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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.    Findings  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.    Electronic supplementary material  The online version of this article (doi:10.1186/s12985-016-0471-0) contains supplementary material, which is available to authorized users.

Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice