Persistence of virus and viral genome in myocardium after coxsackievirus B3-induced murine myocarditis.
Following infection with Coxsackievirus B3 (CVB3), A-strain mice develop ongoing myocarditis that persists after the virus ceases to be cultivatable from heart tissue. We studied the natural history of this virus-induced but apparently autoimmune inflammation by means of in situ hybridization (ISH) and by polymerase chain reaction (PCR). Both ISH and culture allowed detection of virus up to 2 weeks post-infection in virtually all heart tissues. In contrast, PCR revealed the presence of viral genome for a substantially longer period of time, i.e. at least 34 days after CVB3 infection. Similarly, the majority of mice showed myocardial inflammation at this time point. However, the persistence of virus did not correlate with ongoing myocarditis, and vice versa. Most mice with ongoing myocarditis produced heart myosin autoantibodies, most probably as a result of tissue damage. The lack of correlation between presence of ongoing inflammation and persistence of virus supports our previous view that the late phase of CVB3-induced myocarditis is mediated by autoimmunological mechanisms.
Rabausch-Starz
I
I
Department of Pathology, University of Würzburg, Germany.
Schwaiger
A
A
Grünewald
K
K
Müller-Hermelink
H K
HK
Neu
N
N
D000818:Animals; D001323:Autoantibodies / Q000032:analysis; D001483:Base Sequence; D017931:DNA Primers / Q000737:chemistry; D029822:Enterovirus B, Human / Q000254:growth & development*; D005260:Female; D006321:Heart / Q000382:microbiology*; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D008805:Mice, Inbred A; D008969:Molecular Sequence Data; D009205:Myocarditis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D009218:Myosins / Q000276:immunology
D001323:Autoantibodies; D017931:DNA Primers; D009218:Myosins