Susceptibility to coxsackievirus B3-induced chronic myocarditis maps near the murine Tcrα and Myhcα loci on chromosome 14

M. D. Traystman; L. H. Chow; B. M. McManus; A. Herskowitz; M. N. Nesbitt; K. W. Beisel

Susceptibility to coxsackievirus B3-induced chronic myocarditis maps near the murine Tcrα and Myhcα loci on chromosome 14

M. D. Traystman, L. H. Chow, B. M. McManus, A. Herskowitz, M. N. Nesbitt, K. W. Beisel

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8^b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcrα, and Myhcα loci.

Original language	English (US)
Pages (from-to)	721-726
Number of pages	6
Journal	American Journal of Pathology
Volume	138
Issue number	3
State	Published - 1991

All Science Journal Classification (ASJC) codes

Pathology and Forensic Medicine

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title = "Susceptibility to coxsackievirus B3-induced chronic myocarditis maps near the murine Tcrα and Myhcα loci on chromosome 14",

abstract = "This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcrα, and Myhcα loci.",

author = "Traystman, {M. D.} and Chow, {L. H.} and McManus, {B. M.} and A. Herskowitz and Nesbitt, {M. N.} and Beisel, {K. W.}",

year = "1991",

language = "English (US)",

volume = "138",

pages = "721--726",

journal = "American Journal of Pathology",

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T1 - Susceptibility to coxsackievirus B3-induced chronic myocarditis maps near the murine Tcrα and Myhcα loci on chromosome 14

AU - Traystman, M. D.

AU - Chow, L. H.

AU - McManus, B. M.

AU - Herskowitz, A.

AU - Nesbitt, M. N.

AU - Beisel, K. W.

PY - 1991

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N2 - This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcrα, and Myhcα loci.

AB - This study was undertaken to determine the genetic control of host susceptibility to coxsackievirus B3 (CVB3)-induced chronic myocarditis in a mouse model. An autosomal recessive autoimmune myocardial disease (amd) gene (possibly more than one gene), which determined susceptibility to CVB3-induced chronic myocarditis in the A/J and DBA/2J inbred mouse strains, was mapped to a segment of chromosome 14. Data from both the AXB/BXA recombinant inbred (RI) strains and the B10.D2(57N) H-8b congenic mice supported this linkage relationship. Analysis of the AXB/BXA RI strain distribution patterns suggested that amd maps distal to the Np-2, Tcrα, and Myhcα loci.

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