title: Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice.
abstract: BACKGROUND
  Previously, we performed a quantitative trait locus (QTL) mapping study in BXD recombinant inbred mice to identify host genetic factors that confer resistance to influenza A virus infection. We found Lst1 (leukocyte specific transcript 1) as one of the most promising candidate genes in the Qivr17-2 locus because it is non-functional in DBA/2 J mice. Several studies have proposed that LST1 plays a role in the immune response to inflammatory diseases in humans and has additional immune-regulatory functions. Here, we evaluated the relevance of LST1 for the host response to influenza A infection in B6-Lst1 (-/-) mutant mice.
  
  
  RESULTS
  To investigate the role of LST1, we infected B6-Lst1 (-/-) mutant and C57BL/6 N wild-type mice with a low-virulent influenza A virus (PR8M; H1N1). Lst1 deficient mice exhibited significantly increased body weight loss at days 5 and 6 after infection and slightly increased lethality compared to infected wild-type mice. Determination of viral loads, histopathological examination and analysis of immune cell composition in bronchoalveolar lavage of infected lungs did not reveal any obvious differences between KO and wild-type mice.
  
  
  CONCLUSIONS
  The absence of Lst1 leads to a slightly more susceptible phenotype. However, deletion of Lst1 in DBA/2 J mice alone does not explain the high susceptibility of this strain to PR8M influenza infections.
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany. Sarah.Leist@helmholtz-hzi.de.|University of Veterinary Medicine Hannover, Hannover, Germany. Sarah.Leist@helmholtz-hzi.de.
authors.forename: Sarah R
authors.initials: SR
authors.lastname: Leist
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany. Heike.Kollmus@helmholtz-hzi.de.|University of Veterinary Medicine Hannover, Hannover, Germany. Heike.Kollmus@helmholtz-hzi.de.
authors.forename: Heike
authors.initials: H
authors.lastname: Kollmus
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany. Bastian.Hatesuer@helmholtz-hzi.de.|University of Veterinary Medicine Hannover, Hannover, Germany. Bastian.Hatesuer@helmholtz-hzi.de.
authors.forename: Bastian
authors.initials: B
authors.lastname: Hatesuer
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany. Ruth.Lambertz@helmholtz-hzi.de.|University of Veterinary Medicine Hannover, Hannover, Germany. Ruth.Lambertz@helmholtz-hzi.de.
authors.forename: Ruth L O
authors.initials: RL
authors.lastname: Lambertz
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research, 38124, Braunschweig, Germany. Klaus.Schughart@helmholtz-hzi.de.|University of Veterinary Medicine Hannover, Hannover, Germany. Klaus.Schughart@helmholtz-hzi.de.|University of Tennessee Health Science Center, Memphis, Tennessee, United States of America. Klaus.Schughart@helmholtz-hzi.de.
authors.forename: Klaus
authors.initials: K
authors.lastname: Schughart
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D005260:Female; D054884:Host-Pathogen Interactions; D053118:Influenza A Virus, H1N1 Subtype / Q000502:physiology*; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins / Q000172:deficiency*; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D018345:Mice, Knockout; D009976:Orthomyxoviridae Infections / Q000235:genetics* / Q000401:mortality / Q000821:virology*; D010641:Phenotype; D019562:Viral Load
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; C093604:LST1 protein, human; D008565:Membrane Proteins
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