title: The 2009 pandemic H1N1 influenza virus is more pathogenic in pregnant mice than seasonal H1N1 influenza virus.
abstract: Pregnant women can experience high mortality, high rates of abortion, and severe pneumonia when infected with pandemic influenza viruses. In this context, the severity of the 2009 pandemic H1N1 influenza virus compared with seasonal H1N1 influenza virus is not clear. Presently, in a mouse model of pregnancy, the 2009 pandemic H1N1 influenza virus killed up to 60% of pregnant mice and caused abortion in up to 40%, whereas a circulating seasonal H1N1 influenza virus did not cause any deaths or abortions. Higher viral titers and levels of inflammatory cytokines and chemokines such as interleukin (IL)-1α, IL-6, granulocyte colony-stimulating factor, RANTES, monocyte chemotactic protein, and KC (CXCL1), were detected in the lungs of pregnant mice infected with the 2009 pandemic H1N1 influenza virus, compared with the seasonal H1N1 influenza virus. The results of our study with pregnant mice suggest that the observed higher pathogenesis in pregnant women infected with the 2009 pandemic H1N1 influenza virus than the seasonal H1N1 influenza virus may be due to higher viral replication, elevated induction of inflammatory chemokines, and reduced progesterone.
authors.affiliation: Laboratory of Influenza Research, College of Veterinary Medicine, Chungnam National University, Daejeon, South Korea.
authors.forename: Heui Man
authors.initials: HM
authors.lastname: Kim
authors.forename: Young Myong
authors.initials: YM
authors.lastname: Kang
authors.forename: Byung Min
authors.initials: BM
authors.lastname: Song
authors.forename: Hyun Soo
authors.initials: HS
authors.lastname: Kim
authors.forename: Sang Heui
authors.initials: SH
authors.lastname: Seo
mesh_terms: D000818:Animals; D018946:Chemokine CCL5 / Q000378:metabolism; D054360:Chemokine CXCL1 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000378:metabolism; D007249:Inflammation / Q000473:pathology / Q000821:virology; D053118:Influenza A Virus, H1N1 Subtype / Q000472:pathogenicity*; D053582:Interleukin-1alpha / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D018945:Monocyte Chemoattractant Proteins / Q000378:metabolism; D009976:Orthomyxoviridae Infections / Q000453:epidemiology / Q000821:virology*; D058873:Pandemics; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000401:mortality / Q000473:pathology / Q000821:virology*; D014779:Virus Replication
chemical_list: D018946:Chemokine CCL5; D054360:Chemokine CXCL1; D018925:Chemokines; C475895:Cxcl1 protein, mouse; D016207:Cytokines; D053582:Interleukin-1alpha; D015850:Interleukin-6; D018945:Monocyte Chemoattractant Proteins; D016179:Granulocyte Colony-Stimulating Factor