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Article ; Online: HCMV-secreted glycoprotein gpUL4 inhibits TRAIL-mediated apoptosis and NK cell activation.

Vlachava, Virginia-Maria / Seirafian, Sepehr / Fielding, Ceri A / Kollnberger, Simon / Aicheler, Rebecca J / Hughes, Joseph / Baker, Alexander / Weekes, Michael P / Forbes, Simone / Wilkinson, Gavin W G / Wang, Eddie C Y / Stanton, Richard J

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 49, Page(s) e2309077120

Abstract: Human cytomegalovirus (HCMV) is a paradigm of pathogen immune evasion and sustains lifelong persistent infection in the face of exceptionally powerful host immune responses through the concerted action of multiple immune-evasins. These reduce NK cell ... ...

Abstract	Human cytomegalovirus (HCMV) is a paradigm of pathogen immune evasion and sustains lifelong persistent infection in the face of exceptionally powerful host immune responses through the concerted action of multiple immune-evasins. These reduce NK cell activation by inhibiting ligands for activating receptors, expressing ligands for inhibitory receptors, or inhibiting synapse formation. However, these functions only inhibit direct interactions with the infected cell. To determine whether the virus also expresses soluble factors that could modulate NK function at a distance, we systematically screened all 170 HCMV canonical protein-coding genes. This revealed that UL4 encodes a secreted and heavily glycosylated protein (gpUL4) that is expressed with late-phase kinetics and is capable of inhibiting NK cell degranulation. Analyses of gpUL4 binding partners by mass spectrometry identified an interaction with TRAIL. gpUL4 bound TRAIL with picomolar affinity and prevented TRAIL from binding its receptor, thus acting as a TRAIL decoy receptor. TRAIL is found in both soluble and membrane-bound forms, with expression of the membrane-bound form strongly up-regulated on NK cells in response to interferon. gpUL4 inhibited apoptosis induced by soluble TRAIL, while also binding to the NK cell surface in a TRAIL-dependent manner, where it blocked NK cell degranulation and cytokine secretion. gpUL4 therefore acts as an immune-evasin by inhibiting both soluble and membrane-bound TRAIL and is a viral-encoded TRAIL decoy receptor. Interestingly, gpUL4 could also suppress NK responses to heterologous viruses, suggesting that it may act as a systemic virally encoded immunosuppressive agent.
MeSH term(s)	Humans ; Cytomegalovirus/physiology ; Killer Cells, Natural ; Immune Evasion ; Glycoproteins/metabolism ; Apoptosis
Chemical Substances	Glycoproteins
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2309077120
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Article ; Online: ADAM17 targeting by human cytomegalovirus remodels the cell surface proteome to simultaneously regulate multiple immune pathways.

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 33, Page(s) e2303155120

Abstract: Human cytomegalovirus (HCMV) is a major human pathogen whose life-long persistence is enabled by its remarkable capacity to systematically subvert host immune defenses. In exploring the finding that HCMV infection up-regulates tumor necrosis factor ... ...

Abstract	Human cytomegalovirus (HCMV) is a major human pathogen whose life-long persistence is enabled by its remarkable capacity to systematically subvert host immune defenses. In exploring the finding that HCMV infection up-regulates tumor necrosis factor receptor 2 (TNFR2), a ligand for the pro-inflammatory antiviral cytokine TNFα, we found that the underlying mechanism was due to targeting of the protease, A Disintegrin And Metalloproteinase 17 (ADAM17). ADAM17 is the prototype 'sheddase', a family of proteases that cleaves other membrane-bound proteins to release biologically active ectodomains into the supernatant. HCMV impaired ADAM17 surface expression through the action of two virally-encoded proteins in its U
MeSH term(s)	Humans ; Cytomegalovirus/physiology ; Tumor Necrosis Factor-alpha/metabolism ; Proteome/metabolism ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Proteomics ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Cytokines/metabolism ; Cell Membrane/metabolism ; Metalloproteases/metabolism ; ADAM17 Protein/genetics ; ADAM17 Protein/metabolism ; Membrane Glycoproteins/metabolism ; Viral Proteins/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; Proteome ; Receptors, Tumor Necrosis Factor, Type II ; Membrane Proteins ; Cytokines ; Metalloproteases (EC 3.4.-) ; ADAM17 Protein (EC 3.4.24.86) ; UL144 ORF protein, Human herpesvirus 5 ; Membrane Glycoproteins ; Viral Proteins ; ADAM17 protein, human (EC 3.4.24.86) ; UL148 protein, human cytomegalovirus
Language	English
Publishing date	2023-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2303155120
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Article ; Online: Educational impact of early COVID-19 operating room restrictions on neurosurgery resident training in the United States: A multicenter study.

North American Spine Society journal

2022 Volume 9, Page(s) 100104

Abstract: Background: The coronavirus (COVID-19) pandemic has caused unprecedented suspensions of neurosurgical elective surgeries, a large proportion of which involve spine procedures. The goal of this study is to report granular data on the impact of early ... ...

Abstract	Background: The coronavirus (COVID-19) pandemic has caused unprecedented suspensions of neurosurgical elective surgeries, a large proportion of which involve spine procedures. The goal of this study is to report granular data on the impact of early COVID-19 pandemic operating room restrictions upon neurosurgical case volume in academic institutions, with attention to its secondary impact upon neurosurgery resident training. This is the first multicenter quantitative study examining these early effects upon neurosurgery residents caseloads. Methods: A retrospective review of neurosurgical caseloads among seven residency programs between March 2019 and April 2020 was conducted. Cases were grouped by ACGME Neurosurgery Case Categories, subspecialty, and urgency (elective vs. emergent). Residents caseloads were stratified into junior (PGY1-3) and senior (PGY4-7) levels. Descriptive statistics are reported for individual programs and pooled across institutions. Results: When pooling across programs, the 2019 monthly mean (SD) case volume was 214 (123) cases compared to 217 (129) in January 2020, 210 (115) in February 2020, 157 (81), in March 2020 and 82 (39) cases April 2020. There was a 60% reduction in caseload between April 2019 (207 [101]) and April 2020 (82 [39]). Adult spine cases were impacted the most in the pooled analysis, with a 66% decrease in the mean number of cases between March 2020 and April 2020. Both junior and senior residents experienced a similar steady decrease in caseloads, with the largest decreases occurring between March and April 2020 (48% downtrend). Conclusions: Results from our multicenter study reveal considerable decreases in caseloads in the neurosurgical specialty with elective adult spine cases experiencing the most severe decline. Both junior and senior neurosurgical residents experienced dramatic decreases in case volumes during this period. With the steep decline in elective spine cases, it is possible that fellowship directors may see a disproportionate increase in spine fellowships in the coming years. In the face of the emerging Delta and Omicron variants, programs should pay attention toward identifying institution-specific deficiencies and developing plans to mitigate the negative educational effects secondary to such caseloads reduction.
Language	English
Publishing date	2022-02-19
Publishing country	United States
Document type	Journal Article
ISSN	2666-5484
ISSN (online)	2666-5484
DOI	10.1016/j.xnsj.2022.100104
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Article ; Online: Genetic Stability of Bacterial Artificial Chromosome-Derived Human Cytomegalovirus during Culture In Vitro.

Murrell, Isa / Wilkie, Gavin S / Davison, Andrew J / Statkute, Evelina / Fielding, Ceri A / Tomasec, Peter / Wilkinson, Gavin W G / Stanton, Richard J

Journal of virology

2016 Volume 90, Issue 8, Page(s) 3929–3943

Abstract: Unlabelled: Clinical human cytomegalovirus (HCMV) strains invariably mutate when propagatedin vitro Mutations in gene RL13 are selected in all cell types, whereas in fibroblasts mutants in the UL128 locus (UL128L; genes UL128, UL130, and UL131A) are ... ...

Abstract	Unlabelled: Clinical human cytomegalovirus (HCMV) strains invariably mutate when propagatedin vitro Mutations in gene RL13 are selected in all cell types, whereas in fibroblasts mutants in the UL128 locus (UL128L; genes UL128, UL130, and UL131A) are also selected. In addition, sporadic mutations are selected elsewhere in the genome in all cell types. We sought to investigate conditions under which HCMV can be propagated without incurring genetic defects. Bacterial artificial chromosomes (BACs) provide a stable, genetically defined source of viral genome. Viruses were generated from BACs containing the genomes of strains TR, TB40, FIX, and Merlin, as well as from Merlin-BAC recombinants containing variant nucleotides in UL128L from TB40-BAC4 or FIX-BAC. Propagation of viruses derived from TR-BAC, TB40-BAC4, and FIX-BAC in either fibroblast or epithelial cells was associated with the generation of defects around the prokaryotic vector, which is retained in the unique short (US) region of viruses. This was not observed for Merlin-BAC, from which the vector is excised in derived viruses; however, propagation in epithelial cells was consistently associated with mutations in the unique longb' (UL/b') region, all impacting on gene UL141. Viruses derived from Merlin-BAC in fibroblasts had mutations in UL128L, but mutations occurred less frequently with recombinants containing UL128L nucleotides from TB40-BAC4 or FIX-BAC. Viruses derived from a Merlin-BAC derivative in which RL13 and UL128L were either mutated or repressed were remarkably stable in fibroblasts. Thus, HCMV containing a wild-type gene complement can be generatedin vitroby deriving virus from a self-excising BAC in fibroblasts and repressing RL13 and UL128L. Importance: Researchers should aim to study viruses that accurately represent the causative agents of disease. This is problematic for HCMV because clinical strains mutate rapidly when propagatedin vitro, becoming less cell associated, altered in tropism, more susceptible to natural killer cells, and less pathogenic. Following isolation from clinical material, HCMV genomes can be stabilized by cloning into bacterial artificial chromosomes (BACs), and then virus is regenerated by DNA transfection. However, mutations can occur not only during isolation prior to BAC cloning but also when virus is regenerated. We have identified conditions under which BAC-derived viruses containing an intact, wild-type genome can be propagatedin vitrowith minimal risk of mutants being selected, enabling studies of viruses expressing the gene complement of a clinical strain. However, even under these optimized conditions, sporadic mutations can occur, highlighting the advisability of sequencing the HCMV stocks used in experiments.
MeSH term(s)	Cell Line ; Chromosomes, Artificial, Bacterial ; Cytomegalovirus/genetics ; Cytomegalovirus/growth & development ; Epithelial Cells ; Fibroblasts ; Genes, Viral ; Genome, Viral ; Genomic Instability ; Humans ; In Vitro Techniques ; Membrane Glycoproteins/genetics ; Viral Envelope Proteins/genetics ; Virus Cultivation/methods
Chemical Substances	Membrane Glycoproteins ; UL128 protein, human cytomegalovirus ; Viral Envelope Proteins
Language	English
Publishing date	2016-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.02858-15
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Article ; Online: HPV integration detection in CaSki and SiHa using detection of integrated papillomavirus sequences and restriction-site PCR.

Raybould, Rachel / Fiander, Alison / Wilkinson, Gavin W G / Hibbitts, Sam

Journal of virological methods

2014 Volume 206, Page(s) 51–54

Abstract: Human Papillomavirus (HPV) infection is the primary cause of cervical neoplasia. HPV DNA is integrated into the human genome in the majority of cervical cancers. The nature of integration may differ with integration incorporating a single copy of HPV or ... ...

Abstract	Human Papillomavirus (HPV) infection is the primary cause of cervical neoplasia. HPV DNA is integrated into the human genome in the majority of cervical cancers. The nature of integration may differ with integration incorporating a single copy of HPV or occurring in concatenated form. Our understanding of HPV tumorigenesis is largely based on studies using characterised cell lines with defined integration sites; these cell lines provide an invaluable standard for validation of diagnostic assays. Cell lines also further understanding of integration mechanisms in clinical samples. The objective of this study was to explore integration assays and to investigate integration events in cell lines where HPV is integrated in concatenated form. Restriction site PCR and detection of integrated papillomavirus sequences were performed on DNA from SiHa and CaSki. A novel integration site on Xq27.3 and HPV genome rearrangements were detected in CaSki DNA. However, where integration was previously detected by FISH in CaSki, and reported to be integrated in concatenated form, integration was not detected by DIPS or RS-PCR. The data presented illustrate that HPV copy number can hinder integration detection; this needs consideration when interpreting results from tests applied to clinical samples.
MeSH term(s)	Cell Line, Tumor ; Humans ; Papillomaviridae/genetics ; Papillomaviridae/physiology ; Polymerase Chain Reaction ; Sequence Analysis, DNA ; Virus Integration
Language	English
Publishing date	2014-09
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	8013-5
ISSN	1879-0984 ; 0166-0934
ISSN (online)	1879-0984
ISSN	0166-0934
DOI	10.1016/j.jviromet.2014.05.017
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Article ; Online: Human Cytomegalovirus Genomes Sequenced Directly From Clinical Material: Variation, Multiple-Strain Infection, Recombination, and Gene Loss.

The Journal of infectious diseases

2019 Volume 220, Issue 5, Page(s) 781–791

Abstract: The genomic characteristics of human cytomegalovirus (HCMV) strains sequenced directly from clinical pathology samples were investigated, focusing on variation, multiple-strain infection, recombination, and gene loss. A total of 207 datasets generated in ...

Abstract	The genomic characteristics of human cytomegalovirus (HCMV) strains sequenced directly from clinical pathology samples were investigated, focusing on variation, multiple-strain infection, recombination, and gene loss. A total of 207 datasets generated in this and previous studies using target enrichment and high-throughput sequencing were analyzed, in the process enabling the determination of genome sequences for 91 strains. Key findings were that (i) it is important to monitor the quality of sequencing libraries in investigating variation; (ii) many recombinant strains have been transmitted during HCMV evolution, and some have apparently survived for thousands of years without further recombination; (iii) mutants with nonfunctional genes (pseudogenes) have been circulating and recombining for long periods and can cause congenital infection and resulting clinical sequelae; and (iv) intrahost variation in single-strain infections is much less than that in multiple-strain infections. Future population-based studies are likely to continue illuminating the evolution, epidemiology, and pathogenesis of HCMV.
MeSH term(s)	Base Sequence ; Cytomegalovirus/genetics ; Cytomegalovirus Infections/virology ; DNA, Viral/genetics ; Databases, Nucleic Acid ; Datasets as Topic ; Evolution, Molecular ; Genes, Viral ; Genetic Variation ; Genome, Viral/genetics ; Genotype ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation ; Recombination, Genetic ; Sequence Analysis, DNA ; Whole Genome Sequencing
Chemical Substances	DNA, Viral
Language	English
Publishing date	2019-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiz208
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Article ; Online: The pentameric complex drives immunologically covert cell-cell transmission of wild-type human cytomegalovirus.

Murrell, Isa / Bedford, Carmen / Ladell, Kristin / Miners, Kelly L / Price, David A / Tomasec, Peter / Wilkinson, Gavin W G / Stanton, Richard J

Proceedings of the National Academy of Sciences of the United States of America

2017 Volume 114, Issue 23, Page(s) 6104–6109

Abstract: Human cytomegalovirus (HCMV) strains that have been passaged in vitro rapidly acquire mutations that impact viral growth. These laboratory-adapted strains of HCMV generally exhibit restricted tropism, produce high levels of cell-free virus, and develop ... ...

Abstract	Human cytomegalovirus (HCMV) strains that have been passaged in vitro rapidly acquire mutations that impact viral growth. These laboratory-adapted strains of HCMV generally exhibit restricted tropism, produce high levels of cell-free virus, and develop susceptibility to natural killer cells. To permit experimentation with a virus that retained a clinically relevant phenotype, we reconstructed a wild-type (WT) HCMV genome using bacterial artificial chromosome technology. Like clinical virus, this genome proved to be unstable in cell culture; however, propagation of intact virus was achieved by placing the RL13 and UL128 genes under conditional expression. In this study, we show that WT-HCMV produces extremely low titers of cell-free virus but can efficiently infect fibroblasts, epithelial, monocyte-derived dendritic, and Langerhans cells via direct cell-cell transmission. This process of cell-cell transfer required the UL128 locus, but not the RL13 gene, and was significantly less vulnerable to the disruptive effects of IFN, cellular restriction factors, and neutralizing antibodies compared with cell-free entry. Resistance to neutralizing antibodies was dependent on high-level expression of the pentameric gH/gL/gpUL128-131A complex, a feature of WT but not passaged strains of HCMV.
MeSH term(s)	Antibodies, Neutralizing ; Cell Culture Techniques/methods ; Cell Line ; Cells, Cultured ; Chromosomes, Artificial, Bacterial/metabolism ; Cytomegalovirus/genetics ; Cytomegalovirus/metabolism ; Cytomegalovirus/pathogenicity ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/metabolism ; Fibroblasts/metabolism ; Humans ; Membrane Glycoproteins/metabolism ; Mutation ; Phenotype ; Tropism/immunology ; Viral Envelope Proteins/metabolism ; Virus Internalization ; Virus Replication/immunology
Chemical Substances	Antibodies, Neutralizing ; Membrane Glycoproteins ; Viral Envelope Proteins
Language	English
Publishing date	2017-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1704809114
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Article ; Online: Jenner's irony: cowpox taps into T cell evasion.

Wilkinson, Gavin W G / Lehner, Paul J

Cell host & microbe

2009 Volume 6, Issue 5, Page(s) 395–397

Abstract: CPXV12 is the first poxvirus gene product demonstrated to inhibit the transporter associated with antigen processing (TAP). This cowpox virus function acts in concert with a second gene product, CPXV203, to efficiently suppress MHC class I antigen ... ...

Abstract	CPXV12 is the first poxvirus gene product demonstrated to inhibit the transporter associated with antigen processing (TAP). This cowpox virus function acts in concert with a second gene product, CPXV203, to efficiently suppress MHC class I antigen presentation and enhance in vivo virulence.
Language	English
Publishing date	2009-11-16
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2009.11.001
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Article ; Online: Downregulation of HLA-I by the molluscum contagiosum virus mc080 impacts NK-cell recognition and promotes CD8

Elasifer, Hana / Wang, Eddie C Y / Prod'homme, Virginie / Davies, James / Forbes, Simone / Stanton, Richard J / Patel, Mihil / Fielding, Ceri A / Roberts, Dawn / Traherne, James A / Gruber, Nicole / Bugert, Joachim J / Aicheler, Rebecca J / Wilkinson, Gavin W G

The Journal of general virology

2020 Volume 101, Issue 8, Page(s) 863–872

Abstract: Molluscum contagiosum virus (MCV) is a common cause of benign skin lesions in young children and currently the only endemic human poxvirus. Following the infection of primary keratinocytes in the epidermis, MCV induces the proliferation of infected cells ...

Abstract	Molluscum contagiosum virus (MCV) is a common cause of benign skin lesions in young children and currently the only endemic human poxvirus. Following the infection of primary keratinocytes in the epidermis, MCV induces the proliferation of infected cells and this results in the production of wart-like growths. Full productive infection is observed only after the infected cells differentiate. During this prolonged replication cycle the virus must avoid elimination by the host immune system. We therefore sought to investigate the function of the two major histocompatibility complex class-I-related genes encoded by the MCV genes mc033 and mc080. Following insertion into a replication-deficient adenovirus vector, codon-optimized versions of mc033 and mc080 were expressed as endoglycosidase-sensitive glycoproteins that localized primarily in the endoplasmic reticulum. MC080, but not MC033, downregulated cell-surface expression of endogenous classical human leucocyte antigen (HLA) class I and non-classical HLA-E by a transporter associated with antigen processing (TAP)-independent mechanism. MC080 exhibited a capacity to inhibit or activate NK cells in autologous assays in a donor-specific manner. MC080 consistently inhibited antigen-specific T cells being activated by peptide-pulsed targets. We therefore propose that MC080 acts to promote evasion of HLA-I-restricted cytotoxic T cells.
MeSH term(s)	Antigen Presentation/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; Down-Regulation/immunology ; Endoplasmic Reticulum/immunology ; Histocompatibility Antigens Class I/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immune Evasion/immunology ; Keratinocytes/immunology ; Killer Cells, Natural/immunology ; Molluscum contagiosum virus/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Viral Proteins/immunology
Chemical Substances	Histocompatibility Antigens Class I ; Viral Proteins
Language	English
Publishing date	2020-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219316-4
ISSN	1465-2099 ; 0022-1317
ISSN (online)	1465-2099
ISSN	0022-1317
DOI	10.1099/jgv.0.001417
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Article ; Online: Suppression of costimulation by human cytomegalovirus promotes evasion of cellular immune defenses.

Wang, Eddie C Y / Pjechova, Mariana / Nightingale, Katie / Vlahava, Virginia-Maria / Patel, Mihil / Ruckova, Eva / Forbes, Simone K / Nobre, Luis / Antrobus, Robin / Roberts, Dawn / Fielding, Ceri A / Seirafian, Sepehr / Davies, James / Murrell, Isa / Lau, Betty / Wilkie, Gavin S / Suárez, Nicolás M / Stanton, Richard J / Vojtesek, Borivoj /

Davison, Andrew / Lehner, Paul J / Weekes, Michael P / Wilkinson, Gavin W G / Tomasec, Peter

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 19, Page(s) 4998–5003

Abstract: CD58 is an adhesion molecule that is known to play a critical role in costimulation of effector cells and is intrinsic to immune synapse structure. Herein, we describe a virally encoded gene that inhibits CD58 surface expression. Human cytomegalovirus ( ... ...

Abstract	CD58 is an adhesion molecule that is known to play a critical role in costimulation of effector cells and is intrinsic to immune synapse structure. Herein, we describe a virally encoded gene that inhibits CD58 surface expression. Human cytomegalovirus (HCMV) UL148 was necessary and sufficient to promote intracellular retention of CD58 during HCMV infection. Blocking studies with antagonistic anti-CD58 mAb and an HCMV UL148 deletion mutant (HCMV∆UL148) with restored CD58 expression demonstrated that the CD2/CD58 axis was essential for the recognition of HCMV-infected targets by CD8
MeSH term(s)	CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/pathology ; Cell Line, Transformed ; Cytomegalovirus/genetics ; Cytomegalovirus/immunology ; Cytomegalovirus Infections/genetics ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/pathology ; Humans ; Immune Evasion ; Immunity, Cellular ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Viral Fusion Proteins/genetics ; Viral Fusion Proteins/immunology
Chemical Substances	UL148 protein, human cytomegalovirus ; Viral Fusion Proteins
Language	English
Publishing date	2018-04-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1720950115
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