Mouse strain differences in the chemokine response to acute lung infection with a murine gammaherpesvirus.
Mouse strain differences in the chemokine response to acute lung infection with a murine gammaherpesvirus.
复制标题
小鼠品系对鼠伽马疱疹病毒急性肺部感染的趋化因子反应存在差异。
DOI:
10.1089/088282404322875467
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发表时间:
2004
期刊:
影响因子:
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通讯作者:
Rochford,Rosemary
中科院分区:
文献类型:
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作者:
Weinberg,JasonB;Lutzke,MaryL;Alfinito,Rosiane;Rochford,Rosemary
Numerous mouse strain-based differences in the immune response and in susceptibility to numerous pathogens have been described, but it is not known if these differences extend to chemokine responses to viral infection of the lungs. To define mouse strain-based differences in the host chemokine response and susceptibility to infection with murine gammaherpesvirus-68 (MHV-68), we compared the induced chemokine response to MHV-68 infection in the lungs of BALB/c and C57BL/6 mice at 1-15 days post-infection. CC and CXC chemokines were induced in both BALB/c and C57BL/6 following infection but the level of chemokine induction was significantly higher in the BALB/c mice for all chemokines measured. In addition, interferon-γ(IFN-γ) was also induced to a significantly higher level in the lungs of BALB/c infected mice compared to C57BL/6 mice. Interestingly, viral gene expression was lower in the lungs of C57BL/6 mice during the acute phase of replication. Titers of infectious virus were also greater in BALB/c lungs, although they did not achieve statistical significance. In contrast, latent viral load in the spleen, as measured by quantitative real-time PCR, did not significantly differ between mouse strains, suggesting that the establishment of latency is not affected by the amount of virus present during acute infection. This data suggests that robust chemokine response and expression of IFN-γin the lungs of infected BALB/c mice does not correlate with increased resistance to infection. In addition, the significant differences in chemokine responses observed will be important factors to consider in future studies of viral pathogenesis using mouse models.