Zobrazeno 1 - 10
of 41
pro vyhledávání: '"Steven F Baker"'
Autor:
Steven F Baker, Helene Meistermann, Manuel Tzouros, Aaron Baker, Sabrina Golling, Juliane Siebourg Polster, Mitchell P Ledwith, Anthony Gitter, Angelique Augustin, Hassan Javanbakht, Andrew Mehle
Publikováno v:
PLoS Biology, Vol 20, Iss 12, p e3001934 (2022)
Viruses must balance their reliance on host cell machinery for replication while avoiding host defense. Influenza A viruses are zoonotic agents that frequently switch hosts, causing localized outbreaks with the potential for larger pandemics. The hos
Externí odkaz:
https://doaj.org/article/09649af87e6d41eaa961fc4a034da8e8
Autor:
Steven F Baker, Andrew Mehle
Publikováno v:
eLife, Vol 8 (2019)
The evolutionary history of ANP32 proteins impacts how influenza virus jumps from birds to mammals.
Externí odkaz:
https://doaj.org/article/e1cbff39e0fb4d439fb7c0ac8af45060
Autor:
Arindam Mondal, Anthony R Dawson, Gregory K Potts, Elyse C Freiberger, Steven F Baker, Lindsey A Moser, Kristen A Bernard, Joshua J Coon, Andrew Mehle
Publikováno v:
eLife, Vol 6 (2017)
Influenza virus expresses transcripts early in infection and transitions towards genome replication at later time points. This process requires de novo assembly of the viral replication machinery, large ribonucleoprotein complexes (RNPs) composed of
Externí odkaz:
https://doaj.org/article/596f73a4764947edb237f877a986d628
Publikováno v:
PLoS ONE, Vol 11, Iss 6, p e0156906 (2016)
Influenza A virus is a significant public health threat, but little is understood about the viral RNA structure and function. Current vaccines and therapeutic options to control influenza A virus infections are mostly protein-centric and of limited e
Externí odkaz:
https://doaj.org/article/a0ae1b24a67f4c7f8236c79b2a8783ec
Publikováno v:
PLoS ONE, Vol 11, Iss 1, p e0147723 (2016)
Influenza A and B viruses (IAV and IBV, respectively) cause annual seasonal human respiratory disease epidemics. In addition, IAVs have been implicated in occasional pandemics with inordinate health and economic consequences. Studying influenza virus
Externí odkaz:
https://doaj.org/article/21d902d689124aa1b5eea95eb92805f4
Publikováno v:
Seminars in Cell & Developmental Biology. 146:40-56
Effector CD8+T cell interactions are critical in controlling viral infection by directly killing infected cells but overabundant or sustained activation also exacerbates tissue damage. Chemokines promote the trafficking of effector CD8+T cells into i
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9a13ee6103552f1668135d0b31e6fd5f
https://doi.org/10.1101/2022.09.13.507813
https://doi.org/10.1101/2022.09.13.507813
Autor:
Juliane Siebourg Polster, Angélique Augustin, Hassan Javanbakht, Sabrina Golling, Mitchell P. Ledwith, Manuel Tzouros, Andrew Mehle, Aaron Baker, Anthony Gitter, Steven F. Baker, Hélène Meistermann
Viruses must balance their reliance on host cell machinery for replication while avoiding host defense. They often exploit conserved essential host genes whose critical role for the cell limits mutational escape. Conversely, host antiviral genes are
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8a41d5b6afe19e84ebb2656613768a7a
https://doi.org/10.1101/2020.11.09.355982
https://doi.org/10.1101/2020.11.09.355982
Mutations at highly conserved residues in influenza A(H1N1)pdm09 virus affect neuraminidase activity
Autor:
Leidi C. Alvarez-Sánchez, Laura Conde-Ferráez, Guadalupe Ayora-Talavera, Refugio González-Losa, Lesly Romero-Beltran, Marylin Puerto-Solís, Steven F. Baker, Luis Martinez-Sobrido
Publikováno v:
Virus Research. 225:1-9
Influenza virus neuraminidase (NA) plays a pivotal role during viral growth since its sialidase activity allows the efficient release of nascent virions from infected cells. Consequently, mutations in the NA catalytic site affecting sialic acid (SA)
Autor:
Andrew Mehle, Steven F. Baker
Publikováno v:
eLife, Vol 8 (2019)
The evolutionary history of ANP32 proteins impacts how influenza virus jumps from birds to mammals.