard University College of Medicine, Washington, DC, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fayuan","family":"Wen","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Howard University College of Medicine, Washington, DC, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9545-9062","authenticated-orcid":false,"given":"Jin-Hyun","family":"Ahn","sequence":"additional","affiliation":[{"name":"Department of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Inez","family":"Reeves","sequence":"additional","affiliation":[{"name":"Division of Neonatology, Department of Obstetrics and Gynecology, Howard University College of Medicine, Washington, DC, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9352-0643","authenticated-orcid":false,"given":"Min-Hua","family":"Luo","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Virology, CAS Center for Excellence in Brain Science and Intelligence Technology (CEBSIT), Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, Hubei, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qiyi","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Howard University College of Medicine, Washington, DC, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"1083","article-title":"Alternative splicing of PML transcripts predicts coexpression of several carboxy-terminally different protein isoforms","volume":"7","author":"Fagioli M","year":"1992","unstructured":"Fagioli M, Alcalay M, Pandolfi PP, Venturini L, Mencarelli A, Simeone A, Acampora D, Grignani F, Pelicci PG. 1992. 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