TY - JOUR
T1 - Dilated cardiomyopathy in retrovirally infected mice
T2 - A novel model for silent viral DCM?
AU - Beischel, Julie
AU - Larson, Douglas F.
AU - Yu, Qianli
AU - Yang, Bo
AU - Sepúlveda, Ramon Tomas
AU - Kelley, Tara
AU - Watson, Ronald R.
PY - 2004
Y1 - 2004
N2 - Dilated cardiomyopathy (DCM) is a clinically relevant disease that can occur independently or secondary to other diseases such as HIV infection and AIDS. To study this latter process, we used a model in which mice are infected with the LP-BM5 murine AIDS (MAIDS) retrovirus. Cardiac function of control and infected mice was determined through the in vivo analysis of left ventricular pressure-volume loops. Furthermore, the role of myocarditis was investigated through immunohistochemistry for T-cell, B-cell, and macrophage cardiac infiltrates and Northern blot analysis for tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS). End-systolic and end-diastolic volumes were significantly increased and ventricular stiffness was significantly decreased in infected mice, consistent with DCM; however, no staining for inflammatory cellular infiltrates or TNF-α and iNOS was seen. These data support the conclusion that the LP-BM5 HIV model virus causes DCM in the absence of chronic cardiac inflammation. These findings support MAIDS retroviral infection as a new model of idiopathic DCM in which myocarditis does not occur.
AB - Dilated cardiomyopathy (DCM) is a clinically relevant disease that can occur independently or secondary to other diseases such as HIV infection and AIDS. To study this latter process, we used a model in which mice are infected with the LP-BM5 murine AIDS (MAIDS) retrovirus. Cardiac function of control and infected mice was determined through the in vivo analysis of left ventricular pressure-volume loops. Furthermore, the role of myocarditis was investigated through immunohistochemistry for T-cell, B-cell, and macrophage cardiac infiltrates and Northern blot analysis for tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS). End-systolic and end-diastolic volumes were significantly increased and ventricular stiffness was significantly decreased in infected mice, consistent with DCM; however, no staining for inflammatory cellular infiltrates or TNF-α and iNOS was seen. These data support the conclusion that the LP-BM5 HIV model virus causes DCM in the absence of chronic cardiac inflammation. These findings support MAIDS retroviral infection as a new model of idiopathic DCM in which myocarditis does not occur.
KW - Dilated cardiomyopathy
KW - Murine acquired immunodeficiency syndrome
KW - Viral myocarditis
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U2 - 10.1385/CT:4:4:317
DO - 10.1385/CT:4:4:317
M3 - Article
C2 - 15531775
AN - SCOPUS:9244258623
SN - 1530-7905
VL - 4
SP - 317
EP - 325
JO - Cardiovascular toxicology
JF - Cardiovascular toxicology
IS - 4
ER -