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1 ble for a spectrum of pathogenesis including viral myocarditis.
2 hin cardiomyocytes and pericytes, leading to viral myocarditis.
3 lymphoid cell compartment, are protective in viral myocarditis.
4 inflammation and outcome in a mouse model of viral myocarditis.
5     To review how autoimmunity is induced in viral myocarditis.
6  is a characteristic of both human and mouse viral myocarditis.
7 t, and is a potential therapeutic target for viral myocarditis.
8                   CVB3 is a primary cause of viral myocarditis.
9 ces in IFN antagonism to the pathogenesis of viral myocarditis.
10                   Four patients had probable viral myocarditis.
11 M were observed in the subgroup (n=130) with viral myocarditis.
12 +) T regulatory cells, which protect against viral myocarditis.
13 he myocardial inflammatory response in acute viral myocarditis.
14  response during the initial phases of acute viral myocarditis.
15 specific T cell responses during subclinical viral myocarditis.
16 nvestigate non-immune-mediated mechanisms of viral myocarditis.
17 re inflammation and injury, also occurred in viral myocarditis.
18  scheduled to receive ICIs and patients with viral myocarditis.
19 A genome that serves as a model for studying viral myocarditis.
20 CI therapy (pre-ICI group) and patients with viral myocarditis.
21 otential therapeutic target for treatment of viral myocarditis.
22 nisms and potential treatment strategies for viral myocarditis.
23 quent in patients with ICI-M than those with viral myocarditis (27 of 33 patients [82%] vs 85 of 85 [
24                                              Viral myocarditis affects an estimated 5 to 20% of the h
25 ditis, and based on comparisons to non-COVID viral myocarditis an inherently more benign clinical cou
26                                              Viral myocarditis, an inflammatory disease of the heart,
27                                              Viral myocarditis, an inflammatory disease of the myocar
28  222 consecutive patients with biopsy-proven viral myocarditis and CMR were enrolled.
29 ly quantified and compared to other types of viral myocarditis and controls.
30 8-52] years) with a history of biopsy-proven viral myocarditis and drug-refractory VT; 5 patients pre
31 n mediating cardiac injury in the setting of viral myocarditis and is the first demonstration that ca
32 idence that IFN-beta can be a determinant of viral myocarditis and reovirus disease.
33 ew insights into the innate host response to viral myocarditis and the various therapeutic strategies
34 thogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics f
35 subanalysis in 130 adult patients with acute viral myocarditis and viral prodrome within 2 weeks from
36  myocarditis, 4 patients with non-SARS-CoV-2 viral myocarditis, and 5 patients with noninflammatory c
37 usion injury, sepsis, chronic heart failure, viral myocarditis, and cardiac allograft rejection.
38 f sepsis, seven patients with a diagnosis of viral myocarditis, and five control patients without cli
39 myocardial ischemia and reperfusion, sepsis, viral myocarditis, and immune rejection.
40 ntexts of COVID-19 infection, other types of viral myocarditis, and other vaccine-associated cardiac
41 ate the long-term mortality in patients with viral myocarditis, and to establish the prognostic value
42 se myocarditis, the mechanisms that underlie viral myocarditis are poorly understood.
43                       Long-term mortality of viral myocarditis, as well as potential risk factors for
44 n only rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral inf
45  the plasma of mice with acute autoimmune or viral myocarditis but not in those with acute myocardial
46 that the PERK inhibitor GSK2656157 mitigated viral myocarditis by disrupting the TRIM29-PERK connecti
47        TRIM29 deficiency protected mice from viral myocarditis by promoting cardiac antiviral functio
48                 Four serious adverse events (viral myocarditis, diverticulitis, dyspnea, and vestibul
49 therapeutic agent for the treatment of acute viral myocarditis during the viremic phase.
50                                              Viral myocarditis follows a fatal course in approximatel
51                                              Viral myocarditis has been proposed to be divided into 3
52 ong been considered the most common cause of viral myocarditis; however, we previously demonstrated b
53 IFN-beta) is critical for protection against viral myocarditis in mice.
54 he treatment of viral disease in general and viral myocarditis in particular.
55  been speculated that ARVD/C is a sequela of viral myocarditis in some patients, and the role of the
56 e an attractive therapeutic approach against viral myocarditis in the future.
57 endocardial fibroelastosis is a sequela of a viral myocarditis, in particular of that due to mumps vi
58 V-1 model will enable fundamental studies of viral myocarditis, including IFN-gamma modulation as a t
59                   Using this novel model for viral myocarditis induced with Theiler's murine encephal
60                                              Viral myocarditis is a disease with a high morbidity and
61                                              Viral myocarditis is a life-threatening illness that may
62                                              Viral myocarditis is among the most common causes of hea
63                                              Viral myocarditis is an important cause of human morbidi
64                                              Viral myocarditis is an important human disease, and reo
65                                              Viral myocarditis is an important human disease, with a
66 de range of clinical symptoms, biopsy-proven viral myocarditis is associated with a long-term mortali
67 esis of chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and
68                                              Viral myocarditis is remarkably common, being detected i
69                  A major causative agent for viral myocarditis is the B3 strain of coxsackievirus, a
70 5 years +/- 14; 14 men) and 85 patients with viral myocarditis (mean age, 32 years +/- 13; 67 men).
71 e disorders and may be beneficial in chronic viral myocarditis once virus is cleared.
72 hs in the understanding of the etiologies of viral myocarditis or dilated cardiomyopathy (DCM).
73 ackievirus B3 (CVB3) is a causative agent of viral myocarditis, pancreatitis, and meningitis in human
74 ), an important human causative pathogen for viral myocarditis, pancreatitis, and meningitis, has evo
75 s are significant human pathogens that cause viral myocarditis, pancreatitis, and meningitis.
76 kie virus B3 (CVB3)-the most common cause of viral myocarditis-predominantly activates CARD8 in ECs i
77                                        Acute viral myocarditis progresses through several stages, inc
78                                              Viral myocarditis remains a prominent infectious-inflamm
79 sclerosis, acute coronary syndromes, stroke, viral myocarditis, sepsis, ischemia/reperfusion injury,
80 gulated PERK signaling pathways to instigate viral myocarditis, suggesting that targeting the TRIM29-
81 immunity signal transducer IRAK4 exacerbates viral myocarditis through inhibition of interferon produ
82                                              Viral myocarditis (VM) is an important cause of heart fa
83             Using a reovirus murine model of viral myocarditis, we characterized and targeted apoptos
84  The benefits of TIMP-1 blockade in treating viral myocarditis were confirmed by administering, to wi
85                      Pathogenic variants and viral myocarditis were identified in 45.9% of patients w
86 unction, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocki
87 s modulate heart failure pathogenesis during viral myocarditis, yet their identities and functions re