Host Transcription Profile in Nasal Epithelium and Whole Blood of Hospitalized Children Under 2 Years of Age With Respiratory Syncytial Virus Infection.

Autor:	Do LAH; Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Program, in partnership with the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam., Pellet J; Murdoch Children's Research Institute, Melbourne, Australia., van Doorn HR; Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Program, in partnership with the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam.; Centre for Tropical Medicine and Global Health, Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom., Tran AT; Children Hospital 1, Ho Chi Minh City, Vietnam., Nguyen BH; Children Hospital 1, Ho Chi Minh City, Vietnam., Tran TTL; Children Hospital 2, Ho Chi Minh City, Vietnam., Tran QH; Children Hospital 2, Ho Chi Minh City, Vietnam., Vo QB; Children Hospital 2, Ho Chi Minh City, Vietnam., Tran Dac NA; Children Hospital 2, Ho Chi Minh City, Vietnam., Trinh HN; Children Hospital 1, Ho Chi Minh City, Vietnam., Nguyen TTH; Children Hospital 1, Ho Chi Minh City, Vietnam., Le Binh BT; Children Hospital 1, Ho Chi Minh City, Vietnam., Nguyen HMK; Children Hospital 1, Ho Chi Minh City, Vietnam., Nguyen MT; Children Hospital 1, Ho Chi Minh City, Vietnam., Thai QT; Children Hospital 1, Ho Chi Minh City, Vietnam., Vo TV; Children Hospital 1, Ho Chi Minh City, Vietnam., Ngo NQM; Children Hospital 1, Ho Chi Minh City, Vietnam., Dang TKH; Children Hospital 2, Ho Chi Minh City, Vietnam., Cao NH; Children Hospital 2, Ho Chi Minh City, Vietnam., Tran TV; Children Hospital 2, Ho Chi Minh City, Vietnam., Ho LV; Children Hospital 2, Ho Chi Minh City, Vietnam., De Meulder B; European Institute for Systems Biology and Medicine, Lyon, France., Auffray C; European Institute for Systems Biology and Medicine, Lyon, France., Hofstra JJ; Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, The Netherlands., Farrar J; Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Program, in partnership with the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam., Bryant JE; Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Program, in partnership with the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam.; Centre for Tropical Medicine and Global Health, Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom., de Jong M; Oxford University Clinical Research Unit, Wellcome Trust Major Overseas Program, in partnership with the Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam.; Centre for Tropical Medicine and Global Health, Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom.; Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, The Netherlands., Hibberd ML; Genome Institute of Singapore.; London School of Hygiene & Tropical Medicine, United Kingdom.
Jazyk:	angličtina
Zdroj:	The Journal of infectious diseases [J Infect Dis] 2017 Dec 27; Vol. 217 (1), pp. 134-146.
DOI:	10.1093/infdis/jix519
Abstrakt:	Background: Most insights into the cascade of immune events after acute respiratory syncytial virus (RSV) infection have been obtained from animal experiments or in vitro models. Methods: In this study, we investigated host gene expression profiles in nasopharyngeal (NP) swabs and whole blood samples during natural RSV and rhinovirus (hRV) infection (acute versus early recovery phase) in 83 hospitalized patients <2 years old with lower respiratory tract infections. Results: Respiratory syncytial virus infection induced strong and persistent innate immune responses including interferon signaling and pathways related to chemokine/cytokine signaling in both compartments. Interferon-α/β, NOTCH1 signaling pathways and potential biomarkers HIST1H4E, IL7R, ISG15 in NP samples, or BCL6, HIST2H2AC, CCNA1 in blood are leading pathways and hub genes that were associated with both RSV load and severity. The observed RSV-induced gene expression patterns did not differ significantly in NP swab and blood specimens. In contrast, hRV infection did not as strongly induce expression of innate immunity pathways, and significant differences were observed between NP swab and blood specimens. Conclusions: We conclude that RSV induced strong and persistent innate immune responses and that RSV severity may be related to development of T follicular helper cells and antiviral inflammatory sequelae derived from high activation of BCL6. (© The Author(s) 2017. Published by Oxford University Press for the Infectious Diseases Society of America.)
Databáze:	MEDLINE
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