Search

Your search keyword '"Department of Health and Human Services (US)"' showing total 9 results
Start Over Author "Department of Health and Human Services (US)" Publication Year Range Last 3 years
9 results on '"Department of Health and Human Services (US)"'

1. Annual (2023) taxonomic update of RNA-directed RNA polymerase-encoding negative-sense RNA viruses (realm Riboviria: kingdom Orthornavirae: phylum Negarnaviricota)

Author

National Institute of Allergy and Infectious Diseases (US), Antiviral Countermeasures Development Center (US), Department of Agriculture (US), Department of the Army (US), Department of Health and Human Services (US), US Department of Homeland Security, Federal Government of the United States, Kuhn, Jens H. [0000-0002-7800-6045], Abe, Junya [0000-0003-3627-7071], Adkins, Scott [0000-0003-0095-8414], Alkhovsky, Sergey V. [0000-0001-6913-5841], Avsic-Zupanc, Tatjana [0000-0001-6243-0688], Ayllón, María A. [0000-0001-7893-6106], Bahl, Justin [0000-0001-7572-4300], Balkema-Buschmann, A. [0000-0001-7613-9592], Ballinger, Matthew J. [0000-0001-7453-8725], Bejerman, Nicolas [0000-0002-7851-3506], Biedenkopf, Nadine [0000-0002-6061-8019], Blair, Carol D.[0000-0002-2803-0354], Blasdell, Kim R.[0000-0003-2121-0376], Bradfute, Steven B.[0000-0002-1985-751X], Briese, Thomas [0000-0002-4819-8963], Buchholz, Ursula J. [0000-0002-2329-3198], Buchmeier, Michael J.[0000-0002-2387-9287], Bukreyev, Alexander [0000-0002-0342-4824], Burt, Felicity [0000-0002-7238-7799], Büttner, Carmen [0000-0002-2086-2594], Calisher, Charles H. [0000-0003-0213-294X], Cao, Mengji [0000-0003-0396-262X], Casas, Inmaculada [0000-0003-1840-1198], Chandran, Kartik [0000-0003-0232-7077], Charrel, Rémi N.[0000-0002-7675-8251], Chaturvedi, Krishna Kumar [0000-0002-6529-5466], Crane, Anya [0000-0002-2060-2469], De Swart, Rik L.[0000-0003-3599-8969], Debat, Humberto [0000-0003-3056-3739], Dheilly, Nolwenn M.[0000-0002-3675-5013], Di Paola, Nicholas [0000-0002-9694-3913], Di Serio, Francesco [0000-0003-2822-704X], Dietzgen, Ralf G.[0000-0002-7772-2250], Digiaro, Michele [0009-0006-3089-3606], Drexler, J. Felix [0000-0002-3509-0232], Duprex, W. Paul [0000-0003-1716-6376], Elbeaino, Toufic [0000-0003-2211-7907], Ergünay, Koray [0000-0001-5422-1982], Feng, Guozhong [0000-0002-9489-9322], Fooks, Anthony R.[0000-0002-3243-6154], Formenty, Pierre B.H.[0000-0002-9482-5411], Freitas-Astúa, Juliana [0000-0002-0506-6880], Gago-Zachert, Selma [0000-0002-1084-2119], García, María Laura [0000-0001-6468-6943], Garrison, Aura R.[0000-0003-3034-6400], Gaskin, Thomas R. [0000-0002-5644-4431], Gouy de Bellocq, Joelle [0000-0001-5831-6284], Griffiths, Anthony [0000-0001-5435-8364], Groschup, M. H.[0000-0003-0215-185X], Günther, Stephan [0000-0002-6562-0230], Hayashi, Kazusa [0009-0002-9395-0066], Hepojoki, Jussi [0000-0001-5699-214X], Higgins, Colleen M. [0000-0001-9016-2940], Horie, Masayuki [0000-0003-4682-7698], Hughes, Holly R.[0000-0003-1380-8263], Hyndman, Timothy [0000-0002-7047-5023], Jiāng, Dàohóng [0000-0002-3862-7461], Jonson, Gilda B.[0000-0003-0097-8634], Junglen, Sandra [0000-0002-3799-6011], Klempa, B.[0000-0002-6931-1224], Klingström, Jonas [0000-0001-9076-1441], Kondō, Hideki [0000-0001-9220-5350], Koonin, Eugene V. [0000-0003-3943-8299], Krupovic, Mart [0000-0001-5486-0098], Kurath, Gael [0000-0003-3294-560X], Laenen, Lies [0000-0001-9118-8608], Li, Jianrong [0000-0002-7130-1084], Lukashevich, Igor S.[0000-0001-6523-5116], MacDiarmid, Robin M.[0000-0002-7057-2018], Maes, Piet [0000-0002-4571-5232], Marklewitz, Marco [0000-0003-1828-8770], Marshall, Sergio H.[0000-0003-0438-8252], Marzano, Shin-Yi L. [0000-0003-0548-3761], Mühlberger, Elke [0000-0003-3547-9376], Nabeshima, Tomoyuki [0000-0002-6570-096X], Naidu, Rayapati [0000-0002-7273-5116], Natsuaki, Tomohide [0000-0003-1823-7308], Navarro, José A. [0000-0002-0536-6074], Neriya, Yutaro [0000-0002-1385-0050], Netesov, Sergey V. [0000-0002-7786-2464], Neumann, Gabriele [0000-0001-7054-1775], Nowotny, N. [0000-0002-3548-571X], Ochoa-Corona, Francisco M. [0000-0002-4112-8209], Pallás, Vicente [0000-0003-4954-989X], Papa, Anna [0000-0002-6643-3322], Paraskevopoulou, Sofia [0000-0003-2608-2596], Parrish, Colin R. [0000-0002-1836-6655], Pauvolid-Corrêa, Alex [0000-0002-6924-157X], Pawęska, Janusz T. [0000-0001-8776-7519], Pérez, Daniel R. [0000-0002-6569-5689], Pfaff, Florian [0000-0003-0178-6183], Plemper, Richard K. [0000-0003-2034-2107], Postler, Thomas S. [0000-0002-3558-9084], Rabbidge, Lee O. [0009-0001-7962-4881], Radoshitzky, Sheli R. [0000-0001-8976-8056], Ramos-González, Pedro L. [0000-0002-9640-6587], Rehanek, Marius [0000-0002-5710-5060], Resende, Renato O. [0000-0003-3852-1576], Romanowski, Víctor [0000-0001-6378-7929], Rubbenstroth, Dennis [0000-0002-8209-6274], Rubino, Luisa [0000-0002-2073-2415], Runstadler, Jonathan A. [0000-0002-6747-7765], Sabanadzovic, Sead [0000-0002-2995-2633], Salvato, Maria S. [0000-0002-3357-5391], Sasaya, Takahide [0000-0002-5020-9377], Schwemmle, Martin [0000-0002-2972-6855], Shi, Mang [0000-0002-6154-4437], Shimomoto, Yoshifumi [0000-0002-0796-7068], Kavi Sidharthan, Venkidusamy [0000-0003-1561-549X], Sironi, Manuela [0000-0002-2267-5266], Smither, Sophie [0000-0002-7835-3581], Spann, Kirsten [0000-0003-0567-8382], Spengler, Jessica R. [0000-0002-5383-0513], Stenglein, Mark D. [0000-0002-0993-813X], Takada, Ayato [0000-0003-2464-6642], Takeyama, Sawana [0009-0000-3771-5999], Tesh, Robert B. [0000-0002-9226-397X], Thornburg, Natalie J. [0000-0003-3523-3616], Tischler, Nicole D. [0000-0002-4578-4780], Tomitaka, Yasuhiro [0000-0002-6914-4016], Tomonaga, Keizō [0000-0003-0405-7103], Tordo, Noël [0000-0001-5873-059X], Tu, Changchun [0000-0002-8134-7502], Turina, Massimo [0000-0002-9659-9470], Tzanetakis, Ioannis E. [0000-0002-5970-1763], Vaira, Anna Maria [0000-0003-2526-4419], Van den Hoogen, Bernadette [0000-0003-1996-8559], Vanmechelen, Bert [0000-0002-8350-4356], Verbeek, Martin [0000-0002-8973-3803], Von Bargen, Susanne [0000-0001-8321-1572], Wada, Jiro [0000-0001-9846-0846], Wahl, Victoria [0000-0002-6588-4308], Walker, Peter J. [0000-0003-1851-642X], Waltzek, Thomas B. [0000-0001-6383-5978], Whitfield, Anna E. [0000-0002-3538-015X], Wolf, Yuri I. [0000-0002-0247-8708], Xylogianni, Evanthia [0009-0001-8768-0939], Yanagisawa, Hironobu [0000-0002-6729-466X], Ye, Gongyin [0000-0003-4937-8867], Yuan, Zhiming [0000-0002-3234-9616], Zerbini, F. Murilo [0000-0001-8617-0200], Okland, Arnfinn Lodden [0000-0003-3062-4386], Kuhn, Jens H., Abe, Junya, Adkins, Scott, Alkhovsky, Sergey V., Avsic-Zupanc, Tatjana, Ayllón, María A., Bahl, Justin, Balkema-Buschmann, A., Ballinger, Matthew J., Kumar Baranwal, Virendra, Beer, Martin, Bejerman, Nicolas, Bergeron, Éric, Biedenkopf, Nadine, Blair, Carol D., Blasdell, Kim R., Blouin, Arnaud G., Bradfute, Steven B., Briese, Thomas, Brown, Paul A., Buchholz, Ursula J., Buchmeier, Michael J., Bukreyev, Alexander, Burt, Felicity, Büttner, Carmen, Calisher, Charles H., Cao, Mengji, Casas, Inmaculada, Chandran, Kartik, Charrel, Rémi N., Chaturvedi, Krishna Kumar, Chooi, Kar Mun, Crane, Anya, Dal Bó, Elena, de la Torre, J. C., de Souza, William Marciel, De Swart, Rik L., Debat, Humberto, Dheilly, Nolwenn M., Di Paola, Nicholas, Di Serio, Francesco, Dietzgen, Ralf G., Digiaro, Michele, Drexler, J. Felix, Duprex, W. Paul, Dürrwald, Ralf, Easton, Andrew J., Elbeaino, Toufic, Ergünay, Koray, Feng, Guozhong, Firth, Andrew E., Fooks, Anthony R., Formenty, Pierre B.H., Freitas-Astúa, Juliana, Gago-Zachert, Selma, García, María Laura, García-Sastre, Adolfo, Garrison, Aura R., Gaskin, Thomas R., Gong, Wenjie, Gonzalez, Jean-Paul J., Gouy de Bellocq, Joelle, Griffiths, Anthony, Groschup, M. H., Günther, Ines, Günther, Stephan, Hammond, John, Hasegawa, Yusuke, Hayashi, Kazusa, Hepojoki, Jussi, Higgins, Colleen M., Hongo, Seiji, Horie, Masayuki, Hughes, Holly R., Hume, Adam J., Hyndman, Timothy, Ikeda, Kenichi, Jiāng, Dàohóng, Jonson, Gilda B., Junglen, Sandra, Klempa, B., Klingström, Jonas, Kondō, Hideki, Koonin, Eugene V., Krupovic, Mart, Kubota, Kenji, Kurath, Gael, Laenen, Lies, Lambert, Amy J., Li, Jianrong, Li, Jun-Min, Liu, Ran, Lukashevich, Igor S., MacDiarmid, Robin M, Maes, Piet, Marklewitz, Marco, Marshall, Sergio H., Marzano, Shin-Yi L., McCauley, John W., Mirazimi, Ali, Mühlberger, Elke, Nabeshima, Tomoyuki, Naidu, Rayapati, Natsuaki, Tomohide, Navarro, Beatriz, Navarro, José A., Neriya, Yutaro, Netesov, Sergey V., Neumann, Gabriele, Nowotny, N., Nunes, Márcio R.T., Ochoa-Corona, Francisco M., Okada, Tomoyuki, Palacios, Gustavo, Pallás, Vicente, Papa, Anna, Paraskevopoulou, Sofia, Parrish, Colin R., Pauvolid-Corrêa, Alex, Pawęska, Janusz T., Pérez, Daniel R., Pfaff, Florian, Plemper, Richard K., Postler, Thomas S., Rabbidge, Lee O., Radoshitzky, Sheli R., Ramos-González, Pedro L., Rehanek, Marius, Resende, Renato O., Reyes, Carina A., Rodrigues, Thaís C.S., Romanowski, Víctor, Rubbenstroth, Dennis, Rubino, Luisa, Runstadler, Jonathan A., Sabanadzovic, Sead, Sadiq, Sabrina, Salvato, Maria S., Sasaya, Takahide, Schwemmle, Martin, Sharpe, Stephen R., Shi, Mang, Shimomoto, Yoshifumi, Kavi Sidharthan, Venkidusamy, Sironi, Manuela, Smither, Sophie, Song, Jin-Won, Spann, Kirsten, Spengler, Jessica R., Stenglein, Mark D., Takada, Ayato, Takeyama, Sawana, Tatara, Akio, Tesh, Robert B., Thornburg, Natalie J., Tian, Xin, Tischler, Nicole D., Tomitaka, Yasuhiro, Tomonaga, Keizō, Tordo, Noël, Tu, Changchun, Turina, Massimo, Tzanetakis, Ioannis E., Vaira, Anna Maria, Van den Hoogen, Bernadette, Vanmechelen, Bert, Vasilakis, Nikos, Verbeek, Martin, Von Bargen, Susanne, Wada, Jiro, Wahl, Victoria, Walker, Peter J., Waltzek, Thomas B., Whitfield, Anna E., Wolf, Yuri I., Xia, Han, Xylogianni, Evanthia, Yanagisawa, Hironobu, Yano, Kazutaka, Ye, Gongyin, Yuan, Zhiming, Zerbini, F. Murilo, Zhang, Guilin, Zhang, Song, Zhang, Yong-Zhen, Zhao, Lu, Okland, Arnfinn Lodden, National Institute of Allergy and Infectious Diseases (US), Antiviral Countermeasures Development Center (US), Department of Agriculture (US), Department of the Army (US), Department of Health and Human Services (US), US Department of Homeland Security, Federal Government of the United States, Kuhn, Jens H. [0000-0002-7800-6045], Abe, Junya [0000-0003-3627-7071], Adkins, Scott [0000-0003-0095-8414], Alkhovsky, Sergey V. [0000-0001-6913-5841], Avsic-Zupanc, Tatjana [0000-0001-6243-0688], Ayllón, María A. [0000-0001-7893-6106], Bahl, Justin [0000-0001-7572-4300], Balkema-Buschmann, A. [0000-0001-7613-9592], Ballinger, Matthew J. [0000-0001-7453-8725], Bejerman, Nicolas [0000-0002-7851-3506], Biedenkopf, Nadine [0000-0002-6061-8019], Blair, Carol D.[0000-0002-2803-0354], Blasdell, Kim R.[0000-0003-2121-0376], Bradfute, Steven B.[0000-0002-1985-751X], Briese, Thomas [0000-0002-4819-8963], Buchholz, Ursula J. [0000-0002-2329-3198], Buchmeier, Michael J.[0000-0002-2387-9287], Bukreyev, Alexander [0000-0002-0342-4824], Burt, Felicity [0000-0002-7238-7799], Büttner, Carmen [0000-0002-2086-2594], Calisher, Charles H. [0000-0003-0213-294X], Cao, Mengji [0000-0003-0396-262X], Casas, Inmaculada [0000-0003-1840-1198], Chandran, Kartik [0000-0003-0232-7077], Charrel, Rémi N.[0000-0002-7675-8251], Chaturvedi, Krishna Kumar [0000-0002-6529-5466], Crane, Anya [0000-0002-2060-2469], De Swart, Rik L.[0000-0003-3599-8969], Debat, Humberto [0000-0003-3056-3739], Dheilly, Nolwenn M.[0000-0002-3675-5013], Di Paola, Nicholas [0000-0002-9694-3913], Di Serio, Francesco [0000-0003-2822-704X], Dietzgen, Ralf G.[0000-0002-7772-2250], Digiaro, Michele [0009-0006-3089-3606], Drexler, J. Felix [0000-0002-3509-0232], Duprex, W. Paul [0000-0003-1716-6376], Elbeaino, Toufic [0000-0003-2211-7907], Ergünay, Koray [0000-0001-5422-1982], Feng, Guozhong [0000-0002-9489-9322], Fooks, Anthony R.[0000-0002-3243-6154], Formenty, Pierre B.H.[0000-0002-9482-5411], Freitas-Astúa, Juliana [0000-0002-0506-6880], Gago-Zachert, Selma [0000-0002-1084-2119], García, María Laura [0000-0001-6468-6943], Garrison, Aura R.[0000-0003-3034-6400], Gaskin, Thomas R. [0000-0002-5644-4431], Gouy de Bellocq, Joelle [0000-0001-5831-6284], Griffiths, Anthony [0000-0001-5435-8364], Groschup, M. H.[0000-0003-0215-185X], Günther, Stephan [0000-0002-6562-0230], Hayashi, Kazusa [0009-0002-9395-0066], Hepojoki, Jussi [0000-0001-5699-214X], Higgins, Colleen M. [0000-0001-9016-2940], Horie, Masayuki [0000-0003-4682-7698], Hughes, Holly R.[0000-0003-1380-8263], Hyndman, Timothy [0000-0002-7047-5023], Jiāng, Dàohóng [0000-0002-3862-7461], Jonson, Gilda B.[0000-0003-0097-8634], Junglen, Sandra [0000-0002-3799-6011], Klempa, B.[0000-0002-6931-1224], Klingström, Jonas [0000-0001-9076-1441], Kondō, Hideki [0000-0001-9220-5350], Koonin, Eugene V. [0000-0003-3943-8299], Krupovic, Mart [0000-0001-5486-0098], Kurath, Gael [0000-0003-3294-560X], Laenen, Lies [0000-0001-9118-8608], Li, Jianrong [0000-0002-7130-1084], Lukashevich, Igor S.[0000-0001-6523-5116], MacDiarmid, Robin M.[0000-0002-7057-2018], Maes, Piet [0000-0002-4571-5232], Marklewitz, Marco [0000-0003-1828-8770], Marshall, Sergio H.[0000-0003-0438-8252], Marzano, Shin-Yi L. [0000-0003-0548-3761], Mühlberger, Elke [0000-0003-3547-9376], Nabeshima, Tomoyuki [0000-0002-6570-096X], Naidu, Rayapati [0000-0002-7273-5116], Natsuaki, Tomohide [0000-0003-1823-7308], Navarro, José A. [0000-0002-0536-6074], Neriya, Yutaro [0000-0002-1385-0050], Netesov, Sergey V. [0000-0002-7786-2464], Neumann, Gabriele [0000-0001-7054-1775], Nowotny, N. [0000-0002-3548-571X], Ochoa-Corona, Francisco M. [0000-0002-4112-8209], Pallás, Vicente [0000-0003-4954-989X], Papa, Anna [0000-0002-6643-3322], Paraskevopoulou, Sofia [0000-0003-2608-2596], Parrish, Colin R. [0000-0002-1836-6655], Pauvolid-Corrêa, Alex [0000-0002-6924-157X], Pawęska, Janusz T. [0000-0001-8776-7519], Pérez, Daniel R. [0000-0002-6569-5689], Pfaff, Florian [0000-0003-0178-6183], Plemper, Richard K. [0000-0003-2034-2107], Postler, Thomas S. [0000-0002-3558-9084], Rabbidge, Lee O. [0009-0001-7962-4881], Radoshitzky, Sheli R. [0000-0001-8976-8056], Ramos-González, Pedro L. [0000-0002-9640-6587], Rehanek, Marius [0000-0002-5710-5060], Resende, Renato O. [0000-0003-3852-1576], Romanowski, Víctor [0000-0001-6378-7929], Rubbenstroth, Dennis [0000-0002-8209-6274], Rubino, Luisa [0000-0002-2073-2415], Runstadler, Jonathan A. [0000-0002-6747-7765], Sabanadzovic, Sead [0000-0002-2995-2633], Salvato, Maria S. [0000-0002-3357-5391], Sasaya, Takahide [0000-0002-5020-9377], Schwemmle, Martin [0000-0002-2972-6855], Shi, Mang [0000-0002-6154-4437], Shimomoto, Yoshifumi [0000-0002-0796-7068], Kavi Sidharthan, Venkidusamy [0000-0003-1561-549X], Sironi, Manuela [0000-0002-2267-5266], Smither, Sophie [0000-0002-7835-3581], Spann, Kirsten [0000-0003-0567-8382], Spengler, Jessica R. [0000-0002-5383-0513], Stenglein, Mark D. [0000-0002-0993-813X], Takada, Ayato [0000-0003-2464-6642], Takeyama, Sawana [0009-0000-3771-5999], Tesh, Robert B. [0000-0002-9226-397X], Thornburg, Natalie J. [0000-0003-3523-3616], Tischler, Nicole D. [0000-0002-4578-4780], Tomitaka, Yasuhiro [0000-0002-6914-4016], Tomonaga, Keizō [0000-0003-0405-7103], Tordo, Noël [0000-0001-5873-059X], Tu, Changchun [0000-0002-8134-7502], Turina, Massimo [0000-0002-9659-9470], Tzanetakis, Ioannis E. [0000-0002-5970-1763], Vaira, Anna Maria [0000-0003-2526-4419], Van den Hoogen, Bernadette [0000-0003-1996-8559], Vanmechelen, Bert [0000-0002-8350-4356], Verbeek, Martin [0000-0002-8973-3803], Von Bargen, Susanne [0000-0001-8321-1572], Wada, Jiro [0000-0001-9846-0846], Wahl, Victoria [0000-0002-6588-4308], Walker, Peter J. [0000-0003-1851-642X], Waltzek, Thomas B. [0000-0001-6383-5978], Whitfield, Anna E. [0000-0002-3538-015X], Wolf, Yuri I. [0000-0002-0247-8708], Xylogianni, Evanthia [0009-0001-8768-0939], Yanagisawa, Hironobu [0000-0002-6729-466X], Ye, Gongyin [0000-0003-4937-8867], Yuan, Zhiming [0000-0002-3234-9616], Zerbini, F. Murilo [0000-0001-8617-0200], Okland, Arnfinn Lodden [0000-0003-3062-4386], Kuhn, Jens H., Abe, Junya, Adkins, Scott, Alkhovsky, Sergey V., Avsic-Zupanc, Tatjana, Ayllón, María A., Bahl, Justin, Balkema-Buschmann, A., Ballinger, Matthew J., Kumar Baranwal, Virendra, Beer, Martin, Bejerman, Nicolas, Bergeron, Éric, Biedenkopf, Nadine, Blair, Carol D., Blasdell, Kim R., Blouin, Arnaud G., Bradfute, Steven B., Briese, Thomas, Brown, Paul A., Buchholz, Ursula J., Buchmeier, Michael J., Bukreyev, Alexander, Burt, Felicity, Büttner, Carmen, Calisher, Charles H., Cao, Mengji, Casas, Inmaculada, Chandran, Kartik, Charrel, Rémi N., Chaturvedi, Krishna Kumar, Chooi, Kar Mun, Crane, Anya, Dal Bó, Elena, de la Torre, J. C., de Souza, William Marciel, De Swart, Rik L., Debat, Humberto, Dheilly, Nolwenn M., Di Paola, Nicholas, Di Serio, Francesco, Dietzgen, Ralf G., Digiaro, Michele, Drexler, J. Felix, Duprex, W. Paul, Dürrwald, Ralf, Easton, Andrew J., Elbeaino, Toufic, Ergünay, Koray, Feng, Guozhong, Firth, Andrew E., Fooks, Anthony R., Formenty, Pierre B.H., Freitas-Astúa, Juliana, Gago-Zachert, Selma, García, María Laura, García-Sastre, Adolfo, Garrison, Aura R., Gaskin, Thomas R., Gong, Wenjie, Gonzalez, Jean-Paul J., Gouy de Bellocq, Joelle, Griffiths, Anthony, Groschup, M. H., Günther, Ines, Günther, Stephan, Hammond, John, Hasegawa, Yusuke, Hayashi, Kazusa, Hepojoki, Jussi, Higgins, Colleen M., Hongo, Seiji, Horie, Masayuki, Hughes, Holly R., Hume, Adam J., Hyndman, Timothy, Ikeda, Kenichi, Jiāng, Dàohóng, Jonson, Gilda B., Junglen, Sandra, Klempa, B., Klingström, Jonas, Kondō, Hideki, Koonin, Eugene V., Krupovic, Mart, Kubota, Kenji, Kurath, Gael, Laenen, Lies, Lambert, Amy J., Li, Jianrong, Li, Jun-Min, Liu, Ran, Lukashevich, Igor S., MacDiarmid, Robin M, Maes, Piet, Marklewitz, Marco, Marshall, Sergio H., Marzano, Shin-Yi L., McCauley, John W., Mirazimi, Ali, Mühlberger, Elke, Nabeshima, Tomoyuki, Naidu, Rayapati, Natsuaki, Tomohide, Navarro, Beatriz, Navarro, José A., Neriya, Yutaro, Netesov, Sergey V., Neumann, Gabriele, Nowotny, N., Nunes, Márcio R.T., Ochoa-Corona, Francisco M., Okada, Tomoyuki, Palacios, Gustavo, Pallás, Vicente, Papa, Anna, Paraskevopoulou, Sofia, Parrish, Colin R., Pauvolid-Corrêa, Alex, Pawęska, Janusz T., Pérez, Daniel R., Pfaff, Florian, Plemper, Richard K., Postler, Thomas S., Rabbidge, Lee O., Radoshitzky, Sheli R., Ramos-González, Pedro L., Rehanek, Marius, Resende, Renato O., Reyes, Carina A., Rodrigues, Thaís C.S., Romanowski, Víctor, Rubbenstroth, Dennis, Rubino, Luisa, Runstadler, Jonathan A., Sabanadzovic, Sead, Sadiq, Sabrina, Salvato, Maria S., Sasaya, Takahide, Schwemmle, Martin, Sharpe, Stephen R., Shi, Mang, Shimomoto, Yoshifumi, Kavi Sidharthan, Venkidusamy, Sironi, Manuela, Smither, Sophie, Song, Jin-Won, Spann, Kirsten, Spengler, Jessica R., Stenglein, Mark D., Takada, Ayato, Takeyama, Sawana, Tatara, Akio, Tesh, Robert B., Thornburg, Natalie J., Tian, Xin, Tischler, Nicole D., Tomitaka, Yasuhiro, Tomonaga, Keizō, Tordo, Noël, Tu, Changchun, Turina, Massimo, Tzanetakis, Ioannis E., Vaira, Anna Maria, Van den Hoogen, Bernadette, Vanmechelen, Bert, Vasilakis, Nikos, Verbeek, Martin, Von Bargen, Susanne, Wada, Jiro, Wahl, Victoria, Walker, Peter J., Waltzek, Thomas B., Whitfield, Anna E., Wolf, Yuri I., Xia, Han, Xylogianni, Evanthia, Yanagisawa, Hironobu, Yano, Kazutaka, Ye, Gongyin, Yuan, Zhiming, Zerbini, F. Murilo, Zhang, Guilin, Zhang, Song, Zhang, Yong-Zhen, Zhao, Lu, and Okland, Arnfinn Lodden

Abstract

In April 2023, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote on newly proposed taxa, the phylum Negarnaviricota was amended and emended. The phylum was expanded by one new family, 14 new genera, and 140 new species. Two genera and 538 species were renamed. One species was moved, and four were abolished. This article presents the updated taxonomy of Negarnaviricota as now accepted by the ICTV.

Published
2023

2. Defining the causes of sporadic Parkinson’s disease in the global Parkinson’s genetics program (GP2)

Author

National Institute on Aging (US), National Institutes of Health (US), Aligning Science Against Parkinson's, Parkinson Research Foundation, Department of Health and Human Services (US), Towns, Clodagh, Richer, Madeleine, Jasaityte, Simona, Stafford, Eleanor J., Joubert, Julie, Antar, Tarek, Martínez-Carrasco, Alejandro, Makarious, Mary B., Casey, Bradford, Vitale, Dan, Levine, Kristin, Leonard, Hampton, Pantazis, Caroline B., Screven, Laurel A., Hernández, Dena G., Wegel, Claire E., Solle, Justin, Nalls, Mike A., Blauwendraat, Cornelis, Singleton, Andrew B., Tan, Manuela M. X., Iwaki, Hirotaka, Morris, Huw, Global Parkinson’s Genetics Program (GP2), Periñán, María Teresa, National Institute on Aging (US), National Institutes of Health (US), Aligning Science Against Parkinson's, Parkinson Research Foundation, Department of Health and Human Services (US), Towns, Clodagh, Richer, Madeleine, Jasaityte, Simona, Stafford, Eleanor J., Joubert, Julie, Antar, Tarek, Martínez-Carrasco, Alejandro, Makarious, Mary B., Casey, Bradford, Vitale, Dan, Levine, Kristin, Leonard, Hampton, Pantazis, Caroline B., Screven, Laurel A., Hernández, Dena G., Wegel, Claire E., Solle, Justin, Nalls, Mike A., Blauwendraat, Cornelis, Singleton, Andrew B., Tan, Manuela M. X., Iwaki, Hirotaka, Morris, Huw, Global Parkinson’s Genetics Program (GP2), and Periñán, María Teresa

Abstract

The Global Parkinson’s Genetics Program (GP2) will genotype over 150,000 participants from around the world, and integrate genetic and clinical data for use in large-scale analyses to dramatically expand our understanding of the genetic architecture of PD. This report details the workflow for cohort integration into the complex arm of GP2, and together with our outline of the monogenic hub in a companion paper, provides a generalizable blueprint for establishing large scale collaborative research consortia.

Published
2023

3. Mutation L319Q in the PB1 Polymerase Subunit Improves Attenuation of a Candidate Live-Attenuated Influenza A Virus Vaccine

Author

New York Influenza Center of Excellence, National Institute of Allergy and Infectious Diseases (US), Department of Health and Human Services (US), Centers of Excellence for Influenza Research and Surveillance (US), Department of Defense (US), Center for Research for Influenza Pathogenesis (US), Ministerio de Ciencia e Innovación (España), Icahn School of Medicine at Mount Sinai, Nogales, Aitor [0000-0002-2424-7900], Lowen, Anice C. [0000-0002-9829-112X], Chiem, Kevin [0000-0002-3892-5944], García-Sastre, Adolfo [0000-0002-6551-1827], Albrecht, Randy A. [0000-0003-4008-503X], Dewhurst, Stephen [0000-0001-7729-7920], Nogales, Aitor, Steel, John, Liu, Wen-Chun, Lowen, Anice C., Rodriguez, Laura, Chiem, Kevin, Cox, Andrew, García-Sastre, Adolfo, Albrecht, Randy A., Dewhurst, Stephen, Martínez-Sobrido, Luis, New York Influenza Center of Excellence, National Institute of Allergy and Infectious Diseases (US), Department of Health and Human Services (US), Centers of Excellence for Influenza Research and Surveillance (US), Department of Defense (US), Center for Research for Influenza Pathogenesis (US), Ministerio de Ciencia e Innovación (España), Icahn School of Medicine at Mount Sinai, Nogales, Aitor [0000-0002-2424-7900], Lowen, Anice C. [0000-0002-9829-112X], Chiem, Kevin [0000-0002-3892-5944], García-Sastre, Adolfo [0000-0002-6551-1827], Albrecht, Randy A. [0000-0003-4008-503X], Dewhurst, Stephen [0000-0001-7729-7920], Nogales, Aitor, Steel, John, Liu, Wen-Chun, Lowen, Anice C., Rodriguez, Laura, Chiem, Kevin, Cox, Andrew, García-Sastre, Adolfo, Albrecht, Randy A., Dewhurst, Stephen, and Martínez-Sobrido, Luis

Abstract

Influenza A viruses (IAV) remain emerging threats to human public health. Live-attenuated influenza vaccines (LAIV) are one of the most effective prophylactic options to prevent disease caused by influenza infections. However, licensed LAIV remain restricted for use in 2- to 49-year-old healthy and nonpregnant people. Therefore, development of LAIV with increased safety, immunogenicity, and protective efficacy is highly desired. The U.S.-licensed LAIV is based on the master donor virus (MDV) A/Ann Arbor/6/60 H2N2 backbone, which was generated by adaptation of the virus to growth at low temperatures. Introducing the genetic signature of the U.S. MDV into the backbone of other IAV strains resulted in varying levels of attenuation. While the U.S. MDV mutations conferred an attenuated phenotype to other IAV strains, the same amino acid changes did not significantly attenuate the pandemic A/California/04/09 H1N1 (pH1N1) strain. To attenuate pH1N1, we replaced the conserved leucine at position 319 with glutamine (L319Q) in PB1 and analyzed the in vitro and in vivo properties of pH1N1 viruses containing either PB1 L319Q alone or in combination with the U.S. MDV mutations using two animal models of influenza infection and transmission, ferrets and guinea pigs. Our results demonstrated that L319Q substitution in the pH1N1 PB1 alone or in combination with the mutations of the U.S. MDV resulted in reduced pathogenicity (ferrets) and transmission (guinea pigs), and an enhanced temperature sensitive phenotype. These results demonstrate the feasibility of generating an attenuated MDV based on the backbone of a contemporary pH1N1 IAV strain. IMPORTANCE Vaccination represents the most effective strategy to reduce the impact of seasonal IAV infections. Although LAIV are superior in inducing protection and sterilizing immunity, they are not recommended for many individuals who are at high risk for severe disease. Thus, development of safer and more effective LAIV are needed. A concer

Published
2022

4. El exómero: conexión entre la secreción polarizada y el estrés iónico

Author

Ministerio de Economía, Industria y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Junta de Castilla y León, Universidad de Salamanca, University of Toledo, Department of Health and Human Services (US), Moscoso-Romero, Esteban, Moro, Sandra, Poddar, Abhishek, Mulet-Salort, José Miguel, Pérez, Pilar, Chen, Qian, Valdivieso, María Henar, Ministerio de Economía, Industria y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Junta de Castilla y León, Universidad de Salamanca, University of Toledo, Department of Health and Human Services (US), Moscoso-Romero, Esteban, Moro, Sandra, Poddar, Abhishek, Mulet-Salort, José Miguel, Pérez, Pilar, Chen, Qian, and Valdivieso, María Henar

Abstract

El exómero es un complejo proteico que facilita el transporte de vesículas desde la red trans del Golgi (TGN) hasta la membrana plasmática (MP). En Saccharomyces cerevisiae su ausencia causa la retención de un conjunto específico de proteínas cargo en este orgánulo. El exómero de Schizosaccharomyces pombe está compuesto por Cfr1 y Bch1. Los mutantes cfr1¿ y bch1¿ son sensibles a estrés iónico pero no osmótico. Además, la actividad ATPasa en la MP es mayor en un mutante del exómero, lo que sugiere una hiperpolarización de la membrana. Además, en respuesta a estrés por K+, los niveles de Ca2+ intracelular aumentan significativamente más en cfr1¿ que en el silvestre. Los análisis por microscopía muestran una morfología endosomal defectuosa en los mutantes. Esto va acompañado de un incremento de los niveles intracelulares del exportador de K+ Cta3 y el canal de Ca2+ Pck2, que están parcialmente acumulados en el endosoma prevacuolar. Aun así, estos transportadores iónicos llegan a la membrana en los sitios de crecimiento polarizado, lo que demuestra que su transporte desde el TGN ocurre en ausencia del exómero. En los momentos posteriores a su expresión génica en presencia de KCl, la localización polarizada de Cta3 y Pkd2 en la membrana está alterada en los mutantes, de manera que su distribución es asimétrica y subapical. Finalmente, el uso de sondas fluorescentes sugiere que en los mutantes hay una distribución defectuosa de algunos lípidos de la MP en presencia de KCl. Por tanto, el exómero participa en muchos procesos celulares que están alterados en respuesta a estrés por K+. Estos resultados apoyan la idea de que el exómero juega un papel general en el mantenimiento del TGN, la secreción polarizada, y la respuesta a estrés que no está necesariamente relacionado con una función como adaptador de cargo.

Published
2022

5. El exómero: conexión entre la secreción polarizada y el estrés iónico

Author

Moscoso, Esteban, Moro, Sandra, Poddar, Abhishek, Mulet-Salort, José Miguel, Pérez, Pilar, Chen, Qian, Valdivieso, María Henar, Ministerio de Economía, Industria y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Junta de Castilla y León, Universidad de Salamanca, University of Toledo, and Department of Health and Human Services (US)

Abstract

Poster del trabajo presentado en el XV Congreso Nacional de Micología, celebrado en Valencia del 7 al 9 de septiembre de 2022, El exómero es un complejo proteico que facilita el transporte de vesículas desde la red trans del Golgi (TGN) hasta la membrana plasmática (MP). En Saccharomyces cerevisiae su ausencia causa la retención de un conjunto específico de proteínas cargo en este orgánulo. El exómero de Schizosaccharomyces pombe está compuesto por Cfr1 y Bch1. Los mutantes cfr1¿ y bch1¿ son sensibles a estrés iónico pero no osmótico. Además, la actividad ATPasa en la MP es mayor en un mutante del exómero, lo que sugiere una hiperpolarización de la membrana. Además, en respuesta a estrés por K+, los niveles de Ca2+ intracelular aumentan significativamente más en cfr1¿ que en el silvestre. Los análisis por microscopía muestran una morfología endosomal defectuosa en los mutantes. Esto va acompañado de un incremento de los niveles intracelulares del exportador de K+ Cta3 y el canal de Ca2+ Pck2, que están parcialmente acumulados en el endosoma prevacuolar. Aun así, estos transportadores iónicos llegan a la membrana en los sitios de crecimiento polarizado, lo que demuestra que su transporte desde el TGN ocurre en ausencia del exómero. En los momentos posteriores a su expresión génica en presencia de KCl, la localización polarizada de Cta3 y Pkd2 en la membrana está alterada en los mutantes, de manera que su distribución es asimétrica y subapical. Finalmente, el uso de sondas fluorescentes sugiere que en los mutantes hay una distribución defectuosa de algunos lípidos de la MP en presencia de KCl. Por tanto, el exómero participa en muchos procesos celulares que están alterados en respuesta a estrés por K+. Estos resultados apoyan la idea de que el exómero juega un papel general en el mantenimiento del TGN, la secreción polarizada, y la respuesta a estrés que no está necesariamente relacionado con una función como adaptador de cargo., Este trabajo ha sido posible gracias al apoyo del Ministerio de Economía, Industria y Competitividad/Ciencia, Investigación y Universidades/ programa European Regional Development Fund—FEDER—(BFU2017-84508-P y PID2020-115111GB-I00 a M-HV y PGC2018-098924-B-I00 a PP), y de la Junta de Castilla y Leon/programa FEDER (CSI150P20 a PP, y Escalera de Excelencia CLU-2017-03/14-20 al IBFG). SM disfrutó de becas de la Universidad de Salamanca y el Ministerio de Educación, y EMR disfrutó de una beca de la Junta de Castilla y León. Las becas de la Agencia Española de Investigación (AEI) PID2019-104054 GB-I00 y RTC-2017-6468-2-AR financiaron a JM. QC y AP fueron financiados por la “University of Toledo start up fund” y una beca del “National Institute of Health” (R15GM134496).

Published
2022

6. Mutation L319Q in the PB1 Polymerase Subunit Improves Attenuation of a Candidate Live-Attenuated Influenza A Virus Vaccine

Author

Aitor Nogales, John Steel, Wen-Chun Liu, Anice C. Lowen, Laura Rodriguez, Kevin Chiem, Andrew Cox, Adolfo García-Sastre, Randy A. Albrecht, Stephen Dewhurst, Luis Martínez-Sobrido, New York Influenza Center of Excellence, National Institute of Allergy and Infectious Diseases (US), Department of Health and Human Services (US), Centers of Excellence for Influenza Research and Surveillance (US), Department of Defense (US), Center for Research on Influenza Pathogenesis, Ministerio de Ciencia e Innovación (España), Icahn School of Medicine at Mount Sinai, Nogales, Aitor [0000-0002-2424-7900], Lowen, Anice C [0000-0002-9829-112X], Chiem, Kevin [0000-0002-3892-5944], García-Sastre, Adolfo [0000-0002-6551-1827], Albrecht, Randy A [0000-0003-4008-503X], Dewhurst, Stephen [0000-0001-7729-7920], Nogales, Aitor, Lowen, Anice C, Chiem, Kevin, García-Sastre, Adolfo, Albrecht, Randy A, and Dewhurst, Stephen

Subjects
Microbiology (medical), Physiology, Guinea Pigs, Vaccines, Attenuated, Viral Proteins, Influenza A Virus, H1N1 Subtype, Orthomyxoviridae Infections, Protection efficacy, Influenza, Human, Genetics, Transmission, Animals, Humans, Vaccines, General Immunology and Microbiology, Ecology, Ferrets, Cell Biology, Master donor virus, Temperature sensitive, Infectious Diseases, Attenuated, Cold-adapted, Live-attenuated influenza vaccines, Influenza A virus, Influenza Vaccines, Mutation, Guinea pigs
Abstract

15 Pág. Centro de Investigación en Sanidad Animal (CISA), Influenza A viruses (IAV) remain emerging threats to human public health. Live-attenuated influenza vaccines (LAIV) are one of the most effective prophylactic options to prevent disease caused by influenza infections. However, licensed LAIV remain restricted for use in 2- to 49-year-old healthy and nonpregnant people. Therefore, development of LAIV with increased safety, immunogenicity, and protective efficacy is highly desired. The U.S.-licensed LAIV is based on the master donor virus (MDV) A/Ann Arbor/6/60 H2N2 backbone, which was generated by adaptation of the virus to growth at low temperatures. Introducing the genetic signature of the U.S. MDV into the backbone of other IAV strains resulted in varying levels of attenuation. While the U.S. MDV mutations conferred an attenuated phenotype to other IAV strains, the same amino acid changes did not significantly attenuate the pandemic A/California/04/09 H1N1 (pH1N1) strain. To attenuate pH1N1, we replaced the conserved leucine at position 319 with glutamine (L319Q) in PB1 and analyzed the in vitro and in vivo properties of pH1N1 viruses containing either PB1 L319Q alone or in combination with the U.S. MDV mutations using two animal models of influenza infection and transmission, ferrets and guinea pigs. Our results demonstrated that L319Q substitution in the pH1N1 PB1 alone or in combination with the mutations of the U.S. MDV resulted in reduced pathogenicity (ferrets) and transmission (guinea pigs), and an enhanced temperature sensitive phenotype. These results demonstrate the feasibility of generating an attenuated MDV based on the backbone of a contemporary pH1N1 IAV strain. IMPORTANCE Vaccination represents the most effective strategy to reduce the impact of seasonal IAV infections. Although LAIV are superior in inducing protection and sterilizing immunity, they are not recommended for many individuals who are at high risk for severe disease. Thus, development of safer and more effective LAIV are needed. A concern with the current MDV used to generate the U.S.-licensed LAIV is that it is based on a virus isolated in 1960. Moreover, mutations that confer the temperature-sensitive, cold-adapted, and attenuated phenotype of the U.S. MDV resulted in low level of attenuation in the contemporary pandemic A/California/04/09 H1N1 (pH1N1). Here, we show that introduction of PB1 L319Q substitution, alone or in combination with the U.S. MDV mutations, resulted in pH1N1 attenuation. These findings support the development of a novel LAIV MDV based on a contemporary pH1N1 strain as a medical countermeasure against currently circulating H1N1 IAV., This research was partially funded by the New York Influenza Center of Excellence (NYICE) (HHSN 272201400005C), and Emory-UGA (HHSN 272201400004C), members of the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Department of Health and Human Services, Centers of Excellence for Influenza Research and Surveillance (CEIRS) network. The work was also supported by grants W81XWH-18-1-0460-PRMRP-DA (to L.M.-S.) and W81XWH-17-1-0168 (to S.D.) from the Department of Defense (DoD) Peer Reviewed Medical Research Program (PRMRP), as well as NIH R01 AI145332-01 (to L.M.-S.). This research was also partly funded by NIAID grant P01AI097092, by CEIRR (Center for Research on Influenza Pathogenesis and Transmission), a NIAID funded Center of Excellence for Influenza Research and Response (CEIRR, contract # 75N93021C00014) and by the Collaborative Influenza Vaccine Innovation Centers NIAID contract 75N93019C00051 to AG-S. A.N. received a “Ramon y Cajal” Incorporation grant (RYC-2017) from the Spanish Ministry of Science, Innovation. Finally, A.C. received support from NIH grants T32GM068411 and T32GM007356. Use of the Zeiss AxioImager.Z2 microscope and image analysis was performed at the Microscopy CoRE at the Icahn School of Medicine at Mount Sinai.

Published
2022

7. A cholinergic neuroskeletal interface promotes bone formation during postnatal growth and exercise

Author

Stephen Gadomski, Claire Fielding, Andrés García-García, Claudia Korn, Chrysa Kapeni, Sadaf Ashraf, Javier Villadiego, Raquel del Toro, Olivia Domingues, Jeremy N. Skepper, Tatiana Michel, Jacques Zimmer, Regine Sendtner, Scott Dillon, Kenneth E.S. Poole, Gill Holdsworth, Michael Sendtner, Juan J. Toledo-Aral, Cosimo De Bari, Andrew W. McCaskie, Pamela G. Robey, Simón Méndez-Ferrer, National Institutes of Health (US), Gates Cambridge Scholarships, Fundación Ramón Areces, Fundación 'la Caixa', European Commission, German Research Foundation, Federal Ministry of Education and Research (Germany), Instituto de Salud Carlos III, Junta de Andalucía, Versus Arthritis, National Institute of Dental and Craniofacial Research (US), Department of Health and Human Services (US), NIHR Biomedical Research Centre (UK), MRC Cambridge Stem Cell Institute, National Health Institute Blood and Transplant (UK), Wellcome Trust, Cancer Research UK, Poole, Kenneth [0000-0003-4546-7352], McCaskie, Andrew [0000-0001-6476-0832], and Apollo - University of Cambridge Repository

Subjects
anabolic, Glial Cell Line-Derived Neurotrophic Factor Receptors, Anabolic, osteocyte, Cholinergic Agents, Development, bone, cholinergic, Osteogenesis, Genetics, Bone, development, Exercise, Cholinergic, exercise, autonomic, Interleukin-6, Neuroskeletal, Osteocyte, Cell Biology, Skeletal, sympathetic, skeletal, neuroskeletal, Autonomic, Cholinergic Fibers, Molecular Medicine, Sympathetic
Abstract

The autonomic nervous system is a master regulator of homeostatic processes and stress responses. Sympathetic noradrenergic nerve fibers decrease bone mass, but the role of cholinergic signaling in bone has remained largely unknown. Here, we describe that early postnatally, a subset of sympathetic nerve fibers undergoes an interleukin-6 (IL-6)-induced cholinergic switch upon contacting the bone. A neurotrophic dependency mediated through GDNF-family receptor-α2 (GFRα2) and its ligand, neurturin (NRTN), is established between sympathetic cholinergic fibers and bone-embedded osteocytes, which require cholinergic innervation for their survival and connectivity. Bone-lining osteoprogenitors amplify and propagate cholinergic signals in the bone marrow (BM). Moderate exercise augments trabecular bone partly through an IL-6-dependent expansion of sympathetic cholinergic nerve fibers. Consequently, loss of cholinergic skeletal innervation reduces osteocyte survival and function, causing osteopenia and impaired skeletal adaptation to moderate exercise. These results uncover a cholinergic neuro-osteocyte interface that regulates skeletogenesis and skeletal turnover through bone-anabolic effects., S.G. was supported by the NIH-OXCAM Program and the Gates Cambridge Trust. A.G.G. received fellowships from Ramón Areces and La Caixa Foundations. C.K. was supported by Marie Curie Career Integration grant H2020-MSCA-IF-2015-70841. M.S. and R.S. were supported by DFG, Se 697/7-1 and BMBF through the EnergI consortium TP6. J.V. and J.J.T.-A. were supported by Instituto de Salud Carlos III (PI12/02574), Junta de Andalucia (P12-CTS-2739), and, together with S.M.-F., by Red TerCel (ISCIII-Spanish Cell Therapy Network). S.A. and C.D.B. were supported by Versus Arthritis grant 21156. A.W.M. received funding from Versus Arthritis (21156). P.G.R. and S.G. were supported by the DIR, NIDCR, a part of the IRP, NIH, and DHHS (1ZIADE000380). K.E.S.P. acknowledges the support of the Cambridge NIHR Biomedical Research Centre. This work was supported by core support grants from MRC to the Cambridge Stem Cell Institute; National Health Service Blood and Transplant (United Kingdom), European Union’s Horizon 2020 research (ERC-2014-CoG-648765), MRC-AMED grant MR/V005421/1, and a Programme Foundation Award (C61367/A26670) from Cancer Research UK to S.M.-F. This research was funded in part by the Wellcome Trust (203151/Z/16/Z).

Published
2022

8. In Vitro Activity of Cefepime-Taniborbactam against Carbapenemase-Producing Enterobacterales and Pseudomonas aeruginosa Isolates Recovered in Spain

Author

Marta Hernández-García, María García-Castillo, Patricia Ruiz-Garbajosa, Germán Bou, María Siller-Ruiz, Cristina Pitart, Irene Gracia-Ahufinger, Xavier Mulet, Álvaro Pascual, Nuria Tormo, Rafael Cantón, Department of Health and Human Services (US), Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), Red Española de Investigación en Patología Infecciosa, European Commission, and Centro de Investigación Biomédica en Red de Enfermedades Infecciosas (España)

Subjects
Carbapenemase-producing Pseudomonas aeruginosa, Pharmacology, carbapenemase-producing Enterobacterales, Carboxylic Acids, Carbapenemase-producing Enterobacterales, Microbial Sensitivity Tests, beta-Lactamases, Anti-Bacterial Agents, carbapenemase-producing Pseudomonas aeruginosa, Infectious Diseases, Bacterial Proteins, Spain, Susceptibility, Pseudomonas aeruginosa, Humans, Pharmacology (medical), cefepime-taniborbactam susceptibility, Borinic Acids, Cefepime, Azabicyclo Compounds
Abstract

Novel β-lactam-β-lactamase inhibitor combinations currently approved for clinical use are poorly active against metallo-β-lactamase (MBL)-producing strains. We evaluated the in vitro activity of cefepime-taniborbactam (FTB [formerly cefepime-VNRX-5133]) and comparator agents against carbapenemase-producing Enterobacterales (n = 247) and carbapenem-resistant Pseudomonas species (n = 170) clinical isolates prospectively collected from different clinical origins in patients admitted to 8 Spanish hospitals. FTB was the most active agent in both Enterobacterales (97.6% MICFTB, ≤8/4 mg/L) and Pseudomonas (67.1% MICFTB, ≤8/4 mg/L) populations. The MICFTB was >8 mg/L in 6/247 (2.4%) Enterobacterales isolates (3 KPC-producing Klebsiella pneumoniae isolates, 1 VIM-producing Enterobacter cloacae isolate, 1 IMP-producing E. cloacae isolate, and 1 NDM-producing Escherichia coli isolate) and in 56/170 (32.9%) Pseudomonas isolates, 19 of them carbapenemase producers (15 producers of VIM, 2 of GES, 1 of GES+VIM, and 1 of GES+KPC). Against the Enterobacterales isolates with meropenem MICs of >2 mg/L (138/247), FTB was the most active agent against both serine-β-lactamases (107/138) and MBL producers (31/138) (97.2 and 93.5% MICFTB, ≤8/4 mg/L, respectively), whereas the activity of comparators was reduced, particularly against the MBL producers (ceftazidime-avibactam, 94.4 and 12.9%, meropenem-vaborbactam, 85.0 and 64.5%, imipenem-relebactam, 76.6 and 9.7%, ceftolozane-tazobactam, 1.9 and 0%, and piperacillin-tazobactam, 0 and 0%, respectively). Among the meropenem-resistant Pseudomonas isolates (163/170; MIC, >2 mg/L), the activities of FTB against serine-β-lactamase (35/163) and MBL (43/163) producers were 88.6 and 65.1%, respectively, whereas the susceptibilities of comparators were as follows: ceftazidime-avibactam, 88.5 and 16.0%, meropenem-vaborbactam, 8.5 and 7.0%, imipenem-relebactam, 2.9 and 2.3%, ceftolozane-tazobactam, 0 and 2.3%, and piperacillin-tazobactam, 0 and 0%, respectively. Microbiological results suggest FTB as a potential therapeutic option in patients infected with carbapenemase-producing Enterobacterales and carbapenem-resistant Pseudomonas isolates, including MBL producers., This project was sponsored by Venatorx Pharmaceuticals and has been funded in whole or in part with federal funds from the Department of Health and Human Services, Office of the Assistant Secretary for Preparedness and Response, Biomedical Advanced Research and Development Authority, under contract no. HHSO100201900007C. This study was also supported by Plan Nacional de I+D + i 2013–2016 and Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investigación Cooperativa, Ministerio de Economía, Industria y Competitividad, Spanish Network for Research in Infectious Diseases (RD16/0016/0001, RD16/0016/0004, RD16/0016/0006, RD16/0016/0007, RD16/0016/0008, RD16/0016/0010, and REIPI RD16/0016/0011), cofinanced by the European Development Regional Fund “A Way to Achieve Europe” (ERDF), operative program Intelligent Growth 2014–2020 and CIBER en Enfermedades Infecciosas (CIBERINF) (CB21/13/00084).

Published
2022

9. Generation and Characterization of Single-Cycle Infectious Canine Influenza A Virus (sciCIV) and Its Use as Vaccine Platform

Author

Aitor Nogales, Kevin Chiem, Michael Breen, Marta L. DeDiego, Colin R. Parrish, Luis Martínez-Sobrido, New York Influenza Center of Excellence, National Institute of Allergy and Infectious Diseases (US), National Institutes of Health (US), Department of Health and Human Services (US), Centers of Excellence for Influenza Research and Surveillance (US), Ministerio de Ciencia, Innovación y Universidades (España), Nogales, Aitor, Chiem, Kevin, DeDiego, Marta L., Parrish, Colin R, Martínez-Sobrido, Luis, Nogales, Aitor [0000-0002-2424-7900], Chiem, Kevin [0000-0002-3892-5944], DeDiego, Marta L. [0000-0002-7888-7372], Parrish, Colin R [0000-0002-1836-6655], and Martínez-Sobrido, Luis [0000-0001-7084-0804]

Subjects
Single-cycle infectious influenza A virus, Viral vectors, Reverse genetics, Influenza vaccine, Single-cycle influenza virus, Canine influenza virus, Reporter virus, Green fluorescent protein, Humoral response, Reporter gene, Influenza HA-expressing MDCK cells (MDCK-HA)
Abstract

227-256 pp, Influenza A viruses (IAVs) infect a broad range of hosts, including multiple avian and mammalian species. The frequent emergence of novel IAV strains in different hosts, including in humans, results in the need for vigilance and ongoing development of new approaches to fighting or prevent those infections. Canine influenza is a contagious respiratory disease in dogs caused by two subtypes of IAV, the equine-origin H3N8 canine influenza virus (CIV), and the avian-origin H3N2 CIV. A novel approach to influenza vaccination involves single-cycle infectious influenza A viruses (sciIAVs), which are defective for an essential viral gene. They are propagated in complementing cell lines which provide the missing gene in trans. As sciIAV cannot complete their replication cycle in regular cells they are limited to a single round of viral replication. Because of their safety profile and ability to express foreign antigens inside infected cells, sciIAVs have served both as live-attenuated vaccines and as vaccine vectors for the expression of heterologous antigens. Here, we describe experimental procedures for the generation of a single-cycle infectious CIV (sciCIV), where the viral hemagglutinin (HA) gene was exchanged for the gene for green fluorescent protein (GFP). Complementation of the viral HA protein is provided in trans by stable HA-expressing cell lines. Methods for the in vitro characterization of HA deficient but GFP-expressing sciCIV (sciCIV ΔHA/GFP) are described, as well as its use as a potential vaccine., This research was partially funded by the New York Influenza Center of Excellence (NYICE), a member of the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Department of Health and Human Services, Centers of Excellence for Influenza Research and Surveillance (CEIRS) contract No. HHSN272201400005C (NYICE). This research was partially funded by a “Ramon y Cajal” Incorporation grant (RYC-2017) from the Spanish Ministry of Science, Innovation and Universities to A.N.

Published
2022

Catalog

Books, media, physical & digital resources
See catalog results