Dataset Information


Coxsackievirus B3 (CVB3) infection of AJ, B10.A, CSS3 and B6.chr3AJ (heart tissue day 4)

ABSTRACT: The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain. Total RNA obtained from hearts of 3 AJ, 3 B10.A(H2a), 3 CSS3 and 3 B6.chr3AJ that were infected or uninfected with CVB3(CG) at 400pfu/g and collected at day 4 post infection.


ORGANISM(S): Mus musculus  

SUBMITTER: Sean A Wiltshire   Silvia Vidal  Sean Wiltshire 

PROVIDER: E-GEOD-19496 | ArrayExpress | 2011-05-01



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Quantitative trait locus analysis, pathway analysis, and consomic mapping show genetic variants of Tnni3k, Fpgt, or H28 control susceptibility to viral myocarditis.

Wiltshire Sean A SA   Leiva-Torres Gabriel André GA   Vidal Silvia M SM  

Journal of immunology (Baltimore, Md. : 1950) 20110427 11

Coxsackievirus B3 (CVB3) infection is the most common cause of viral myocarditis. The pathogenesis of viral myocarditis is strongly controlled by host genetic factors. Although certain indispensable components of immunity have been identified, the genes and pathways underlying natural variation between individuals remain unclear. Previously, we isolated the viral myocarditis susceptibility 1 (Vms1) locus on chromosome 3, which influences pathogenesis. We hypothesized that confirmation and furthe  ...[more]

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