Non-Coding Rnas and Retroviruses
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Herpes Simplex Virus Latency in Isolated Human Neurons [Herpesviruses/Neuron-Specific Marker/Human Leukocyte Interferon/(E)-5-(2-Bromovinyl)-2'-Deoxyuridine]
Proc. Natl. Acad. Sci. USA Vol. 81, pp. 6217-6221, October 1984 Microbiology Herpes simplex virus latency in isolated human neurons [herpesviruses/neuron-specific marker/human leukocyte interferon/(E)-5-(2-bromovinyl)-2'-deoxyuridine] BRIAN WIGDAHL, CAROL A. SMITH, HELEN M. TRAGLIA, AND FRED RAPP* Department of Microbiology and Cancer Research Center, The Pennsylvania State University College of Medicine, Hershey, PA 17033 Communicated by Gertrude Henle, June 6, 1984 ABSTRACT Herpes simplex virus is most probably main- latency was maintained after inhibitor removal by increasing tained in the ganglion neurons of the peripheral nervous sys- the incubation temperature from 370C to 40.50C, and virus tem of humans in a latent form that can reactivate to produce replication was reactivated by decreasing the temperature recurrent disease. As an approximation of this cell-virus inter- (20, 22). As determined by DNA blot hybridization, the la- action, we have constructed a herpes simplex virus latency in tently infected HEL-F cell and neuron populations con- vitro model system using human fetus sensory neurons as the tained detectable quantities of most, if not all, HSV-1 Hin- host cell. Human fetus neurons were characterized as neuronal dIII, Xba I, and BamHI DNA fragments (21). Furthermore, in origin by the detection of the neuropeptide substance P and there was no detectable alteration in size or molarity of the the neuron-specific plasma membrane A2B5 antigen. Virus la- HSV-1 junction or terminal DNA fragments obtained by tency was established by blocking complete expression of the HindIII, Xba I, or BamHI digestion of DNA isolated from virus genome by treatment of infected human neurons with a latently infected HEL-F cells or neurons (21). -
Role of CCCH-Type Zinc Finger Proteins in Human Adenovirus Infections
viruses Review Role of CCCH-Type Zinc Finger Proteins in Human Adenovirus Infections Zamaneh Hajikhezri 1, Mahmoud Darweesh 1,2, Göran Akusjärvi 1 and Tanel Punga 1,* 1 Department of Medical Biochemistry and Microbiology, Uppsala University, 75123 Uppsala, Sweden; [email protected] (Z.H.); [email protected] (M.D.); [email protected] (G.A.) 2 Department of Microbiology and Immunology, Al-Azhr University, Assiut 11651, Egypt * Correspondence: [email protected]; Tel.: +46-733-203-095 Received: 28 October 2020; Accepted: 16 November 2020; Published: 18 November 2020 Abstract: The zinc finger proteins make up a significant part of the proteome and perform a huge variety of functions in the cell. The CCCH-type zinc finger proteins have gained attention due to their unusual ability to interact with RNA and thereby control different steps of RNA metabolism. Since virus infections interfere with RNA metabolism, dynamic changes in the CCCH-type zinc finger proteins and virus replication are expected to happen. In the present review, we will discuss how three CCCH-type zinc finger proteins, ZC3H11A, MKRN1, and U2AF1, interfere with human adenovirus replication. We will summarize the functions of these three cellular proteins and focus on their potential pro- or anti-viral activities during a lytic human adenovirus infection. Keywords: human adenovirus; zinc finger protein; CCCH-type; ZC3H11A; MKRN1; U2AF1 1. Zinc Finger Proteins Zinc finger proteins are a big family of proteins with characteristic zinc finger (ZnF) domains present in the protein sequence. The ZnF domains consists of various ZnF motifs, which are short 30–100 amino acid sequences, coordinating zinc ions (Zn2+). -
Non-Coding Rnas: Strategy for Viruses' Offensive
non-coding RNA Review Non-Coding RNAs: Strategy for Viruses’ Offensive Alessia Gallo 1,*, Matteo Bulati 1, Vitale Miceli 1 , Nicola Amodio 2 and Pier Giulio Conaldi 1,3 1 Department of Research, IRCCS ISMETT (Istituto Mediterraneo per i Trapianti e Terapie ad alta specializzazione), Via E.Tricomi 5, 90127 Palermo, Italy; [email protected] (M.B.); [email protected] (V.M.); [email protected] (P.G.C.) 2 Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, 88100 Catanzaro, Italy; [email protected] 3 UPMC Italy (University of Pittsburgh Medical Center Italy), Discesa dei Giudici 4, 90133 Palermo, Italy * Correspondence: [email protected]; Tel.: +39-91-21-92-649 Received: 7 August 2020; Accepted: 8 September 2020; Published: 10 September 2020 Abstract: The awareness of viruses as a constant threat for human public health is a matter of fact and in this resides the need of understanding the mechanisms they use to trick the host. Viral non-coding RNAs are gaining much value and interest for the potential impact played in host gene regulation, acting as fine tuners of host cellular defense mechanisms. The implicit importance of v-ncRNAs resides first in the limited genomes size of viruses carrying only strictly necessary genomic sequences. The other crucial and appealing characteristic of v-ncRNAs is the non-immunogenicity, making them the perfect expedient to be used in the never-ending virus-host war. In this review, we wish to examine how DNA and RNA viruses have evolved a common strategy and which the crucial host pathways are targeted through v-ncRNAs in order to grant and facilitate their life cycle. -
Shared Ancestry of Herpes Simplex Virus 1 Strain Patton with Recent Clinical Isolates from Asia and with Strain KOS63
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Virology Manuscript Author . Author manuscript; Manuscript Author available in PMC 2018 December 01. Published in final edited form as: Virology. 2017 December ; 512: 124–131. doi:10.1016/j.virol.2017.09.016. Shared ancestry of herpes simplex virus 1 strain Patton with recent clinical isolates from Asia and with strain KOS63 Aldo Pourcheta, Richard Copinb, Matthew C. Mulveyc, Bo Shopsina,b, Ian Mohra, and Angus C. Wilsona,# aDepartment of Microbiology, New York University School of Medicine, New York, New York, USA bDepartment of Medicine, New York University School of Medicine, New York, New York, USA cBeneVir Biopharm, Inc., Gaithersburg, Maryland, USA Abstract Herpes simplex virus 1 (HSV-1) is a widespread pathogen that persists for life, replicating in surface tissues and establishing latency in peripheral ganglia. Increasingly, molecular studies of latency use cultured neuron models developed using recombinant viruses such as HSV-1 GFP- US11, a derivative of strain Patton expressing green fluorescent protein (GFP) fused to the viral US11 protein. Visible fluorescence follows viral DNA replication, providing a real time indicator of productive infection and reactivation. Patton was isolated in Houston, Texas, prior to 1973, and distributed to many laboratories. Although used extensively, the genomic structure and phylogenetic relationship to other strains is poorly known. We report that wild type Patton and the GFP-US11 recombinant contain the full complement of HSV-1 genes and differ within the unique regions at only eight nucleotides, changing only two amino acids. Although isolated in North America, Patton is most closely related to Asian viruses, including KOS63. -
Where Do We Stand After Decades of Studying Human Cytomegalovirus?
microorganisms Review Where do we Stand after Decades of Studying Human Cytomegalovirus? 1, 2, 1 1 Francesca Gugliesi y, Alessandra Coscia y, Gloria Griffante , Ganna Galitska , Selina Pasquero 1, Camilla Albano 1 and Matteo Biolatti 1,* 1 Laboratory of Pathogenesis of Viral Infections, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] (F.G.); gloria.griff[email protected] (G.G.); [email protected] (G.G.); [email protected] (S.P.); [email protected] (C.A.) 2 Complex Structure Neonatology Unit, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] * Correspondence: [email protected] These authors contributed equally to this work. y Received: 19 March 2020; Accepted: 5 May 2020; Published: 8 May 2020 Abstract: Human cytomegalovirus (HCMV), a linear double-stranded DNA betaherpesvirus belonging to the family of Herpesviridae, is characterized by widespread seroprevalence, ranging between 56% and 94%, strictly dependent on the socioeconomic background of the country being considered. Typically, HCMV causes asymptomatic infection in the immunocompetent population, while in immunocompromised individuals or when transmitted vertically from the mother to the fetus it leads to systemic disease with severe complications and high mortality rate. Following primary infection, HCMV establishes a state of latency primarily in myeloid cells, from which it can be reactivated by various inflammatory stimuli. Several studies have shown that HCMV, despite being a DNA virus, is highly prone to genetic variability that strongly influences its replication and dissemination rates as well as cellular tropism. In this scenario, the few currently available drugs for the treatment of HCMV infections are characterized by high toxicity, poor oral bioavailability, and emerging resistance. -
Global Mapping of Herpesvirus-‐Host Protein Complexes Reveals a Novel Transcription
Global mapping of herpesvirus-host protein complexes reveals a novel transcription strategy for late genes By Zoe Hartman Davis A dissertation submitted in partial satisfaction of the Requirements for the degree of Doctor of Philosophy in Infectious Disease and Immunity in the Graduate Division of the University of California, Berkeley Committee in charge: Professor Britt A. Glaunsinger, Chair Professor Laurent Coscoy Professor Qiang Zhou Spring 2015 Abstract Global mapping of herpesvirus-host protein complexes reveals a novel transcription strategy for late genes By Zoe Hartman Davis Doctor of Philosophy in Infectious Diseases and Immunity University of California, Berkeley Professor Britt A. Glaunsinger, Chair Mapping host-pathogen interactions has proven instrumental for understanding how viruses manipulate host machinery and how numerous cellular processes are regulated. DNA viruses such as herpesviruses have relatively large coding capacity and thus can target an extensive network of cellular proteins. To identify the host proteins hijacked by this pathogen, we systematically affinity tagged and purified all 89 proteins of Kaposi’s sarcoma-associated herpesvirus (KSHV) from human cells. Mass spectrometry of this material identified over 500 high-confidence virus-host interactions. KSHV causes AIDS-associated cancers and its interaction network is enriched for proteins linked to cancer and overlaps with proteins that are also targeted by HIV-1. This work revealed many new interactions between viral and host proteins. I have focused on one interaction in particular, that of a previously uncharacterized KSHV protein, ORF24, with cellular RNA polymerase II (RNAP II). All DNA viruses encode a class of genes that are expressed only late in the infectious cycle, following replication of the viral genome. -
Broadly Neutralizing Anti- Hiv-1 Antibodies Do Not Inhibit Hiv-1 Env-Mediated Cell-Cell Fusion
bioRxiv preprint doi: https://doi.org/10.1101/2021.06.08.447628; this version posted June 8, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. BROADLY NEUTRALIZING ANTI- HIV-1 ANTIBODIES DO NOT INHIBIT HIV-1 ENV-MEDIATED CELL-CELL FUSION Nejat Düzgüneş*, Michael Yee and Deborah Chau Department of Biomedical Sciences, Arthur A. Dugoni School of Dentistry University of the Pacific, 155 Fifth Street San Francisco, CA 94103, USA ABSTRACT PG9, PG16, PGT121, and PGT145 antibodies were identified from culture media of activated memory B-cells of an infected donor and shown to neutralize many HIV-1 strains. Since HIV-1 spreads via both free virions and cell-cell fusion, we examined the effect of the antibodies on HIV-1 Env-mediated cell-cell fusion. Clone69TRevEnv cells that express Env in the absence of tetracycline were labeled with Calcein-AM Green, and incubated with CD4+ SupT1 cells labeled with CellTrace™ Calcein Red-Orange, with or without antibodies. Monoclonal antibodies PG9, PG16, 2G12, PGT121, and PGT145 (at up to 50 µg/mL) had little or no inhibitory effect on fusion between HIV-Env and SupT1 cells. By contrast, Hippeastrum hybrid agglutinin completely inhibited fusion. Our results indicate that transmission of the virus or viral genetic material would not be inhibited by these broadly neutralizing antibodies. Thus, antibodies generated by HIV-1 vaccines should be screened for their inhibitory effect on Env-mediated cell-cell fusion. -
Evaluating the Role of CRM1-Mediated Export for Adenovirus Gene Expression
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Available online at www.sciencedirect.com R Virology 315 (2003) 224–233 www.elsevier.com/locate/yviro Evaluating the role of CRM1-mediated export for adenovirus gene expression Christoph C. Carter,1 Reza Izadpanah, and Eileen Bridge* Department of Microbiology, 32 Pearson Hall, Miami University, Oxford, OH 45056, USA Received 25 March 2003; accepted 30 June 2003 Abstract A complex of the Adenovirus (Ad) early region 1b 55-kDa (E1b-55kDa) and early region 4 ORF6 34-kDa (E4-34kDa) proteins promotes viral late gene expression. E1b-55kDa and E4-34kDa have leucine-rich nuclear export signals (NESs) similar to that of HIV Rev. It was proposed that E1b-55kDa and/or E4-34kDa might promote the export of Ad late mRNA via their Rev-like NESs, and the transport receptor CRM1. We treated infected cells with the cytotoxin leptomycin B to inhibit CRM1-mediated export; treatment initially delays the onset of late gene expression, but this activity completely recovers as the late phase progresses. We find that the E1b-55kDa NES is not required to promote late gene expression. Previous results showed that E4-34kDa-mediated late gene expression does not require an intact NES (J. Virol. 74 (2000), 6684–6688). Our results indicate that these Ad regulatory proteins promote late gene expression without intact NESs or active CRM1. © 2003 Elsevier Inc. All rights reserved. Keywords: Adenovirus; E1b 55kDa; CRM1; Leptomycin B; E4; RNA export; NES Introduction RNP through the nuclear pore complex (reviewed by Cullen, 2000). -
Human Cytomegalovirus Primary Infection and Reactivation: Insights from Virion-Carried Molecules
fmicb-11-01511 July 16, 2020 Time: 8:16 # 1 REVIEW published: 14 July 2020 doi: 10.3389/fmicb.2020.01511 Human Cytomegalovirus Primary Infection and Reactivation: Insights From Virion-Carried Molecules Yu-Qing Wang1,2 and Xiang-Yu Zhao1* 1 Peking University People’s Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Key Laboratory of Hematopoietic Stem Cell Transplantation, Beijing, China, 2 PKU-THU Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China Human cytomegalovirus (HCMV), a ubiquitous beta-herpesvirus, is able to establish lifelong latency after initial infection. Periodical reactivation occurs after immunosuppression, remaining a major cause of death in immunocompromised patients. HCMV has to reach a structural and functional balance with the host at Edited by: its earliest entry. Virion-carried mediators are considered to play pivotal roles in viral Akio Adachi, adaptation into a new cellular environment upon entry. Additionally, one clear difference Kansai Medical University, Japan between primary infection and reactivation is the idea that virion-packaged factors are Reviewed by: Eain Anthony Murphy, already formed such that those molecules can be used swiftly by the virus. In contrast, SUNY Upstate Medical University, virion-carried mediators have to be transcribed and translated; thus, they are not readily United States Sarah Elizabeth Jackson, available during reactivation. Hence, understanding virion-carried -
Review Article DNA Oncogenic Virus-Induced Oxidative Stress, Genomic Damage, and Aberrant Epigenetic Alterations
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Crossref Hindawi Oxidative Medicine and Cellular Longevity Volume 2017, Article ID 3179421, 16 pages https://doi.org/10.1155/2017/3179421 Review Article DNA Oncogenic Virus-Induced Oxidative Stress, Genomic Damage, and Aberrant Epigenetic Alterations 1 1 2 Mankgopo Magdeline Kgatle, Catherine Wendy Spearman, Asgar Ali Kalla, and 1 Henry Norman Hairwadzi 1Division of Hepatology, Department of Medicine, Faculty of Health Sciences, Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa 2Division of Rheumatology, Department of Medicine, Faculty of Health Sciences, Groote Schuur Hospital, Cape Town, South Africa Correspondence should be addressed to Mankgopo Magdeline Kgatle; [email protected] Received 27 January 2017; Revised 1 May 2017; Accepted 23 May 2017; Published 27 June 2017 Academic Editor: Peeter Karihtala Copyright © 2017 Mankgopo Magdeline Kgatle et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Approximately 20% of human cancers is attributable to DNA oncogenic viruses such as human papillomavirus (HPV), hepatitis B virus (HBV), and Epstein-Barr virus (EBV). Unrepaired DNA damage is the most common and overlapping feature of these DNA oncogenic viruses and a source of genomic instability and tumour development. Sustained DNA damage results from unceasing production of reactive oxygen species and activation of inflammasome cascades that trigger genomic changes and increased propensity of epigenetic alterations. Accumulation of epigenetic alterations may interfere with genome-wide cellular signalling machineries and promote malignant transformation leading to cancer development. -
Viral Epigenomes in Human Tumorigenesis
Oncogene (2010) 29, 1405–1420 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 $32.00 www.nature.com/onc REVIEW Viral epigenomes in human tumorigenesis AF Fernandez1 and M Esteller1,2 1Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Catalonia, Spain and 2Institucio Catalana de Recerca i Estudis Avanc¸ats (ICREA), Barcelona, Catalonia, Spain Viruses are associated with 15–20% of human cancers is altered in cancer (Fraga and Esteller, 2005; Chuang worldwide. In the last century, many studies were directed and Jones, 2007; Lujambio et al., 2007). towards elucidating the molecular mechanisms and genetic DNA methylation mainly occurs on cytosines that alterations by which viruses cause cancer. The importance precede guanines to yield 5-methylcytosine; these of epigenetics in the regulation of gene expression has dinucleotide sites are usually referred to as CpGs prompted the investigation of virus and host interactions (Herman and Baylin, 2003). CpGs are asymmetrically not only at the genetic level but also at the epigenetic level. distributed into CpG-poor regions and dense regions In this study, we summarize the published epigenetic called ‘CpG islands’, which are located in the promoter information relating to the genomes of viruses directly or regions of approximately half of all genes. These CpG indirectly associated with the establishment of tumori- islands are usually unmethylated in normal cells, with genic processes. We also review aspects such as viral the exceptions listed below, whereas the sporadic CpG replication and latency associated with epigenetic changes sites in the rest of the genome are generally methylated and summarize what is known about epigenetic alterations (Jones and Takai, 2001). -
Herpesviral Latency—Common Themes
pathogens Review Herpesviral Latency—Common Themes Magdalena Weidner-Glunde * , Ewa Kruminis-Kaszkiel and Mamata Savanagouder Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Tuwima Str. 10, 10-748 Olsztyn, Poland; [email protected] (E.K.-K.); [email protected] (M.S.) * Correspondence: [email protected] Received: 22 January 2020; Accepted: 14 February 2020; Published: 15 February 2020 Abstract: Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.