P
Patricia Jeannin
Researcher at Pasteur Institute
Publications - 19
Citations - 893
Patricia Jeannin is an academic researcher from Pasteur Institute. The author has contributed to research in topics: Zika virus & Flavivirus. The author has an hindex of 10, co-authored 16 publications receiving 809 citations. Previous affiliations of Patricia Jeannin include World Health Organization & Centre national de la recherche scientifique.
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Journal ArticleDOI
Evolution of H5N1 avian influenza viruses in Asia
Jean Thierry Aubin,Saliha Azebi,Amanda Balish,Jill Banks,Niranjan Bhat,Rick A. Bright,Ian Brown,Philippe Buchy,Ana Maria Burguiere,Hua Ian Chen,Peter K.C. Cheng,Nancy J. Cox,Alice Crosier,Aaron Curns,Frédérique Cuvelier,Guohua Deng,Julia Desheva,Stéphanie Desvaux,Nguyen Hong Diep,Ruben O. Donis,Ruben O. Donis,A. R. Douglas,Scott F. Dowell,Nguyen Tien Dung,Lindsay Edwards,Keiji Fukuda,Rebecca Garten,Elena A. Govorkova,Victoria Gregory,Alan W. Hampson,Nguyen Thi Hong Hanh,Scott A. Harper,A. Hay,Erich Hoffmann,Diane J. Hulse,Masaki Imai,Shigeyuki Itamura,Samadhan Jadhao,Patricia Jeannin,Chun Kang,Jackie Katz,Jae Hong Kim,Alexander Klimov,Yong Kuk Kwon,Chang-Won Lee,Phuong Song Lien,Yanbing Li,Wilina Lim,Yi Pu Lin,Stephen Lindstom,La Morris Loftin,Jan Mabry,Le Quynh Mai,Taronna R. Maines,Jean Claude Manuguerra,Masaji Mase,Yumi Matsuoka,Margaret McCarron,Marie-Jo Medina,Doan Nguyen,Ai Ninomiya,Masatsugu Obuchi,Takato Odagiri,Malik Peiris,Michael L. Perdue,Jean Marc Reynes,James Robertson,Claudine Rousseaux,Takehiko Saito,Somchai Sangkitporn,Michael W. Shaw,James Mark Simmerman,Marek J. Slomka,Catherine K. Smith,San Sorn,Erica Spackman,Klaus Stöhr,David L. Suarez,Haan Woo Sung,David E. Swayne,Maryse Tardy-Panit,Masato Tashiro,Pranee Thawatsupha,Terrence M. Tumpey,Timothy M. Uyeki,Phan Van Tu,Sylvie van der Werf,Sirenda Vong,Richard J. Webby,Robert G. Webster,John Wood,Xiyan Xu,Guan Yi,Wenging Zhang +93 more
TL;DR: Human infections were from a virus clade undergoing antigenic drift that showed resistance to adamantanes but sensitivity to neuraminidase inhibitors.
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Enzymatic properties of the neuraminidase of seasonal H1N1 influenza viruses provide insights for the emergence of natural resistance to oseltamivir.
Marie-Anne Rameix-Welti,Vincent Enouf,Frédérique Cuvelier,Patricia Jeannin,Sylvie van der Werf +4 more
TL;DR: These frequencies are in sharp contrast with those observed for H1N1 viruses during previous seasons (0 to <1%) [4]–[8].
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HIV controller CD4+ T cells respond to minimal amounts of Gag antigen due to high TCR avidity.
Benoît Vingert,Santiago Perez-Patrigeon,Patricia Jeannin,Olivier Lambotte,Olivier Lambotte,Faroudy Boufassa,Fabrice Lemaître,William W. Kwok,Ioannis Theodorou,Jean-François Delfraissy,Jean-François Delfraissy,Jacques Thèze,Lisa A. Chakrabarti +12 more
TL;DR: HIV controllers harbor a pool of memory CD4+ T cells with the intrinsic ability to recognize minimal amounts of Gag antigen, which may explain how they maintain an active antiviral response in the face of very low viremia.
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Mother-to-Child Transmission of HTLV-1 Epidemiological Aspects, Mechanisms and Determinants of Mother-to-Child Transmission
Florent Percher,Patricia Jeannin,Sandra Martin-Latil,Antoine Gessain,Philippe V. Afonso,Aurore Vidy-Roche,Pierre-Emmanuel Ceccaldi +6 more
TL;DR: Most of the mechanisms underlying HTLV-1 transmission during breast feeding remain largely unknown, such as the sites of infection and cellular targets as well as the role of milk factors.
Journal ArticleDOI
HIV Controllers Maintain a Population of Highly Efficient Th1 Effector Cells in Contrast to Patients Treated in the Long Term
Benoît Vingert,Daniela Benati,Olivier Lambotte,Pierre de Truchis,Laurence Slama,Patricia Jeannin,Moran Galperin,Santiago Perez-Patrigeon,Faroudy Boufassa,William W. Kwok,Fabrice Lemaître,Jean-François Delfraissy,Jacques Thèze,Lisa A. Chakrabarti +13 more
TL;DR: HIV controllers maintained a population of highly efficient Th1 effectors directed against Gag in spite of a persistently low antigenemia, while patients treated in the long term showed a loss of CD4 effector functions.