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Article ; Online: Clinical and microbiological investigation into mixed growth urine cultures.

Folaranmi, Tolulope / Harley, Clare / Jolly, Jim / Kirby, Andrew

2022 Volume 71, Issue 5

Abstract: Introduction. ...

Abstract	Introduction.
MeSH term(s)	Anti-Bacterial Agents/therapeutic use ; Bacteria ; Escherichia coli ; Humans ; Retrospective Studies ; Urinalysis/methods ; Urinary Tract Infections/microbiology
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2022-05-27
Publishing country	England
Document type	Journal Article
ZDB-ID	218356-0
ISSN	1473-5644 ; 0022-2615
ISSN (online)	1473-5644
ISSN	0022-2615
DOI	10.1099/jmm.0.001544
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Article ; Online: HIV envelope tail truncation confers resistance to SERINC5 restriction.

Haider, Tafhima / Snetkov, Xenia / Jolly, Clare

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

2021 Volume 118, Issue 21

Abstract: SERINC5 is a potent lentiviral restriction factor that gets incorporated into nascent virions and inhibits viral fusion and infectivity. The envelope glycoprotein (Env) is a key determinant for SERINC restriction, but many aspects of this relationship ... ...

Abstract	SERINC5 is a potent lentiviral restriction factor that gets incorporated into nascent virions and inhibits viral fusion and infectivity. The envelope glycoprotein (Env) is a key determinant for SERINC restriction, but many aspects of this relationship remain incompletely understood, and the mechanism of SERINC5 restriction remains unresolved. Here, we have used mutants of HIV-1 and HIV-2 to show that truncation of the Env cytoplasmic tail (ΔCT) confers complete resistance of both viruses to SERINC5 and SERINC3 restriction. Critically, fusion of HIV-1 ΔCT virus was not inhibited by SERINC5 incorporation into virions, providing a mechanism to explain how EnvCT truncation allows escape from restriction. Neutralization and inhibitor assays showed ΔCT viruses have an altered Env conformation and fusion kinetics, suggesting that EnvCT truncation dysregulates the processivity of entry, in turn allowing Env to escape targeting by SERINC5. Furthermore, HIV-1 and HIV-2 ΔCT viruses were also resistant to IFITMs, another entry-targeting family of restriction factors. Notably, while the EnvCT is essential for Env incorporation into HIV-1 virions and spreading infection in T cells, HIV-2 does not require the EnvCT. Here, we reveal a mechanism by which human lentiviruses can evade two potent Env-targeting restriction factors but show key differences in the capacity of HIV-1 and HIV-2 to exploit this. Taken together, this study provides insights into the interplay between HIV and entry-targeting restriction factors, revealing viral plasticity toward mechanisms of escape and a key role for the long lentiviral EnvCT in regulating these processes.
MeSH term(s)	Antigens, Differentiation/genetics ; Antigens, Differentiation/immunology ; Cell Line ; Gene Expression Regulation ; HEK293 Cells ; HIV Infections/genetics ; HIV Infections/immunology ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/immunology ; HIV-1/pathogenicity ; HIV-2/genetics ; HIV-2/immunology ; HIV-2/pathogenicity ; HeLa Cells ; Humans ; Immune Evasion ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/immunology ; Membrane Proteins/genetics ; Membrane Proteins/immunology ; Protein Domains ; Protein Isoforms/genetics ; Protein Isoforms/immunology ; Signal Transduction ; Stem Cells ; Virion/genetics ; Virion/immunology ; Virion/pathogenicity ; Virus Internalization ; env Gene Products, Human Immunodeficiency Virus/genetics ; env Gene Products, Human Immunodeficiency Virus/immunology
Chemical Substances	Antigens, Differentiation ; Membrane Glycoproteins ; Membrane Proteins ; Protein Isoforms ; SERINC3 protein, human ; SERINC5 protein, human ; env Gene Products, Human Immunodeficiency Virus ; leu-13 antigen
Language	English
Publishing date	2021-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.2101450118
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Zs.A 1148: Show issues

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Article ; Online: Proteomic analysis of the developing mammalian brain links PCDH19 to the Wnt/β-catenin signalling pathway.

de Nys, Rebekah / Gardner, Alison / van Eyk, Clare / Mincheva-Tasheva, Stefka / Thomas, Paul / Bhattacharjee, Rudrarup / Jolly, Lachlan / Martinez-Garay, Isabel / Fox, Ian W J / Kamath, Karthik Shantharam / Kumar, Raman / Gecz, Jozef

Molecular psychiatry

2024

Abstract: Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into ... ...

Abstract	Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into the molecular role of PCDH19 in the brain, we investigated the PCDH19 interactome in the developing mouse hippocampus and cortex. Combined with a meta-analysis of all reported PCDH19 interacting proteins, our results show that PCDH19 interacts with proteins involved in actin, microtubule, and gene regulation. We report CAPZA1, αN-catenin and, importantly, β-catenin as novel PCDH19 interacting proteins. Furthermore, we show that PCDH19 is a regulator of β-catenin transcriptional activity, and that this pathway is disrupted in CE individuals. Overall, our results support the involvement of PCDH19 in the cytoskeletal network and point to signalling pathways where PCDH19 plays critical roles.
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-024-02482-z
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Zs.A 4812: Show issues

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Article ; Online: A Conserved Tryptophan in the Envelope Cytoplasmic Tail Regulates HIV-1 Assembly and Spread.

Snetkov, Xenia / Haider, Tafhima / Mesner, Dejan / Groves, Nicholas / van Engelenburg, Schuyler B / Jolly, Clare

Viruses

2022 Volume 14, Issue 1

Abstract: The HIV-1 envelope (Env) is an essential determinant of viral infectivity, tropism and spread between T cells. Lentiviral Env contain an unusually long 150 amino acid cytoplasmic tail (EnvCT), but the function of the EnvCT and many conserved domains ... ...

Abstract	The HIV-1 envelope (Env) is an essential determinant of viral infectivity, tropism and spread between T cells. Lentiviral Env contain an unusually long 150 amino acid cytoplasmic tail (EnvCT), but the function of the EnvCT and many conserved domains within it remain largely uncharacterised. Here, we identified a highly conserved tryptophan motif at position 757 (W757) in the LLP-2 alpha helix of the EnvCT as a key determinant for HIV-1 replication and spread between T cells. Alanine substitution at this position potently inhibited HIV-1 cell-cell spread (the dominant mode of HIV-1 dissemination) by preventing recruitment of Env and Gag to sites of cell-cell contact, inhibiting virological synapse (VS) formation and spreading infection. Single-molecule tracking and super-resolution imaging showed that mutation of W757 dysregulates Env diffusion in the plasma membrane and increases Env mobility. Further analysis of Env function revealed that W757 is also required for Env fusion and infectivity, which together with reduced VS formation, result in a potent defect in viral spread. Notably, W757 lies within a region of the EnvCT recently shown to act as a supporting baseplate for Env. Our data support a model in which W757 plays a key role in regulating Env biology, modulating its temporal and spatial recruitment to virus assembly sites and regulating the inherent fusogenicity of the Env ectodomain, thereby supporting efficient HIV-1 replication and spread.
MeSH term(s)	CD4-Positive T-Lymphocytes ; Cell Membrane/metabolism ; HEK293 Cells ; HIV Envelope Protein gp41 ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/physiology ; HeLa Cells ; Humans ; T-Lymphocytes/metabolism ; T-Lymphocytes/virology ; Tryptophan/metabolism ; Virion/metabolism ; Virus Assembly/physiology ; Virus Internalization ; Virus Replication ; env Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	HIV Envelope Protein gp41 ; env Gene Products, Human Immunodeficiency Virus ; Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2022-01-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14010129
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Article ; Online: Loss of Nef-mediated CD3 down-regulation in the HIV-1 lineage increases viral infectivity and spread.

Mesner, Dejan / Hotter, Dominik / Kirchhoff, Frank / Jolly, Clare

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

2020 Volume 117, Issue 13, Page(s) 7382–7391

Abstract: Nef is an accessory protein of primate lentiviruses that is essential for efficient replication and pathogenesis of HIV-1. A conserved feature of Nef proteins from different lentiviral lineages is the ability to modulate host protein trafficking and down- ...

Abstract	Nef is an accessory protein of primate lentiviruses that is essential for efficient replication and pathogenesis of HIV-1. A conserved feature of Nef proteins from different lentiviral lineages is the ability to modulate host protein trafficking and down-regulate a number of cell surface receptors to enhance replication and promote immune evasion. Notably, the inability of Nef to down-regulate CD3 from infected T cells distinguishes HIV-1 Nef and its direct simian precursors from other primate lentiviruses. Why HIV-1 does not employ this potential immune evasion strategy is not fully understood. Using chimeric HIV-1 constructs expressing lentiviral Nef proteins that differ in their ability to down-modulate CD3, we show that retaining CD3 on the surface of infected primary T cells results in increased viral replication and cell-to-cell spread. We identified increased expression of envelope (Env) trimers at the cell surface and increased Env incorporation into virions as the determinants for the Nef- and CD3-dependent enhancement of viral infectivity. Importantly, this was independent of Nef-mediated antagonism of the host restriction factor SERINC5. CD3 retention on the surface of infected primary T cells also correlated with increased T cell signaling, activation, and cell death during cell-to-cell spread. Taken together, our results show that loss of an otherwise conserved function of Nef has a positive effect on HIV-1 replication, allowing for more efficient replication while potentially contributing to HIV-1 pathogenesis by triggering T cell activation and cell death during viral spread.
MeSH term(s)	CD3 Complex/metabolism ; CD4 Antigens/metabolism ; CD4-Positive T-Lymphocytes ; Down-Regulation ; HIV Seropositivity ; HIV-1/genetics ; HIV-1/metabolism ; HIV-1/pathogenicity ; Humans ; Immune Evasion ; Lymphocyte Activation ; Membrane Proteins/metabolism ; Primary Cell Culture ; Simian Immunodeficiency Virus/pathogenicity ; T-Lymphocytes/immunology ; Viral Regulatory and Accessory Proteins/metabolism ; Virion/metabolism ; Virus Replication ; env Gene Products, Human Immunodeficiency Virus/immunology ; env Gene Products, Human Immunodeficiency Virus/metabolism ; nef Gene Products, Human Immunodeficiency Virus/genetics ; nef Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	CD3 Complex ; CD4 Antigens ; Membrane Proteins ; NEF protein, SIV ; Viral Regulatory and Accessory Proteins ; env Gene Products, Human Immunodeficiency Virus ; nef Gene Products, Human Immunodeficiency Virus ; nef protein, Human immunodeficiency virus 1 ; nef protein, Human immunodeficiency virus 2
Language	English
Publishing date	2020-03-16
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.1921135117
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Zs.A 1148: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Cell-to-cell transmission of retroviruses: Innate immunity and interferon-induced restriction factors.

Jolly, Clare

Virology

2011 Volume 411, Issue 2, Page(s) 251–259

Abstract: It has been known for some time that retroviruses can disseminate between immune cells either by conventional cell-free transmission or by directed cell-to-cell spread. Over the past few years there has been increasing interest in how retroviruses may ... ...

Abstract	It has been known for some time that retroviruses can disseminate between immune cells either by conventional cell-free transmission or by directed cell-to-cell spread. Over the past few years there has been increasing interest in how retroviruses may use cell-to-cell spread to promote more rapid infection kinetics and circumvent humoral immunity. Effective humoral immune responses are intimately linked with innate immunity and the interplay between retroviruses and innate immunity is a rapidly expanding area of research that has been advanced considerably by the identification of cellular restriction factors that provide barriers to retroviral infection. The effect of innate immunity and restriction factors on retroviral cell-to-cell spread has been comparatively little studied; however recent work suggests this maybe changing. Here I will review some recent advances in what is a budding area of retroviral research.
MeSH term(s)	Humans ; Immunity, Innate ; Interferons/immunology ; Retroviridae/immunology ; Retroviridae/pathogenicity
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2011-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2010.12.031
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Article ; Online: T cell polarization at the virological synapse.

Jolly, Clare

Viruses

2010 Volume 2, Issue 6, Page(s) 1261–1278

Abstract: Cell-to-cell spread of HIV-1 between CD4(+) T cells takes place at multimolecular structures called virological synapses. A defining feature of the virological synapse is polarization of viral assembly and budding at sites of T cell-T cell contact. ... ...

Abstract	Cell-to-cell spread of HIV-1 between CD4(+) T cells takes place at multimolecular structures called virological synapses. A defining feature of the virological synapse is polarization of viral assembly and budding at sites of T cell-T cell contact. Recent work is beginning to address how viral proteins are targeted to the virological synapse and the molecular mechanisms that regulate HIV-1 egress by cell-to-cell spread. This review discusses our current understanding of these processes and considers how T cell polarization during other forms of intercellular communication may provide insight into HIV-1 assembly and dissemination.
Language	English
Publishing date	2010-05-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v2061261
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Conference proceedings ; Online: Investigating the role of T cell signalling during HIV-1 cell-cell spread.

Shivkumar, Maitreyi / Ann-Kathrin, Reuschl / Dejan, Mesner / Clare, Jolly

2020

Keywords	covid19
Language	English
Publishing date	2020-03-31
Publisher	Microbiology Society
Publishing country	uk
Document type	Conference proceedings ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Evolution of enhanced innate immune suppression by SARS-CoV-2 Omicron subvariants.

Reuschl, Ann-Kathrin / Thorne, Lucy G / Whelan, Matthew V X / Ragazzini, Roberta / Furnon, Wilhelm / Cowton, Vanessa M / De Lorenzo, Giuditta / Mesner, Dejan / Turner, Jane L E / Dowgier, Giulia / Bogoda, Nathasha / Bonfanti, Paola / Palmarini, Massimo / Patel, Arvind H / Jolly, Clare / Towers, Greg J

Nature microbiology

2024 Volume 9, Issue 2, Page(s) 451–463

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) human adaptation resulted in distinct lineages with enhanced transmissibility called variants of concern (VOCs). Omicron is the first VOC to evolve distinct globally dominant subvariants. Here ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) human adaptation resulted in distinct lineages with enhanced transmissibility called variants of concern (VOCs). Omicron is the first VOC to evolve distinct globally dominant subvariants. Here we compared their replication in human cell lines and primary airway cultures and measured host responses to infection. We discovered that subvariants BA.4 and BA.5 have improved their suppression of innate immunity when compared with earlier subvariants BA.1 and BA.2. Similarly, more recent subvariants (BA.2.75 and XBB lineages) also triggered reduced innate immune activation. This correlated with increased expression of viral innate antagonists Orf6 and nucleocapsid, reminiscent of VOCs Alpha to Delta. Increased Orf6 levels suppressed host innate responses to infection by decreasing IRF3 and STAT1 signalling measured by transcription factor phosphorylation and nuclear translocation. Our data suggest that convergent evolution of enhanced innate immune antagonist expression is a common pathway of human adaptation and link Omicron subvariant dominance to improved innate immune evasion.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Cell Line ; Immune Evasion ; Immunity, Innate
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article
ISSN	2058-5276
ISSN (online)	2058-5276
DOI	10.1038/s41564-023-01588-4
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Article ; Online: Executable network of SARS-CoV-2-host interaction predicts drug combination treatments.

Howell, Rowan / Clarke, Matthew A / Reuschl, Ann-Kathrin / Chen, Tianyi / Abbott-Imboden, Sean / Singer, Mervyn / Lowe, David M / Bennett, Clare L / Chain, Benjamin / Jolly, Clare / Fisher, Jasmin

NPJ digital medicine

2022 Volume 5, Issue 1, Page(s) 18

Abstract: The COVID-19 pandemic has pushed healthcare systems globally to a breaking point. The urgent need for effective and affordable COVID-19 treatments calls for repurposing combinations of approved drugs. The challenge is to identify which combinations are ... ...

Abstract	The COVID-19 pandemic has pushed healthcare systems globally to a breaking point. The urgent need for effective and affordable COVID-19 treatments calls for repurposing combinations of approved drugs. The challenge is to identify which combinations are likely to be most effective and at what stages of the disease. Here, we present the first disease-stage executable signalling network model of SARS-CoV-2-host interactions used to predict effective repurposed drug combinations for treating early- and late stage severe disease. Using our executable model, we performed in silico screening of 9870 pairs of 140 potential targets and have identified nine new drug combinations. Camostat and Apilimod were predicted to be the most promising combination in effectively supressing viral replication in the early stages of severe disease and were validated experimentally in human Caco-2 cells. Our study further demonstrates the power of executable mechanistic modelling to enable rapid pre-clinical evaluation of combination therapies tailored to disease progression. It also presents a novel resource and expandable model system that can respond to further needs in the pandemic.
Language	English
Publishing date	2022-02-14
Publishing country	England
Document type	Journal Article
ISSN	2398-6352
ISSN (online)	2398-6352
DOI	10.1038/s41746-022-00561-5
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