| Literature DB >> 28279344 |
Géraldine Engels1, Alexandra Maximiliane Hierweger2, Julia Hoffmann3, René Thieme4, Swantje Thiele3, Stephanie Bertram3, Carola Dreier3, Patricia Resa-Infante3, Henning Jacobsen3, Kristin Thiele4, Malik Alawi5, Daniela Indenbirken5, Adam Grundhoff5, Svenja Siebels6, Nicole Fischer6, Violeta Stojanovska7, Damián Muzzio8, Federico Jensen9, Khalil Karimi10, Hans-Willi Mittrücker11, Petra Clara Arck12, Gülsah Gabriel13.
Abstract
Pregnant women are at high risk for severe influenza disease outcomes, yet insights into the underlying mechanisms are limited. Here, we present models of H1N1 infection in syngenic and allogenic pregnant mice; infection in the latter mirrors the severe course of 2009 pandemic influenza in pregnant women. We found that the anti-viral immune response in the pregnant host was significantly restricted as compared to the non-pregnant host. This included a reduced type I interferon response as well as impaired migration of CD8+ T cells into the lung. The multi-faceted failure to mount an anti-viral response in allogenic pregnant mice resulted in a less stringent selective environment that promoted the emergence of 2009 H1N1 virus variants that specifically counteract type I interferon response and mediate increased viral pathogenicity. These insights underscore the importance of influenza vaccination compliance in pregnant women and may open novel therapeutic avenues.Entities:
Keywords: NS1 R211K mutation; allogenic mating; influenza; leukocyte homing; mice; pandemic; pregnancy; progesterone; type I response; viral quasi species
Mesh:
Year: 2017 PMID: 28279344 DOI: 10.1016/j.chom.2017.02.020
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023