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3. Proteomic analysis of circulating immune cells identifies cellular phenotypes associated with COVID-19 severity

Author

Potts, Martin, Fletcher-Etherington, Alice, Nightingale, Katie, Mescia, Federica, Bergamaschi, Laura, Calero-Nieto, Fernando J., Antrobus, Robin, Williamson, James, Parsons, Harriet, Huttlin, Edward L., Kingston, Nathalie, Göttgens, Berthold, Bradley, John R., Lehner, Paul J., Matheson, Nicholas J., Smith, Kenneth G.C., Wills, Mark R., Lyons, Paul A., and Weekes, Michael P.

Published
2023
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6. A prospective study of risk factors associated with seroprevalence of SARS-CoV-2 antibodies in healthcare workers at a large UK teaching hospital

Author

Cooper, Daniel J, Lear, Sara, Watson, Laura, Shaw, Ashley, Ferris, Mark, Doffinger, Rainer, Bousfield, Rachel, Sharrocks, Katherine, Weekes, Michael P., Warne, Ben, Sparkes, Dominic, Jones, Nick K, Rivett, Lucy, Routledge, Matthew, Chaudhry, Afzal, Dempsey, Katherine, Matson, Montgomery, Lakha, Adil, Gathercole, George, O'Connor, Olivia, Wilson, Emily, Shahzad, Orthi, Toms, Kieran, Thompson, Rachel, Halsall, Ian, Halsall, David, Houghton, Sally, Papadia, Sofia, Kingston, Nathalie, Stirrups, Kathleen E, Graves, Barbara, Townsend, Paul, Walker, Neil, Stark, Hannah, De Angelis, Daniela, Seaman, Shaun, Dougan, Gordon, Bradley, John R, Török, M. Estée, Goodfellow, Ian, and Baker, Stephen

Published
2022
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7. SARS-CoV-2 spike N-terminal domain modulates TMPRSS2-dependent viral entry and fusogenicity

Author

Baker, Stephen, Dougan, Gordon, Hess, Christoph, Kingston, Nathalie, Lehner, Paul J., Lyons, Paul A., Matheson, Nicholas J., Owehand, Willem H., Saunders, Caroline, Summers, Charlotte, Thaventhiran, James E.D., Toshner, Mark, Weekes, Michael P., Maxwell, Patrick, Shaw, Ashley, Bucke, Ashlea, Calder, Jo, Canna, Laura, Domingo, Jason, Elmer, Anne, Fuller, Stewart, Harris, Julie, Hewitt, Sarah, Kennet, Jane, Jose, Sherly, Kourampa, Jenny, Meadows, Anne, O’Brien, Criona, Price, Jane, Publico, Cherry, Rastall, Rebecca, Ribeiro, Carla, Rowlands, Jane, Ruffolo, Valentina, Tordesillas, Hugo, Bullman, Ben, Dunmore, Benjamin J., Fawke, Stuart, Gräf, Stefan, Hodgson, Josh, Huang, Christopher, Hunter, Kelvin, Jones, Emma, Legchenko, Ekaterina, Matara, Cecilia, Martin, Jennifer, Mescia, Federica, O’Donnell, Ciara, Pointon, Linda, Shih, Joy, Sutcliffe, Rachel, Tilly, Tobias, Treacy, Carmen, Tong, Zhen, Wood, Jennifer, Wylot, Marta, Betancourt, Ariana, Bower, Georgie, Cossetti, Chiara, De Sa, Aloka, Epping, Madeline, Gleadall, Nick, Grenfell, Richard, Hinch, Andrew, Jackson, Sarah, Jarvis, Isobel, Krishna, Ben, Nice, Francesca, Omarjee, Ommar, Perera, Marianne, Potts, Martin, Richoz, Nathan, Romashova, Veronika, Stefanucci, Luca, Strezlecki, Mateusz, Turner, Lori, De Bie, Eckart M.D.D., Bunclark, Katherine, Josipovic, Masa, Mackay, Michael, Allison, John, Butcher, Helen, Caputo, Daniela, Clapham-Riley, Debbie, Dewhurst, Eleanor, Furlong, Anita, Graves, Barbara, Gray, Jennifer, Ivers, Tasmin, Le Gresley, Emma, Linger, Rachel, Meloy, Sarah, Muldoon, Francesca, Ovington, Nigel, Papadia, Sofia, Phelan, Isabel, Stark, Hannah, Stirrups, Kathleen E., Townsend, Paul, Walker, Neil, Webster, Jennifer, Scholtes, Ingrid, Hein, Sabine, King, Rebecca, Meng, Bo, Datir, Rawlings, Choi, Jinwook, Bradley, John R., Smith, Kenneth G.C., Lee, Joo Hyeon, and Gupta, Ravindra K.

Published
2022
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8. Epstein-Barr virus BALF0/1 subverts the Caveolin and ERAD pathways to target B cell receptor complexes for degradation.

Author

Pei Tung Yiu, Stephanie, Yifei Liao, Jinjie Yan, Weekes, Michael P., and Gewurz, Benjamin E.

Subjects
B cell receptors, B cells, IMMUNOGLOBULIN heavy chains, B cell lymphoma, CAVEOLAE
Abstract

Epstein-Barr virus (EBV) establishes persistent infection, causes infectious mononucleosis, is a major trigger for multiple sclerosis and contributes to multiple cancers. Yet, knowledge remains incomplete about how the virus remodels host B cells to support lytic replication. We previously identified that EBV lytic replication results in selective depletion of plasma membrane (PM) B cell receptor (BCR) complexes, composed of immunoglobulin and the CD79A and CD79B signaling chains. Here, we used proteomic and biochemical approaches to identify that the EBV early lytic protein BALF0/1 is responsible for EBV lytic cycle BCR degradation. Mechanistically, an immunoglobulin heavy chain (HC) cytoplasmic tail KVK motif was required for ubiquitin-mediated BCR degradation, while CD79A and CD79B were dispensable. BALF0/1 subverted caveolin-mediated endocytosis to internalize PM BCR complexes and to deliver them to the endoplasmic reticulum. BALF0/1 stimulated immunoglobulin HC cytoplasmic tail ubiquitination, which together with the ATPase valosin-containing protein/p97 drove ER-associated degradation of BCR complexes by cytoplasmic proteasomes. BALF0/1 knockout reduced the viral load of secreted EBV particles from B cells that expressed a monoclonal antibody against EBV glycoprotein 350 but not a control anti-influenza hemagglutinin antibody and increased viral particle immunoglobulin incorporation. Consistent with downmodulation of PM BCR, BALF0/1 overexpression reduced viability of a diffuse large B cell lymphoma cell line whose survival is dependent upon BCR signaling. Collectively, our results suggest that EBV BALF0/1 downmodulates immunoglobulin upon lytic reactivation to block BCR signaling and support virion release, but await the development of suitable models to test its roles in EBV reactivation in vivo. [ABSTRACT FROM AUTHOR]

Published
2025
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9. Coagulation factor V is a T-cell inhibitor expressed by leukocytes in COVID-19

Author

Wang, Jun, Kotagiri, Prasanti, Lyons, Paul A., Al-Lamki, Rafia S., Mescia, Federica, Bergamaschi, Laura, Turner, Lorinda, Morgan, Michael D., Calero-Nieto, Fernando J., Bach, Karsten, Mende, Nicole, Wilson, Nicola K., Watts, Emily R., Maxwell, Patrick H., Chinnery, Patrick F., Kingston, Nathalie, Papadia, Sofia, Stirrups, Kathleen E., Walker, Neil, Gupta, Ravindra K., Menon, David K., Allinson, Kieren, Aitken, Sarah J., Toshner, Mark, Weekes, Michael P., Nathan, James A., Walmsley, Sarah R., Ouwehand, Willem H., Kasanicki, Mary, Göttgens, Berthold, Marioni, John C., Smith, Kenneth G.C., Pober, Jordan S., and Bradley, John R.

Published
2022
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11. Genomic epidemiology of SARS-CoV-2 in a UK university identifies dynamics of transmission

Author

Aggarwal, Dinesh, Warne, Ben, Jahun, Aminu S., Hamilton, William L., Fieldman, Thomas, du Plessis, Louis, Hill, Verity, Blane, Beth, Watkins, Emmeline, Wright, Elizabeth, Hall, Grant, Ludden, Catherine, Myers, Richard, Hosmillo, Myra, Chaudhry, Yasmin, Pinckert, Malte L., Georgana, Iliana, Izuagbe, Rhys, Leek, Danielle, Nsonwu, Olisaeloka, Hughes, Gareth J., Packer, Simon, Page, Andrew J., Metaxaki, Marina, Fuller, Stewart, Weale, Gillian, Holgate, Jon, Brown, Christopher A., Howes, Rob, McFarlane, Duncan, Dougan, Gordon, Pybus, Oliver G., Angelis, Daniela De, Maxwell, Patrick H., Peacock, Sharon J., Weekes, Michael P., Illingworth, Chris, Harrison, Ewan M., Matheson, Nicholas J., and Goodfellow, Ian G.

Published
2022
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14. Hypoxia inducible factors regulate hepatitis B virus replication by activating the basal core promoter

Author

Wing, Peter A.C., Liu, Peter Jianrui, Harris, James M., Magri, Andrea, Michler, Thomas, Zhuang, Xiaodong, Borrmann, Helene, Minisini, Rosalba, Frampton, Nicholas R., Wettengel, Jochen M., Mailly, Laurent, D’Arienzo, Valentina, Riedl, Tobias, Nobre, Luis, Weekes, Michael P., Pirisi, Mario, Heikenwalder, Mathias, Baumert, Thomas F., Hammond, Ester M., Mole, David R., Protzer, Ulrike, Balfe, Peter, and McKeating, Jane A.

Published
2021
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15. Longitudinal analysis reveals that delayed bystander CD8+ T cell activation and early immune pathology distinguish severe COVID-19 from mild disease

Author

Bergamaschi, Laura, Mescia, Federica, Turner, Lorinda, Hanson, Aimee L., Kotagiri, Prasanti, Dunmore, Benjamin J., Ruffieux, Hélène, De Sa, Aloka, Huhn, Oisín, Morgan, Michael D., Gerber, Pehuén Pereyra, Wills, Mark R., Baker, Stephen, Calero-Nieto, Fernando J., Doffinger, Rainer, Dougan, Gordon, Elmer, Anne, Goodfellow, Ian G., Gupta, Ravindra K., Hosmillo, Myra, Hunter, Kelvin, Kingston, Nathalie, Lehner, Paul J., Matheson, Nicholas J., Nicholson, Jeremy K., Petrunkina, Anna M., Richardson, Sylvia, Saunders, Caroline, Thaventhiran, James E.D., Toonen, Erik J.M., Weekes, Michael P., Göttgens, Berthold, Toshner, Mark, Hess, Christoph, Bradley, John R., Lyons, Paul A., and Smith, Kenneth G.C.

Published
2021
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16. Rapid implementation of SARS-CoV-2 sequencing to investigate cases of health-care associated COVID-19: a prospective genomic surveillance study

Author

Meredith, Luke W, Hamilton, William L, Warne, Ben, Houldcroft, Charlotte J, Hosmillo, Myra, Jahun, Aminu S, Curran, Martin D, Parmar, Surendra, Caller, Laura G, Caddy, Sarah L, Khokhar, Fahad A, Yakovleva, Anna, Hall, Grant, Feltwell, Theresa, Forrest, Sally, Sridhar, Sushmita, Weekes, Michael P, Baker, Stephen, Brown, Nicholas, Moore, Elinor, Popay, Ashley, Roddick, Iain, Reacher, Mark, Gouliouris, Theodore, Peacock, Sharon J, Dougan, Gordon, Török, M Estée, and Goodfellow, Ian

Published
2020
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18. Point of Care Nucleic Acid Testing for SARS-CoV-2 in Hospitalized Patients: A Clinical Validation Trial and Implementation Study

Author

Baker, Stephen, Bradley, John, Dougan, Gordon, Goodfellow, Ian, Gupta, Ravindra K., Lehner, Paul J., Lyons, Paul, Matheson, Nicholas J., Smith, Kenneth G.C., Toshner, Mark, Weekes, Michael P., Brown, Nick, Curran, Martin, Palmar, Surendra, Zhang, Hongyi, Enoch, David, Chapman, Daniel, Shaw, Ashley, Mendoza, Vivien, Jose, Sherly, Bermperi, Areti, Zerrudo, Julie Ann, Kourampa, Evgenia, Saunders, Caroline, de Jesus, Ranalie, Domingo, Jason, Pasquale, Ciro, Vergese, Bensi, Vargas, Phoebe, Fabiculana, Marivic, Perales, Marlyn, Skells, Richard, Mynott, Lee, Blake, Elizabeth, Bates, Amy, Vallier, Anne-laure, Williams, Alexandra, Phillips, David, Chiu, Edmund, Overhill, Alex, Ramenante, Nicola, Sipple, Jamal, Frost, Steven, Knock, Helena, Hardy, Richard, Foster, Emily, Davidson, Fiona, Rundell, Viona, Bundi, Purity, Abeseabe, Richmond, Clark, Sarah, Vicente, Isabel, Collier, Dami A., Assennato, Sonny M., Warne, Ben, Sithole, Nyarie, Sharrocks, Katherine, Ritchie, Allyson, Ravji, Pooja, Routledge, Matthew, Sparkes, Dominic, Skittrall, Jordan, Smielewska, Anna, Ramsey, Isobel, Goel, Neha, Tassell, Rhys, Lineham, Michelle, Vaghela, Devan, Leong, Clare, Mok, Hoi Ping, Mendoza, Vivienne, Demiris, Nikos, Besser, Martin, Siedner, Mark J., Waddington, Claire S., and Lee, Helen

Published
2020
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22. Suppression of costimulation by human cytomegalovirus promotes evasion of cellular immune defenses

Author

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., and Tomasec, Peter

Published
2018

23. High-Definition Analysis of Host Protein Stability during Human Cytomegalovirus Infection Reveals Antiviral Factors and Viral Evasion Mechanisms

Author

Nightingale, Katie, Lin, Kai-Min, Ravenhill, Benjamin J., Davies, Colin, Nobre, Luis, Fielding, Ceri A., Ruckova, Eva, Fletcher-Etherington, Alice, Soday, Lior, Nichols, Hester, Sugrue, Daniel, Wang, Eddie C.Y., Moreno, Pablo, Umrania, Yagnesh, Huttlin, Edward L., Antrobus, Robin, Davison, Andrew J., Wilkinson, Gavin W.G., Stanton, Richard J., Tomasec, Peter, and Weekes, Michael P.

Published
2018
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24. Transferrin receptor 1 is a reticulocyte-specific receptor for Plasmodium vivax

Author

Gruszczyk, Jakub, Kanjee, Usheer, Chan, Li-Jin, Menant, Sébastien, Malleret, Benoit, Lim, Nicholas T. Y., Schmidt, Christoph Q., Mok, Yee-Foong, Lin, Kai-Min, Pearson, Richard D., Rangel, Gabriel, Smith, Brian J., Call, Melissa J., Weekes, Michael P., Griffin, Michael D. W., Murphy, James M., Abraham, Jonathan, Sriprawat, Kanlaya, Menezes, Maria J., Ferreira, Marcelo U., Russell, Bruce, Renia, Laurent, Duraisingh, Manoj T., and Tham, Wai-Hong

Published
2018

33. Monoclonal antibodies targeting nonstructural viral antigens can activate ADCC against human cytomegalovirus

Author

Vlahava, Virginia-Maria, Murrell, Isa, Zhuang, Lihui, Aicheler, Rebecca J., Lim, Eleanor, Miners, Kelly L., Ladell, Kristin, Suarez, Nicolas M., Price, David A., Davison, Andrew J., Wilkinson, Gavin W.G., Wills, Mark R., Weekes, Michael P., Wang, Eddie C.Y., and Stanton, Richard J.

Subjects
Care and treatment, Development and progression, Genetic aspects, Health aspects, Killer cells -- Genetic aspects -- Health aspects, Monoclonal antibodies -- Health aspects, Viral antigens -- Health aspects, Immune response -- Genetic aspects, Cytomegalovirus infections -- Development and progression -- Care and treatment -- Genetic aspects
Abstract

Introduction Human cytomegalovirus (HCMV) establishes lifelong infection in the face of robust humoral and cell-mediated immune responses. The virus is a significant cause of morbidity and mortality in immunocompromised individuals [...], Human cytomegalovirus (HCMV) is a ubiquitous pathogen that causes severe disease following congenital infection and in immunocompromised individuals. No vaccines are licensed, and there are limited treatment options. We now show that the addition of anti-HCMV antibodies (Abs) can activate NK cells prior to the production of new virions, through Ab- dependent cellular cytotoxicity (ADCC), overcoming viral immune evasins. Quantitative proteomics defined the most abundant HCMV proteins on the cell surface, and we screened these targets to identify the viral antigens responsible for activating ADCC. Surprisingly, these were not structural glycoproteins; instead, the immune evasins US28, RL11, UL5, UL141, and UL16 each individually primed ADCC. We isolated human monoclonal Abs (mAbs) specific for UL16 or UL141 from a seropositive donor and optimized them for ADCC. Cloned Abs targeting a single antigen (UL141) were sufficient to mediate ADCC against HCMV-infected cells, even at low concentrations. Collectively, these findings validated an unbiased methodological approach to the identification of immunodominant viral antigens, providing a pathway toward an immunotherapeutic strategy against HCMV and potentially other pathogens.

Published
2021
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34. HCMV pUL135 Remodels the Actin Cytoskeleton to Impair Immune Recognition of Infected Cells

Author

Stanton, Richard J., Prod’homme, Virginie, Purbhoo, Marco A., Moore, Melanie, Aicheler, Rebecca J., Heinzmann, Marcus, Bailer, Susanne M., Haas, Jürgen, Antrobus, Robin, Weekes, Michael P., Lehner, Paul J., Vojtesek, Borivoj, Miners, Kelly L., Man, Stephen, Wilkie, Gavin S., Davison, Andrew J., Wang, Eddie C.Y., Tomasec, Peter, and Wilkinson, Gavin W.G.

Published
2014
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38. ADAM17 targeting by human cytomegalovirus remodels the cell surface proteome to simultaneously regulate multiple immune pathways.

Author

Rubina, Anzelika, Patel, Mihil, Nightingale, Katie, Potts, Martin, Fielding, Ceri A., Kollnberger, Simon, Lau, Betty, Ladell, Kristin, Miners, Kelly L., Nichols, Jenna, Nobre, Luis, Roberts, Dawn, Trinca, Terrence M., Twohig, Jason P., Vlahava, Virginia-Maria, Davison, Andrew J., Price, David A., Tomasec, Peter, Wilkinson, Gavin W. G., and Weekes, Michael P.

Subjects
HUMAN cytomegalovirus, TUMOR necrosis factor receptors, CELL membranes, RESPONSE inhibition
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 UL/b' region, UL148 and UL148D. Proteomic plasma membrane profiling of cells infected with an HCMV double-deletion mutant for UL148 and UL148D with restored ADAM17 expression, combined with ADAM17 functional blockade, showed that HCMV stabilized the surface expression of 114 proteins (P < 0.05) in an ADAM17-dependent fashion. These included reported substrates of ADAM17 with established immunological functions such as TNFR2 and jagged1, but also numerous unreported host and viral targets, such as nectin1, UL8, and UL144. Regulation of TNFα-induced cytokine responses and NK inhibition during HCMV infection were dependent on this impairment of ADAM17. We therefore identify a viral immunoregulatory mechanism in which targeting a single sheddase enables broad regulation of multiple critical surface receptors, revealing a paradigm for viral-encoded immunomodulation. [ABSTRACT FROM AUTHOR]

Published
2023
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39. Human cytomegalovirus: taking the strain

Author

Wilkinson, Gavin W. G., Davison, Andrew J., Tomasec, Peter, Fielding, Ceri A., Aicheler, Rebecca, Murrell, Isa, Seirafian, Sepher, Wang, Edward C. Y., Weekes, Michael, Lehner, Paul J., Wilkie, Gavin S., and Stanton, Richard J.

Published
2015
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40. SARS-CoV-2 B.1.617.2 Delta variant replication and immune evasion

Author

Mlcochova, Petra, Kemp, Steven A., Dhar, Mahesh Shanker, Papa, Guido, Meng, Bo, Ferreira, Isabella A. T. M., Datir, Rawlings, Collier, Dami A., Albecka, Anna, Singh, Sujeet, Pandey, Rajesh, Brown, Jonathan, Zhou, Jie, Goonawardane, Niluka, Mishra, Swapnil, Whittaker, Charles, Mellan, Thomas, Marwal, Robin, Datta, Meena, Sengupta, Shantanu, Ponnusamy, Kalaiarasan, Radhakrishnan, Venkatraman Srinivasan, Abdullahi, Adam, Charles, Oscar, Chattopadhyay, Partha, Devi, Priti, Caputo, Daniela, Peacock, Tom, Wattal, Chand, Goel, Neeraj, Satwik, Ambrish, Vaishya, Raju, Agarwal, Meenakshi, Chauhan, Himanshu, Dikid, Tanzin, Gogia, Hema, Lall, Hemlata, Verma, Kaptan, Singh, Manoj K., Soni, Namita, Meena, Namonarayan, Madan, Preeti, Singh, Priyanka, Sharma, Ramesh, Sharma, Rajeev, Kabra, Sandhya, Kumar, Sattender, Kumari, Swati, Sharma, Uma, Chaudhary, Urmila, Sivasubbu, Sridhar, Scaria, Vinod, Oberoi, J. K., Raveendran, Reena, Datta, S., Das, Saumitra, Maitra, Arindam, Chinnaswamy, Sreedhar, Biswas, Nidhan Kumar, Parida, Ajay, Raghav, Sunil K., Prasad, Punit, Sarin, Apurva, Mayor, Satyajit, Ramakrishnan, Uma, Palakodeti, Dasaradhi, Seshasayee, Aswin Sai Narain, Thangaraj, K., Bashyam, Murali Dharan, Dalal, Ashwin, Bhat, Manoj, Shouche, Yogesh, Pillai, Ajay, Abraham, Priya, Potdar, Varsha Atul, Cherian, Sarah S., Desai, Anita Sudhir, Pattabiraman, Chitra, Manjunatha, M. V., Mani, Reeta S., Udupi, Gautam Arunachal, Nandicoori, Vinay, Tallapaka, Karthik Bharadwaj, Sowpati, Divya Tej, Kawabata, Ryoko, Morizako, Nanami, Sadamasu, Kenji, Asakura, Hiroyuki, Nagashima, Mami, Yoshimura, Kazuhisa, Ito, Jumpei, Kimura, Izumi, Uriu, Keiya, Kosugi, Yusuke, Suganami, Mai, Oide, Akiko, Yokoyama, Miyabishara, Chiba, Mika, Saito, Akatsuki, Butlertanaka, Erika P., Tanaka, Yuri L., Ikeda, Terumasa, Motozono, Chihiro, Nasser, Hesham, Shimizu, Ryo, Yuan, Yue, Kitazato, Kazuko, Hasebe, Haruyo, Nakagawa, So, Wu, Jiaqi, Takahashi, Miyoko, Fukuhara, Takasuke, Shimizu, Kenta, Tsushima, Kana, Kubo, Haruko, Shirakawa, Kotaro, Kazuma, Yasuhiro, Nomura, Ryosuke, Horisawa, Yoshihito, Takaori-Kondo, Akifumi, Tokunaga, Kenzo, Ozono, Seiya, Baker, Stephen, Dougan, Gordon, Hess, Christoph, Kingston, Nathalie, Lehner, Paul J., Lyons, Paul A., Matheson, Nicholas J., Owehand, Willem H., Saunders, Caroline, Summers, Charlotte, Thaventhiran, James E. D., Toshner, Mark, Weekes, Michael P., Maxwell, Patrick, Shaw, Ashley, Bucke, Ashlea, Calder, Jo, Canna, Laura, Domingo, Jason, Elmer, Anne, Fuller, Stewart, Harris, Julie, Hewitt, Sarah, Kennet, Jane, Jose, Sherly, Kourampa, Jenny, Meadows, Anne, O'Brien, Criona, Price, Jane, Publico, Cherry, Rastall, Rebecca, Ribeiro, Carla, Rowlands, Jane, Ruffolo, Valentina, Tordesillas, Hugo, Bullman, Ben, Dunmore, Benjamin J., Fawke, Stuart, Graf, Stefan, Hodgson, Josh, Huang, Christopher, Hunter, Kelvin, Jones, Emma, Legchenko, Ekaterina, Matara, Cecilia, Martin, Jennifer, Mescia, Federica, O'Donnell, Ciara, Pointon, Linda, Pond, Nicole, Shih, Joy, Sutcliffe, Rachel, Tilly, Tobias, Treacy, Carmen, Tong, Zhen, Wood, Jennifer, Wylot, Marta, Bergamaschi, Laura, Betancourt, Ariana, Bower, Georgie, Cossetti, Chiara, De Sa, Aloka, Epping, Madeline, Gleadall, Nick, Grenfell, Richard, Hinch, Andrew, Huhn, Oisin, Jackson, Sarah, Jarvis, Isobel, Krishna, Ben, Lewis, Daniel, Marsden, Joe, Nice, Francesca, Okecha, Georgina, Omarjee, Ommar, Perera, Marianne, Potts, Martin, Richoz, Nathan, Romashova, Veronika, Yarkoni, Natalia Savinykh, Sharma, Rahul, Stefanucci, Luca, Stephens, Jonathan, Strezlecki, Mateusz, Turner, Lori, De Bie, Eckart M. D. D., Bunclark, Katherine, Josipovic, Masa, Mackay, Michael, Rossi, Sabrina, Selvan, Mayurun, Spencer, Sarah, Yong, Cissy, Allison, John, Butcher, Helen, Clapham-Riley, Debbie, Dewhurst, Eleanor, Furlong, Anita, Graves, Barbara, Gray, Jennifer, Ivers, Tasmin, Kasanicki, Mary, Le Gresley, Emma, Linger, Rachel, Meloy, Sarah, Muldoon, Francesca, Ovington, Nigel, Papadia, Sofia, Phelan, Isabel, Stark, Hannah, Stirrups, Kathleen E., Townsend, Paul, Walker, Neil, Webster, Jennifer, Scholtes, Ingrid, Hein, Sabine, King, Rebecca, Mavousian, Antranik, Lee, Joo Hyeon, Bassi, Jessica, Silacci-Fegni, Chiara, Saliba, Christian, Pinto, Dora, Irie, Takashi, Yoshida, Isao, Hamilton, William L., Sato, Kei, Bhatt, Samir, Flaxman, Seth, James, Leo C., Corti, Davide, Piccoli, Luca, Barclay, Wendy S., Rakshit, Partha, Agrawal, Anurag, Gupta, Ravindra K., (INSACOG), Indian SARS-CoV-2 Genomics Consortium, Consortium, Genotype to Phenotype Japan (G2P-Japan), Collaboration, CITIID-NIHR BioResource COVID-19, Gupta, Ravindra K [0000-0001-9751-1808], Apollo - University of Cambridge Repository, and Gupta, Ravindra K. [0000-0001-9751-1808]

Subjects
Male, COVID-19 Vaccines, medicine.drug_class, Health Personnel, India, Monoclonal antibody, Virus Replication, Antibodies, Cell Line, Cell Fusion, Immune system, 13/100, medicine, Humans, Neutralizing antibody, Antibodies, Neutralizing, Female, Kinetics, SARS-CoV-2, Spike Glycoprotein, Coronavirus, Vaccination, Immune Evasion, Neutralizing, 631/326/596/4130, Syncytium, Multidisciplinary, Cell fusion, biology, article, Vaccine efficacy, 631/250/254, Virology, Spike Glycoprotein, Coronavirus, 13/31, biology.protein, Antibody, Infection
Abstract

The B.1.617.2 (Delta) variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first identified in the state of Maharashtra in late 2020 and spread throughout India, outcompeting pre-existing lineages including B.1.617.1 (Kappa) and B.1.1.7 (Alpha)1. In vitro, B.1.617.2 is sixfold less sensitive to serum neutralizing antibodies from recovered individuals, and eightfold less sensitive to vaccine-elicited antibodies, compared with wild-type Wuhan-1 bearing D614G. Serum neutralizing titres against B.1.617.2 were lower in ChAdOx1 vaccinees than in BNT162b2 vaccinees. B.1.617.2 spike pseudotyped viruses exhibited compromised sensitivity to monoclonal antibodies to the receptor-binding domain and the amino-terminal domain. B.1.617.2 demonstrated higher replication efficiency than B.1.1.7 in both airway organoid and human airway epithelial systems, associated with B.1.617.2 spike being in a predominantly cleaved state compared with B.1.1.7 spike. The B.1.617.2 spike protein was able to mediate highly efficient syncytium formation that was less sensitive to inhibition by neutralizing antibody, compared with that of wild-type spike. We also observed that B.1.617.2 had higher replication and spike-mediated entry than B.1.617.1, potentially explaining the B.1.617.2 dominance. In an analysis of more than 130 SARS-CoV-2-infected health care workers across three centres in India during a period of mixed lineage circulation, we observed reduced ChAdOx1 vaccine effectiveness against B.1.617.2 relative to non-B.1.617.2, with the caveat of possible residual confounding. Compromised vaccine efficacy against the highly fit and immune-evasive B.1.617.2 Delta variant warrants continued infection control measures in the post-vaccination era., A study of SARS-CoV-2 variants examining their transmission, infectivity, and potential resistance to therapies provides insights into the biology of the Delta variant and its role in the global pandemic.

Published
2022
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42. MALARIA: A forward genetic screen identifies erythrocyte CD55 as essential for Plasmodium falciparum invasion

Author

Egan, Elizabeth S., Jiang, Rays H. Y., Moechtar, Mischka A., Barteneva, Natasha S., Weekes, Michael P., Nobre, Luis V., Gygi, Steven P., Paulo, Joao A., Frantzreb, Charles, Tani, Yoshihiko, Takahashi, Junko, Watanabe, Seishi, Goldberg, Jonathan, Paul, Aditya S., Brugnara, Carlo, Root, David E., Wiegand, Roger C., Doench, John G., and Duraisingh, Manoj T.

Published
2015
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43. Combined Point-of-Care Nucleic Acid and Antibody Testing for SARS-CoV-2 following Emergence of D614G Spike Variant

Author

Baker, Stephen, Bradley, John, Dougan, Gordon, Goodfellow, Ian, Gupta, Ravi, Lehner, Paul J., Lyons, Paul, Matheson, Nicholas J., Smith, Kenneth G.C., Toshner, Mark, Weekes, Michael P., Brown, Nick, Curran, Martin, Palmar, Surendra, Zhang, Hongyi, Enoch, David, Chapman, Daniel, Shaw, Ashley, Jose, Sherly, Bermperi, Areti, Zerrudo, Julie Ann, Kourampa, Evgenia, Watson, Laura, Worsley, Jieniean, Saunders, Caroline, de Jesus, Ranalie, Domingo, Jason, Pasquale, Ciro, Vergese, Bensi, Vargas, Phoebe, Fabiculana, Marivic, Perales, Marlyn, Mynott, Lee, Blake, Elizabeth, Bates, Amy, Vallier, Anne-Laure, Williams, Alexandra, Phillips, David, Chiu, Edmund, Overhill, Alex, Ramenatte, Nicola, Sipple, Jamal, Frost, Steven, Knock, Helena, Hardy, Richard, Foster, Emily, Davidson, Fiona, Rundell, Viona, Bundi, Purity, Abeseabe, Richmond, Clark, Sarah, Vicente, Isabel, Elmer, Anne, Ribeiro, Carla, Kourampa, Jenny, Kennet, Jane, Rowlands, Jane, Meadows, Anne, O’Brien, Criona, Rastall, Rebecca, Crucusio, Cherry, Hewitt, Sarah, Price, Jane, Calder, Jo, Canna, Laura, Bucke, Ashlea, Tordesillas, Hugo, Harris, Julie, Ruffolo, Valentina, Graves, Barbara, Butcher, Helen, Caputo, Daniela, Le Gresley, Emma, Dunmore, Benjamin J., Martin, Jennifer, Legchenko, Ekaterina, Treacy, Carmen, Huang, Christopher, Wood, Jennifer, Sutcliffe, Rachel, Hodgson, Josh, Shih, Joy, Graf, Stefan, Tong, Zhen, Mescia, Federica, Tilly, Tobias, O’Donnell, Ciara, Hunter, Kelvin, Pointon, Linda, Pond, Nicole, Wylot, Marta, Jones, Emma, Fawke, Stuart, Bullman, Ben, Turner, Lori, Jarvis, Isobel, Omarjee, Ommar, De Sa, Aloka, Marsden, Joe, Betancourt, Ariana, Perera, Marianne, Epping, Maddie, Richoz, Nathan, Bower, Georgie, Sharma, Rahul, Nice, Francesca, Huhn, Oisin, Savoinykh Yarkoni, Natalia, Romashova, Nika, Lewis, Daniel, Hinch, Andrew, Cossetti, Chiara, Strezlecki, Mateusz, Grenfell, Richard, Stark, Hannah, Walker, Neil, Stirrups, Kathy, Ovington, Nigel, Dewhust, Eleanor, Li, Emily, Papadia, Sofia, Kingston, Nathalie, Lever, Andrew, Torok, Estee, Hamilton, William, Hall, Grant, Jahun, Aminu, Chaudhry, Yasmin, Pinckert, Malte, Georgana, Iliana, Yakovleva, Anna, Caller, Laura, Caddy, Sarah, Feltwell, Theresa, Khokhar, Fahad, Meredith, Luke, Holdcroft, Charlotte, Parmar, Surendra, Mlcochova, Petra, Collier, Dami, Ritchie, Allyson, Assennato, Sonny M., Hosmillo, Myra, Goel, Neha, Meng, Bo, Chatterjee, Krishna, Mendoza, Vivien, Temperton, Nigel, Kiss, Leo, James, Leo C., Ciazynska, Katarzyna A., Xiong, Xiaoli, Briggs, John A.G., Nathan, James A., Bergamaschi, Laura, Barmpounakis, Petros, Demeris, Nikos, Skells, Richard, Lyons, Paul A., Baker, Steven, Allain, Jean Pierre, Bousfield, Rachel, Wilson, Michael, Sparkes, Dominic, Amoroso, Glenn, Gkrania-Klotsas, Effrosyni, Hardwick, Susie, Boyle, Adrian, and Gupta, Ravindra K.

Published
2020
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44. Selective modulation of cell surface proteins during vaccinia infection: A resource for identifying viral immune evasion strategies.

Author

Depierreux, Delphine M., Altenburg, Arwen F., Soday, Lior, Fletcher-Etherington, Alice, Anthrobus, Robin, Ferguson, Brian J., Weekes, Michael P., and Smith, Geoffrey L.

Subjects
CELL membranes, VACCINIA, CYTOKINE receptors, EPHRINS, KILLER cells, VIRUS diseases
Abstract

The interaction between immune cells and virus-infected targets involves multiple plasma membrane (PM) proteins. A systematic study of PM protein modulation by vaccinia virus (VACV), the paradigm of host regulation, has the potential to reveal not only novel viral immune evasion mechanisms, but also novel factors critical in host immunity. Here, >1000 PM proteins were quantified throughout VACV infection, revealing selective downregulation of known T and NK cell ligands including HLA-C, downregulation of cytokine receptors including IFNAR2, IL-6ST and IL-10RB, and rapid inhibition of expression of certain protocadherins and ephrins, candidate activating immune ligands. Downregulation of most PM proteins occurred via a proteasome-independent mechanism. Upregulated proteins included a decoy receptor for TRAIL. Twenty VACV-encoded PM proteins were identified, of which five were not recognised previously as such. Collectively, this dataset constitutes a valuable resource for future studies on antiviral immunity, host-pathogen interaction, poxvirus biology, vector-based vaccine design and oncolytic therapy. Author summary: Vaccinia virus (VACV) is the vaccine used to eradicate smallpox and an excellent model for studying host-pathogen interactions. Many VACV-mediated immune evasion strategies are known, however how immune cells recognise VACV-infected cells is incompletely understood because of the complexity of surface proteins regulating such interactions. Here, a systematic study of proteins on the cell surface at different times during infection with VACV is presented. This shows not only the precise nature and kinetics of appearance of VACV proteins, but also the selective alteration of cellular surface proteins. The latter thereby identified potential novel immune evasion strategies and host proteins regulating immune activation. Comprehensive comparisons with published datasets provided further insight into mechanisms used to regulate surface protein expression. Such comparisons also identified proteins that are targeted by both VACV and human cytomegalovirus (HCMV), and which are therefore likely to represent host proteins regulating immune recognition and activation. Collectively, this work provides a valuable resource for studying viral immune evasion mechanisms and novel host proteins critical in host immunity. [ABSTRACT FROM AUTHOR]

Published
2022
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48. Genetic Evidence for Erythrocyte Receptor Glycophorin B Expression Levels Defining a Dominant Plasmodium falciparum Invasion Pathway into Human Erythrocytes

Author

Dankwa, Selasi, Chaand, Mudit, Kanjee, Usheer, Jiang, Rays HY, Nobre, Luis V, Goldberg, Jonathan M, Bei, Amy K, Moechtar, Mischka A, Grüring, Christof, Ahouidi, Ambroise D, Ndiaye, Daouda, Dieye, Tandakha N, Mboup, Souleymane, Weekes, Michael P, Duraisingh, Manoj T, Weekes, Michael [0000-0003-3196-5545], and Apollo - University of Cambridge Repository

Subjects
cultured erythrocyte, Proteomics, Erythrocytes, Plasmodium falciparum, malaria, transcriptional variation, Computational Biology, Receptors, Cell Surface, Ligands, Molecular Pathogenesis, glycophorin, parasitic diseases, Humans, Glycophorins, host cell invasion, red blood cells, Protein Binding
Abstract

Plasmodium falciparum, the parasite that causes the deadliest form of malaria, has evolved multiple proteins known as invasion ligands that bind to specific erythrocyte receptors to facilitate invasion of human erythrocytes. The EBA-175/glycophorin A (GPA) and Rh5/basigin ligand-receptor interactions, referred to as invasion pathways, have been the subject of intense study. In this study, we focused on the less-characterized sialic acid-containing receptors glycophorin B (GPB) and glycophorin C (GPC). Through bioinformatic analysis, we identified extensive variation in glycophorin B (GYPB) transcript levels in individuals from Benin, suggesting selection from malaria pressure. To elucidate the importance of the GPB and GPC receptors relative to the well-described EBA-175/GPA invasion pathway, we used an ex vivo erythrocyte culture system to decrease expression of GPA, GPB, or GPC via lentiviral short hairpin RNA transduction of erythroid progenitor cells, with global surface proteomic profiling. We assessed the efficiency of parasite invasion into knockdown cells using a panel of wild-type P. falciparum laboratory strains and invasion ligand knockout lines, as well as P. falciparum Senegalese clinical isolates and a short-term-culture-adapted strain. For this, we optimized an invasion assay suitable for use with small numbers of erythrocytes. We found that all laboratory strains and the majority of field strains tested were dependent on GPB expression level for invasion. The collective data suggest that the GPA and GPB receptors are of greater importance than the GPC receptor, supporting a hierarchy of erythrocyte receptor usage in P. falciparum.

Published
2017

49. Applying prospective genomic surveillance to support investigation of hospital-onset COVID-19

Author

Curran, Martin D, Parmar, Surendra, Hosmillo, Myra, Chaudhry, Yasmin, Pinckert, Malte L, Georgana, Iliana, Izuagbe, Rhys, Ferris, Mark, Workman, Chris, Jones, Nick K, Rivett, Lucy, Sparkes, Dominic, Routledge, Matthew, Enoch, David, Whitehorn, James, Moody, Christine, Brennan, Liam, Smith, Richard, Tsui, Rachel, Bousfield, Rachel, Pocock, Joanna, Toleman, Michelle, Payne, Helen, Coscione, Suny, Myers, Chloe, Sharrocks, Katherine, Ravji, Pooja, Leong, Clare, Ramsay, Isobel, Hamilton, William L, Fieldman, Tom, Jahun, Aminu, Warne, Ben, Illingworth, Christopher J R, Jackson, Chris, Blane, Beth, Moore, Elinor, Weekes, Michael P, Peacock, Sharon J, De Angelis, Daniela, Goodfellow, Ian, Gouliouris, Theodore, and Török, M Estée

Published
2021
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50. Comparative Cell Surface Proteomic Analysis of the Primary Human T Cell and Monocyte Responses to Type I Interferon.

Author

Soday, Lior, Potts, Martin, Hunter, Leah M., Ravenhill, Benjamin J., Houghton, Jack W., Williamson, James C., Antrobus, Robin, Wills, Mark R., Matheson, Nicholas J., and Weekes, Michael P.

Subjects
TYPE I interferons, T cells, SURFACE analysis, VIRAL envelope proteins, INTERFERON beta 1b, GENES, PROTEOMICS
Abstract

The cellular response to interferon (IFN) is essential for antiviral immunity, IFN-based therapy and IFN-related disease. The plasma membrane (PM) provides a critical interface between the cell and its environment, and is the initial portal of entry for viruses. Nonetheless, the effect of IFN on PM proteins is surprisingly poorly understood, and has not been systematically investigated in primary immune cells. Here, we use multiplexed proteomics to quantify IFNα2a-stimulated PM protein changes in primary human CD14+ monocytes and CD4+ T cells from five donors, quantifying 606 and 482 PM proteins respectively. Comparison of cell surface proteomes revealed a remarkable invariance between donors in the overall composition of the cell surface from each cell type, but a marked donor-to-donor variability in the effects of IFNα2a. Furthermore, whereas only 2.7% of quantified proteins were consistently upregulated by IFNα2a at the surface of CD4+ T cells, 6.8% of proteins were consistently upregulated in primary monocytes, suggesting that the magnitude of the IFNα2a response varies according to cell type. Among these differentially regulated proteins, we found the viral target Endothelin-converting enzyme 1 (ECE1) to be an IFNα2a-stimulated protein exclusively upregulated at the surface of CD4+ T cells. We therefore provide a comprehensive map of the cell surface of IFNα2a-stimulated primary human immune cells, including previously uncharacterized interferon stimulated genes (ISGs) and candidate antiviral factors. [ABSTRACT FROM AUTHOR]

Published
2021
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