Coxsackievirus experimental heart diseases

被引:60
作者
Gauntt, C
Huber, S
机构
[1] Univ Texas, Hlth Sci Ctr, Dept Microbiol, San Antonio, TX 78229 USA
[2] Univ Vermont, Dept Pathol, Colchester, VT USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2003年 / 8卷
关键词
myocarditis; animal models; coxsackieviruses; persistent viral RNA; polymerase chain reaction; autoimmunity; cytokines; review;
D O I
10.2741/928
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Many microorganisms, particularly viruses, can cause myocarditis, an inflammatory disease of the heart. The frequency of and major factors that contribute to this disease, including a pronounced gender (male) bias, age and genetic background parameters are discussed, along with signs and symptoms of disease in infants to adults. Individuals with acute disease generally recover without sequelae; the chronic form can develop into idiopathic dilated cardiomyopathy and death can follow. Among viruses most frequently associated with cases in the U. S., the coxsackieviruses group B (CVB) are major etiologic agents. The association between the CVB and disease is based on detection of viral RNA in heart biopsy specimens by polymerase chain reaction assays. Excellent CVB?, particularly coxsackievirus B3 (CVB3)?, mouse models of the disease have identified mechanisms of induction and establishment of chronic myocarditis. CVB3-murine models share many biologic parameters of the acute and chronic diseases in humans, and show that cardiopathologic alterations result from virus-induced and immunologic reactions in heart tissues. Several immune responses to a CVB3 infection that become cardiopathogenic, instead of protective, are discussed in an attempt to explain why immunosuppressive treatments are not effective. Bed rest and supportive therapy are the current treatment for patients with myocarditis.
引用
收藏
页码:E23 / E35
页数:13
相关论文
共 81 条
[1]   VIRUS AND HEART [J].
ABELMANN, WH .
CIRCULATION, 1971, 44 (05) :950-&
[2]   Meta-analysis of the association of enteroviruses with human heart disease [J].
Baboonian, C ;
Treasure, T .
HEART, 1997, 78 (06) :539-543
[3]  
Beck MA, 1997, CURR TOP MICROBIOL, V223, P81
[4]   Clinical coxsackievirus B isolates differ from laboratory strains in their interaction with two cell surface receptors [J].
Bergelson, JM ;
Modlin, JF ;
WielandAlter, W ;
Cunningham, JA ;
Crowell, RL ;
Finberg, RW .
JOURNAL OF INFECTIOUS DISEASES, 1997, 175 (03) :697-700
[5]   Molecular aspects of myocarditis [J].
Neil E. Bowles ;
Jeffrey A. Towbin .
Current Infectious Disease Reports, 2000, 2 (4) :308-314
[6]   NEARLY 10 DECADES OF INTEREST IN IDIOPATHIC PERICARDITIS [J].
CHRISTIAN, HA .
AMERICAN HEART JOURNAL, 1951, 42 (05) :645-651
[7]  
Crowell RL, 1997, CURR TOP MICROBIOL, V223, P1
[8]   CYTOTOXIC AND VIRAL NEUTRALIZING ANTIBODIES CROSS-REACT WITH STREPTOCOCCAL-M PROTEIN, ENTEROVIRUSES, AND HUMAN CARDIAC MYOSIN [J].
CUNNINGHAM, MW ;
ANTONE, SM ;
GULIZIA, JM ;
MCMANUS, BM ;
FISCHETTI, VA ;
GAUNTT, CJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (04) :1320-1324
[9]   From infection to autoimmunity [J].
Fairweather, D ;
Kaya, Z ;
Shellam, GR ;
Lawson, CM ;
Rose, NR .
JOURNAL OF AUTOIMMUNITY, 2001, 16 (03) :175-186
[10]   Contractile depression and expression of proinflammatory cytokines and iNOS in viral myocarditis [J].
Freeman, GL ;
Colston, JT ;
Zabalgoitia, M ;
Chandrasekar, B .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1998, 274 (01) :H249-H258