Myocarditis is a rare cause of sudden death in childhood. We describe the sudden death of a child from viral myocarditis, which we demonstrate was likely caused by an uncontrolled inflammatory response to a disseminated adenovirus serotype 3 infection originating in the tonsil. CASE REPORTAn 11-year old boy collapsed suddenly at home. He was transferred to a hospital by ambulance. Cardiopulmonary resuscitation was unsuccessful, and he was pronounced dead. He had visited his general practitioner (GP) 1 day earlier with a sore throat and was treated with antibiotics for tonsillitis. No investigations were carried out by his GP or on arrival at the hospital due to his sudden death. He had no past medical history of note, and there was no family history of cardiac illness or sudden death. No recent foreign travel was reported, nor was there contact with persons from abroad. A postmortem was carried out at the direction of the coroner.Much of the postmortem examination was normal. His tonsils were mildly enlarged and showed a surface purulent exudate. However, on postmortem examination, his heart was enlarged (weight, 214.2 g; expected weight, 124 g). On sectioning, the myocardium appeared diffusely abnormal with areas of petechiae and pallor. There was no evidence of myocardial hypertrophy. Microscopically, there was a severe myocardial infiltrate diffusely present composed of lymphocytes, histiocytes, and plasma cells with occasional eosinophils and neutrophils (Fig. 1). There were admixed areas of necrosis and hemorrhage. There was no evidence of fibrosis or myofiber hypertrophy. Immunohistochemical staining revealed that the infiltrate was predominantly lymphohistiocytic (CD45 positive). CD3 staining confirmed that this was a T-lymphocytemediated response (Fig. 2).All routine investigations, including swabs for bacterial culture, blood cultures, meningococcal PCR, and pneumococcal PCR, were negative. Toxicology testing for alcohol and drugs was negative. Target-specific immunoglobulin M assays were performed for Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus, parvovirus B19, and rubella virus, along with complement fixation testing for total antibodies to Mycoplasma pneumoniae, Chlamydia group, and adenovirus and latex agglutination testing for Toxoplasma gondii. All serological investigations were negative. In addition, no viruses were observed in the lung or myocardial tissue by electron microscopy. Cerebrospinal fluid Gram staining and culture were negative.The most common viral etiologies of myocarditis are Coxsackie group B viruses and members of the adenovirus genus (3, 5). Therefore, molecular methods were employed to investigate the presence of these viruses. Total viral RNA/DNA was extracted from serum using the Qiagen QIAmp viral RNA mini kit, and total viral DNA was extracted from myocardial and pulmonary tissue using the QIAamp DNA mini kit (Qiagen) in accordance with the manufacturer's instructions. Enterovirus RNA was not detected in lung or myocardial tissue using a nested reverse trans...
EBV gene expression in CHL carriers differs from those that resolve infection and should be interpreted alongside HLA polymorphisms.
Studies have identified solid organ transplant recipients who remain asymptomatic despite maintaining CHL. Factors which determine the CHL state remain poorly understood but are likely to involve immunological control of the viral infection. We monitored expression of PD-1, a marker of T-cell exhaustion and viral persistence, on CD8 T cells in patients who resolved EBV infection as determined by undetectable EBV DNA (REI) and CHL patients. PD-1 expression on CD8 T cells was increased in the first year post-transplant irrespective of EBV outcome, and most CD8 T cells continued to express PD-1 for up to three yr post-transplant. Although all patient groups showed similar frequencies of EBV-specific CD8+ T cells, PD-1 expression on these cells increased in the post-transplant groups compared with the pretransplant patients. Functional studies of EBV-specific CD8+ T cells stimulated with BZLF or LMP2 peptide pools revealed monofunctional IFN-γ responses. Our results indicate that PD-1 expression on CD8 T cells post-transplant may result from factors other than antigenic stimulation.
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