tetano
Editor, Senior Moderator
Virol J. 2016 Jan 27;13(1):17. doi: 10.1186/s12985-016-0471-0.
[h=1]Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice.[/h] Leist SR[SUP]1,[/SUP][SUP]2[/SUP], Kollmus H[SUP]3,[/SUP][SUP]4[/SUP], Hatesuer B[SUP]5,[/SUP][SUP]6[/SUP], Lambertz RL[SUP]7,[/SUP][SUP]8[/SUP], Schughart K[SUP]9,[/SUP][SUP]10,[/SUP][SUP]11[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]FINDINGS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
PMID: 26817701 [PubMed - in process] Free full text
[h=1]Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice.[/h] Leist SR[SUP]1,[/SUP][SUP]2[/SUP], Kollmus H[SUP]3,[/SUP][SUP]4[/SUP], Hatesuer B[SUP]5,[/SUP][SUP]6[/SUP], Lambertz RL[SUP]7,[/SUP][SUP]8[/SUP], Schughart K[SUP]9,[/SUP][SUP]10,[/SUP][SUP]11[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]FINDINGS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
PMID: 26817701 [PubMed - in process] Free full text