Additional file 1: Figure S1. of Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice

Abstract

Targeting and genotyping strategy of the Lst1 KO strain. Mice were genotyped by using different primer pairs leading to PCR products which allowed the identification of wild-type (310 bp), KO (400 bp) and heterozygous animals (310 bp and 400 bp) (A). Primers (blue arrows) used for genotyping: Lst1-fwd: 5′ - GTG CGT GCT CAG TCA CAC TA – 3′; Lst1-rev: 3′ - AGG CCA ACA ATA AGT CCT TAC – 5′; neofwd: 3′ - TCA TTC TCA GTA TTG TTT TGC C – 5′. Abbreviations: lacZ: ß-galactosidase coding sequence from the E.coli lacZ gene, hubiP: promoter from the human ubiquitin C gene, neor: coding sequence for neomycin phosphotransferase, p(A): polyadenylation signal, black arrow: direction of gene transcription, black boxes: Lst1 coding region. To confirm the knock-out of the Lst1 gene in C57BL/6 N-Lst1tm1(KOMP)Vlcg mice we performed reverse transcription. Figure S2. No difference in changes of body weight or survival rate between Lst1 KO and C57BL/6 J mice after infection with H3N2 influenza A virus Male C57BL/6 N-Lst1 tm1(KOMP)Vlcg (n = 7) and C57BL/6 J mice (n = 10) were infected intranasally with 2x10³ FFU H3N2 virus (A/HK/01/68) in 20 μl PBS. Body weight (A) and survival (B) were determined for each day p.i. for a period of 14 days. Percent weight change is shown with reference to the starting body weight. Significances were calculated using non-parametric Mann Whitney U test. (p < 0.01 for day 1) and Logrank test for survival rates (not significant). (PDF 230 kb

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