| First Author | Leist SR | Year | 2016 |
| Journal | Virol J | Volume | 13 |
| Pages | 17 | PubMed ID | 26817701 |
| Mgi Jnum | J:235700 | Mgi Id | MGI:5800392 |
| Doi | 10.1186/s12985-016-0471-0 | Citation | Leist SR, et al. (2016) Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice. Virol J 13:17 |
| abstractText | 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. |
