Marek’s Disease Virus

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Virology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 30296

Special Issue Editors

Department of Animal and Food Sciences, University of Delaware, Newark, DE 19716, USA
Interests: MDV; meq; lymphomagenesis; vaccine development; immune patterning; avian immunology
Institute of Virology, Freie Universität Berlin, 14163 Berlin, Germany
Interests: MDV; viroimmunology; lymphocytes; avian immunology; antivirals
Special Issues, Collections and Topics in MDPI journals
Institute of Virology, Freie Universität Berlin, 14163 Berlin, Germany
Interests: MDV; tumorigenesis; telomere integration; viral telomerase RNA; viral chemokines; HHV-6; VZV
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Marek’s disease virus (MDV) is a highly oncogenic alphaherpesvirus of chickens and an enormous burden to poultry production worldwide. Despite the control of losses due to Marek’s disease through the widespread use of vaccines, MDV remains a major threat to chickens and field strains have increased in virulence over the past decades. MDV research has led to a profound increase in knowledge of virus-induced pathogenesis and tumor development. However, a more detailed and mechanistic understanding of viral and host factors that contribute to virus replication and pathogenesis, as well as the development of new vaccines and antiviral strategies, are needed to better protect chickens from this deadly disease in the future. This Special Issue will publish manuscripts that provide deeper insights into important aspects of MDV infection, lytic replication, latency, pathogenesis, and immune system interactions, as well as a greater understanding of the evolution of increased virulence of MDV field strains.

We’re looking forward to your contributions!

Prof. Dr. Mark S. Parcells
Dr. Luca D. Bertzbach
Prof. Dr. Benedikt B. Kaufer
Guest Editors

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Keywords

  • Marek’s disease virus
  • alphaherpesvirus replication
  • tumorigenesis
  • telomere integration
  • immunosuppression
  • imperfect vaccination

Published Papers (12 papers)

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Editorial

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2 pages, 172 KiB  
Editorial
A Special Issue on Marek’s Disease Virus—The Editors’ View
by Benedikt B. Kaufer, Mark S. Parcells and Luca D. Bertzbach
Microorganisms 2023, 11(3), 805; https://doi.org/10.3390/microorganisms11030805 - 21 Mar 2023
Viewed by 1151
Abstract
Marek’s disease virus (MDV), an Alphaherpesvirus belonging to the genus Mardivirus, causes T cell lymphomas in chickens and remains one of the greatest threats to poultry production worldwide [...] Full article
(This article belongs to the Special Issue Marek’s Disease Virus)

Research

Jump to: Editorial, Review

15 pages, 1717 KiB  
Article
Identification and Validation of Ikaros (IKZF1) as a Cancer Driver Gene for Marek’s Disease Virus-Induced Lymphomas
by Alec Steep, Evin Hildebrandt, Hongen Xu, Cari Hearn, Dmitrij Frishman, Masahiro Niikura, John R. Dunn, Taejoong Kim, Steven J. Conrad, William M. Muir and Hans H. Cheng
Microorganisms 2022, 10(2), 401; https://doi.org/10.3390/microorganisms10020401 - 09 Feb 2022
Cited by 4 | Viewed by 2154
Abstract
Marek’s disease virus (MDV) is the causative agent for Marek’s disease (MD), which is characterized by T-cell lymphomas in chickens. While the viral Meq oncogene is necessary for transformation, it is insufficient, as not every bird infected with virulent MDV goes on to [...] Read more.
Marek’s disease virus (MDV) is the causative agent for Marek’s disease (MD), which is characterized by T-cell lymphomas in chickens. While the viral Meq oncogene is necessary for transformation, it is insufficient, as not every bird infected with virulent MDV goes on to develop a gross tumor. Thus, we postulated that the chicken genome contains cancer driver genes; i.e., ones with somatic mutations that promote tumors, as is the case for most human cancers. To test this hypothesis, MD tumors and matching control tissues were sequenced. Using a custom bioinformatics pipeline, 9 of the 22 tumors analyzed contained one or more somatic mutation in Ikaros (IKFZ1), a transcription factor that acts as the master regulator of lymphocyte development. The mutations found were in key Zn-finger DNA-binding domains that also commonly occur in human cancers such as B-cell acute lymphoblastic leukemia (B-ALL). To validate that IKFZ1 was a cancer driver gene, recombinant MDVs that expressed either wild-type or a mutated Ikaros allele were used to infect chickens. As predicted, birds infected with MDV expressing the mutant Ikaros allele had high tumor incidences (~90%), while there were only a few minute tumors (~12%) produced in birds infected with the virus expressing wild-type Ikaros. Thus, in addition to Meq, key somatic mutations in Ikaros or other potential cancer driver genes in the chicken genome are necessary for MDV to induce lymphomas. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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11 pages, 763 KiB  
Article
Deletion of the Viral Thymidine Kinase in a Meq-Deleted Recombinant Marek’s Disease Virus Reduces Lymphoid Atrophy but Is Less Protective
by Steven J. Conrad, Eniope B. Oluwayinka, Mohammad Heidari, Jody K. Mays and John R. Dunn
Microorganisms 2022, 10(1), 7; https://doi.org/10.3390/microorganisms10010007 - 22 Dec 2021
Cited by 1 | Viewed by 2329
Abstract
Marek’s disease (MD) is a ubiquitous disease of domesticated chickens and its etiologic agent is the Gallid alphaherpesvirus 2 (GaHV-2), also known as Marek’s disease virus (MDV). MD is currently controlled by vaccination using live attenuated strains of MDV (e.g., CVI988/Rispens), non-pathogenic serotypes [...] Read more.
Marek’s disease (MD) is a ubiquitous disease of domesticated chickens and its etiologic agent is the Gallid alphaherpesvirus 2 (GaHV-2), also known as Marek’s disease virus (MDV). MD is currently controlled by vaccination using live attenuated strains of MDV (e.g., CVI988/Rispens), non-pathogenic serotypes of MDV (GaHV-3), or non-pathogenic strains of the related Melagrid alphaherpesvirus 1 (MeHV-1). One attractive strategy for the production of new vaccine strains is a recombinant MDV attenuated by the deletion of the major viral oncogene meq. However, meq-deleted variants of MDV cause atrophy of the bursa and thymus in maternal antibody-negative chickens, and the resulting immunosuppression makes them unsuitable. Herein we detail our attempt to mitigate the lymphoid atrophy caused by meq-deleted MDV by further attenuation of the virus through ablation of the viral thymidine kinase (tk) gene. We demonstrate that ablation of the viral tk from the meq-deleted virus rMd5B40/Δmeq resulted in a virus attenuated for replication in vitro and which spared chickens from atrophy of the lymphoid organs in vivo. When the rMd5B40/Δmeqtk/GFP was used as a vaccine it was protective against challenge with the vv+MDV strain 686, but the protection was less than that provided by the CVI988/Rispens vaccine. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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11 pages, 1141 KiB  
Communication
A Cell Culture System to Investigate Marek’s Disease Virus Integration into Host Chromosomes
by Yu You, Tereza Vychodil, Giulia Aimola, Renato L. Previdelli, Thomas W. Göbel, Luca D. Bertzbach and Benedikt B. Kaufer
Microorganisms 2021, 9(12), 2489; https://doi.org/10.3390/microorganisms9122489 - 01 Dec 2021
Cited by 5 | Viewed by 2131
Abstract
Marek’s disease virus (MDV) is a highly oncogenic alphaherpesvirus that causes a devastating neoplastic disease in chickens. MDV has been shown to integrate its genome into the telomeres of latently infected and tumor cells, which is crucial for efficient tumor formation. Telomeric repeat [...] Read more.
Marek’s disease virus (MDV) is a highly oncogenic alphaherpesvirus that causes a devastating neoplastic disease in chickens. MDV has been shown to integrate its genome into the telomeres of latently infected and tumor cells, which is crucial for efficient tumor formation. Telomeric repeat arrays present at the ends of the MDV genome facilitate this integration into host telomeres; however, the integration mechanism remains poorly understood. Until now, MDV integration could only be investigated qualitatively upon infection of chickens. To shed further light on the integration mechanism, we established a quantitative integration assay using chicken T cell lines, the target cells for MDV latency and transformation. We optimized the infection conditions and assessed the establishment of latency in these T cells. The MDV genome was efficiently maintained over time, and integration was confirmed in these cells by fluorescence in situ hybridization (FISH). To assess the role of the two distinct viral telomeric repeat arrays in the integration process, we tested various knockout mutants in our in vitro integration assay. Efficient genome maintenance and integration was thereby dependent on the presence of the telomeric repeat arrays in the virus genome. Taken together, we developed and validated a novel in vitro integration assay that will shed light on the integration mechanism of this highly oncogenic virus into host telomeres. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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16 pages, 2195 KiB  
Article
CRISPR-Mediated Gene Activation (CRISPRa) of pp38/pp24 Orchestrates Events Triggering Lytic Infection in Marek’s Disease Virus-Transformed Cell Lines
by Poornima Roy, Katy Moffat, Venugopal Nair and Yongxiu Yao
Microorganisms 2021, 9(8), 1681; https://doi.org/10.3390/microorganisms9081681 - 08 Aug 2021
Cited by 5 | Viewed by 2795
Abstract
Marek’s disease (MD) is an immunosuppressive and highly contagious lymphoproliferative disease caused by Marek’s disease virus (MDV) in poultry. Lymphoblastoid cell lines (LCLs) generated ex vivo from MD lymphomas are considered excellent models to study virus-host molecular interactions. LCLs mostly have latently infected [...] Read more.
Marek’s disease (MD) is an immunosuppressive and highly contagious lymphoproliferative disease caused by Marek’s disease virus (MDV) in poultry. Lymphoblastoid cell lines (LCLs) generated ex vivo from MD lymphomas are considered excellent models to study virus-host molecular interactions. LCLs mostly have latently infected MDV genome, but many of them also have varying populations of lytically-infected cells, thus making them very suitable to examine the molecular events associated with the switch from latent to lytic infection. MDV-encoded phosphoprotein 38 (pp38) is readily detectable in lytically-infected LCLs and hence considered as a biomarker for lytic infection. Whilst previous studies have suggested that pp38 is essential for the early cytolytic infection of B-cells, its role in the switch from latent to lytic infection of LCLs is still unclear. pp24, another phosphorylated protein in the same protein complex, shares the same promoter and N-terminal 65 amino acids as pp38. In this study we employed CRISPR activation (CRISPRa) technology for targeted activation of pp38/pp24 in LCLs to investigate their role in inducing lytic infection. Our results show that enforced expression of pp38/pp24 through CRISPRa induces orchestrated upregulation of other MDV genes including ICP4, gB, Meq and pp14 as well as differential expression of host genes thereby facilitating lytic infection. Our results also show that pp38/pp24 expression induces the lytic switch through inhibiting apoptosis. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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12 pages, 1750 KiB  
Article
Characterization of a Novel Viral Interleukin 8 (vIL-8) Splice Variant Encoded by Marek’s Disease Virus
by Yu You, Ibrahim T. Hagag, Ahmed Kheimar, Luca D. Bertzbach and Benedikt B. Kaufer
Microorganisms 2021, 9(7), 1475; https://doi.org/10.3390/microorganisms9071475 - 09 Jul 2021
Cited by 1 | Viewed by 3166
Abstract
Marek’s disease virus (MDV) is a highly cell-associated oncogenic alphaherpesvirus that causes lymphomas in various organs in chickens. Like other herpesviruses, MDV has a large and complex double-stranded DNA genome. A number of viral transcripts are generated by alternative splicing, a process that [...] Read more.
Marek’s disease virus (MDV) is a highly cell-associated oncogenic alphaherpesvirus that causes lymphomas in various organs in chickens. Like other herpesviruses, MDV has a large and complex double-stranded DNA genome. A number of viral transcripts are generated by alternative splicing, a process that drastically extends the coding capacity of the MDV genome. One of the spliced genes encoded by MDV is the viral interleukin 8 (vIL-8), a CXC chemokine that facilitates the recruitment of MDV target cells and thereby plays an important role in MDV pathogenesis and tumorigenesis. We recently identified a novel vIL-8 exon (vIL-8-E3′) by RNA-seq; however, it remained elusive whether the protein containing the vIL-8-E3′ is expressed and what role it may play in MDV replication and/or pathogenesis. To address these questions, we first generated recombinant MDV harboring a tag that allows identification of the spliced vIL-8-E3′ protein, revealing that it is indeed expressed. We subsequently generated knockout viruses and could demonstrate that the vIL-8-E3′ protein is dispensable for MDV replication as well as secretion of the functional vIL-8 chemokine. Finally, infection of chickens with this vIL-8-E3′ knockout virus revealed that the protein is not important for MDV replication and pathogenesis in vivo. Taken together, our study provides novel insights into the splice forms of the CXC chemokine of this highly oncogenic alphaherpesvirus. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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23 pages, 4483 KiB  
Article
Epigenetic Silencing of MicroRNA-126 Promotes Cell Growth in Marek’s Disease
by Isabelle Gennart, Astrid Petit, Laetitia Wiggers, Srđan Pejaković, Nicolas Dauchot, Sylvie Laurent, Damien Coupeau and Benoît Muylkens
Microorganisms 2021, 9(6), 1339; https://doi.org/10.3390/microorganisms9061339 - 21 Jun 2021
Cited by 2 | Viewed by 2426
Abstract
During latency, herpesvirus infection results in the establishment of a dormant state in which a restricted set of viral genes are expressed. Together with alterations of the viral genome, several host genes undergo epigenetic silencing during latency. These epigenetic dysregulations of cellular genes [...] Read more.
During latency, herpesvirus infection results in the establishment of a dormant state in which a restricted set of viral genes are expressed. Together with alterations of the viral genome, several host genes undergo epigenetic silencing during latency. These epigenetic dysregulations of cellular genes might be involved in the development of cancer. In this context, Gallid alphaherpesvirus 2 (GaHV-2), causing Marek’s disease (MD) in susceptible chicken, was shown to impair the expression of several cellular microRNAs (miRNAs). We decided to focus on gga-miR-126, a host miRNA considered a tumor suppressor through signaling pathways controlling cell proliferation. Our objectives were to analyze the cause and the impact of miR-126 silencing during GaHV-2 infection. This cellular miRNA was found to be repressed at crucial steps of the viral infection. In order to determine whether miR-126 low expression level was associated with specific epigenetic signatures, DNA methylation patterns were established in the miR-126 gene promoter. Repression was associated with hypermethylation at a CpG island located in the miR-126 host gene epidermal growth factor like-7 (EGFL-7). A strategy was developed to conditionally overexpress miR-126 and control miRNAs in transformed CD4+ T cells propagated from Marek’s disease (MD) lymphoma. This functional assay showed that miR-126 restoration specifically diminishes cell proliferation. We identified CT10 regulator of kinase (CRK), an adaptor protein dysregulated in several human malignancies, as a candidate target gene. Indeed, CRK protein levels were markedly reduced by the miR-126 restoration. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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9 pages, 30251 KiB  
Communication
US3 Serine/Threonine Protein Kinase from MDV-1, MDV-2, and HVT Differentially Regulate Viral Gene Expression and Replication
by Yifei Liao, Xin Fang, Mohammad AI-Mahmood, Qinglei Li, Blanca Lupiani and Sanjay M. Reddy
Microorganisms 2021, 9(4), 785; https://doi.org/10.3390/microorganisms9040785 - 09 Apr 2021
Cited by 3 | Viewed by 2199
Abstract
Gallid alphaherpesvirus 2 (GaHV-2), commonly known as Marek’s disease virus type 1 (MDV-1), is an oncogenic avian alphaherpesvirus, and along with its close relatives—Gallid alphaherpesvirus 3 (GaHV-3) or MDV-2 and Meleagrid alphaherpesvirus 1 (MeHV-1) or turkey herpesvirus (HVT)—belongs to the Mardivirus genus. [...] Read more.
Gallid alphaherpesvirus 2 (GaHV-2), commonly known as Marek’s disease virus type 1 (MDV-1), is an oncogenic avian alphaherpesvirus, and along with its close relatives—Gallid alphaherpesvirus 3 (GaHV-3) or MDV-2 and Meleagrid alphaherpesvirus 1 (MeHV-1) or turkey herpesvirus (HVT)—belongs to the Mardivirus genus. We and others previously showed that MDV-1 US3 protein kinase plays an important role in viral replication and pathogenesis, which could be partially compensated by MDV-2 and HVT US3. In this study, we further studied the differential roles of MDV-1, MDV-2 and HVT US3 in regulating viral gene expression and replication. Our results showed that MDV-2 and HVT US3 could differentially compensate MDV-1 US3 regulation of viral gene expression in vitro. MDV-2 and HVT US3 could also partially rescue the replication deficiency of MDV-1 US3 null virus in the spleen and thymus, as determined by immunohistochemistry analysis of MDV-1 pp38 protein. Importantly, using immunohistochemistry and dual immunofluorescence assays, we found that MDV-2 US3, but not HVT US3, fully compensated MDV-1 US3 regulation of MDV-1 replication in bursal B lymphocytes. In conclusion, our study provides the first comparative analysis of US3 from MDV-1, MDV-2 and HVT in regulating viral gene expression in cell culture and MDV-1 replication in lymphocytes. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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7 pages, 13551 KiB  
Communication
Manipulation of Promyelocytic Leukemia Protein Nuclear Bodies by Marek’s Disease Virus Encoded US3 Protein Kinase
by Yifei Liao, Blanca Lupiani and Sanjay M. Reddy
Microorganisms 2021, 9(4), 685; https://doi.org/10.3390/microorganisms9040685 - 26 Mar 2021
Cited by 4 | Viewed by 1800
Abstract
Promyelocytic leukemia protein nuclear bodies (PML-NBs) are dynamic nuclear structures, shown to be important for herpesvirus replication; however, their role in regulating Marek’s disease virus (MDV) infection has not been studied. MDV is an oncogenic alphaherpesvirus that causes lymphoproliferative disease in chickens. MDV [...] Read more.
Promyelocytic leukemia protein nuclear bodies (PML-NBs) are dynamic nuclear structures, shown to be important for herpesvirus replication; however, their role in regulating Marek’s disease virus (MDV) infection has not been studied. MDV is an oncogenic alphaherpesvirus that causes lymphoproliferative disease in chickens. MDV encodes a US3 serine/threonine protein kinase that is important for MDV replication and gene expression. In this study, we studied the role of MDV US3 in regulating PML-NBs. Using an immunofluorescence assay, we found that MDV US3 disrupts PML and SP100 in a kinase dependent manner. In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100. These findings provide the first evidence for the interplay between MDV proteins and PML-NBs. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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17 pages, 1940 KiB  
Article
In Vivo Inhibition of Marek’s Disease Virus in Transgenic Chickens Expressing Cas9 and gRNA against ICP4
by Arjun Challagulla, Kristie A. Jenkins, Terri E. O’Neil, Shunning Shi, Kirsten R. Morris, Terry G. Wise, Prasad N. Paradkar, Mark L. Tizard, Timothy J. Doran and Karel A. Schat
Microorganisms 2021, 9(1), 164; https://doi.org/10.3390/microorganisms9010164 - 13 Jan 2021
Cited by 19 | Viewed by 3044
Abstract
Marek’s disease (MD), caused by MD herpesvirus (MDV), is an economically important disease in chickens. The efficacy of the existing vaccines against evolving virulent stains may become limited and necessitates the development of novel antiviral strategies to protect poultry from MDV strains with [...] Read more.
Marek’s disease (MD), caused by MD herpesvirus (MDV), is an economically important disease in chickens. The efficacy of the existing vaccines against evolving virulent stains may become limited and necessitates the development of novel antiviral strategies to protect poultry from MDV strains with increased virulence. The CRISPR/Cas9 system has emerged as a powerful genome editing tool providing an opportunity to develop antiviral strategies for the control of MDV infection. Here, we characterized Tol2 transposon constructs encoding Cas9 and guide RNAs (gRNAs) specific to the immediate early infected-cell polypeptide-4 (ICP4) of MDV. We generated transgenic chickens that constitutively express Cas9 and ICP4-gRNAs (gICP4) and challenged them via intraabdominal injection of MDV-1 Woodlands strain passage-19 (p19). Transgenic chickens expressing both gRNA/Cas9 had a significantly reduced replication of MDV in comparison to either transgenic Cas9-only or the wild-type (WT) chickens. We further confirmed that the designed gRNAs exhibited sequence-specific virus interference in transgenic chicken embryo fibroblast (CEF) expressing Cas9/gICP4 when infected with MDV but not with herpesvirus of turkeys (HVT). These results suggest that CRISPR/Cas9 can be used as an antiviral approach to control MDV infection in chickens, allowing HVT to be used as a vector for recombinant vaccines. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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13 pages, 2816 KiB  
Article
Mardivirus Infection and Persistence in Feathers of a Chicken Model Harboring a Local Autoimmune Response
by Gisela F. Erf, Gilles Le Pape, Sylvie Rémy and Caroline Denesvre
Microorganisms 2020, 8(10), 1613; https://doi.org/10.3390/microorganisms8101613 - 20 Oct 2020
Cited by 1 | Viewed by 1989
Abstract
Herpesvirus of turkey (HVT) is commonly used as a vaccine to protect chickens against Marek’s disease. Following vaccination, HVT infects feathers where it can be detected in all chicken lines examined. Unlike the parental Brown line (BL), Smyth line (SL) chickens develop vitiligo, [...] Read more.
Herpesvirus of turkey (HVT) is commonly used as a vaccine to protect chickens against Marek’s disease. Following vaccination, HVT infects feathers where it can be detected in all chicken lines examined. Unlike the parental Brown line (BL), Smyth line (SL) chickens develop vitiligo, due to autoimmune destruction of melanocytes in feathers. Previous reports showed a strong inflammatory response in Smyth chickens’ feathers at vitiligo onset, that subsided once melanocytes were destroyed, and depigmentation was complete. Here, we questioned whether the local autoimmune response in the Smyth model influences HVT infection and persistence in feathers. For this, one-day-old SL and BL chickens were vaccinated with Newcastle disease (rHVT-ND). Vitiligo was scored and HVT loads in pigmented and non-pigmented growing feathers were quantified regularly over 20 weeks. Chickens of both lines showed moderate HVT loads in feathers. At the onset of active vitiligo, the HVT load was significantly higher in SL compared to BL feathers. However, no difference in HVT loads was noticed between pigmented and non-pigmented feathers from SL chickens. Therefore, surprisingly, the inflammatory response in feathers of SL chickens did not inhibit HVT infection and persistence, but on the contrary, temporarily promoted HVT infection in feathers. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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Review

Jump to: Editorial, Research

17 pages, 1429 KiB  
Review
Methods for the Manipulation of Herpesvirus Genome and the Application to Marek’s Disease Virus Research
by Yifei Liao, Kanika Bajwa, Sanjay M. Reddy and Blanca Lupiani
Microorganisms 2021, 9(6), 1260; https://doi.org/10.3390/microorganisms9061260 - 10 Jun 2021
Cited by 3 | Viewed by 3018
Abstract
Herpesviruses are a group of double-strand DNA viruses that infect a wide range of hosts, including humans and animals. In the past decades, numerous methods have been developed to manipulate herpesviruses genomes, from the introduction of random mutations to specific genome editing. The [...] Read more.
Herpesviruses are a group of double-strand DNA viruses that infect a wide range of hosts, including humans and animals. In the past decades, numerous methods have been developed to manipulate herpesviruses genomes, from the introduction of random mutations to specific genome editing. The development of genome manipulation methods has largely advanced the study of viral genes function, contributing not only to the understanding of herpesvirus biology and pathogenesis, but also the generation of novel vaccines and therapies to control and treat diseases. In this review, we summarize the major methods of herpesvirus genome manipulation with emphasis in their application to Marek’s disease virus research. Full article
(This article belongs to the Special Issue Marek’s Disease Virus)
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