Fatal Myocarditis Associated with Acute Parvovirus B19 and Human Herpesvirus 6 Coinfection

Abstract

We report on the case of a healthy young boy who developed a fulminant myocarditis due to acute coinfection with erythrovirus (parvovirus B19) and human herpesvirus 6 (HHV-6) in the absence of an antiviral immune response. We suggest that the HHV-6-induced immunosuppression enhanced dissemination of parvovirus B19, which led to fatal myocarditis. CASE REPORTAn 11-year-old boy was admitted with a 3-day history of fever that progressed within a few hours to acute distress. He had no notable medical history; in particular, there were no signs of a preexisting immunodeficiency. On examination he was lethargic and cyanotic with tachypnea and had a fever (41.3°C). His blood pressure was 73/31 mm Hg, and his pulse was 201 beats/min. Erythema and exudates on the tonsils were noted, as were cervical lymphadenopathies and a rash involving both arms and the neck. Examination of the head, lungs, and abdomen was normal. There were no focal neurological signs. He was intubated. Intravenous dopamine and dobutamine were given. Arterial blood gas analysis showed a pH of 7.26 and partial O 2 pressure of 3.48 kPa, with an O 2 saturation level of 43.4%. Cardiac arrest occurred suddenly; resuscitation efforts were successful only for a short time, and the patient died of congestive heart failure 55 min later.Biochemical laboratory findings were normal except for Creactive protein (64.5 mg/liter; normal level, Ͻ10 mg/liter), creatinine kinase (6.60 kat/liter; normal level, 0.10 to 3.17 kat/liter), and troponin T (0.59 ng/ml; normal level, Ͻ0

High Prevalence of Cardiac Parvovirus B19 Infection in Patients With Isolated Left Ventricular Diastolic Dysfunction

“…6 Coinfection with PVB19 and HHV6, as seen in 7 of 37 (19%) of our patients, has been previously reported in fulminant myocarditis, and it has been suggested that HHV6-induced immunosuppression can lead to enhanced dissemination of PVB19. 26 However, HHV6, as seen in 9 of 37 (24%) of our patients, is thought to exhibit a unique spectrum of biological properties that make it an immunosuppressive agent of it own. In this context, it should be noted that vasculotropism of HHV6 has also recently been demonstrated in human cardiac microvessels.…”

High Prevalence of Viral Genomes and Multiple Viral Infections in the Myocardium of Adults With “Idiopathic” Left Ventricular Dysfunction

“…Polymerase chain reaction (PCR)/reverse transcription PCR (RT-PCR) was performed for the detection of enteroviruses (including coxsackievirus and echovirus), adenovirus, 12 parvovirus B19, 9,13 human herpesvirus type 6, 13 human cytomegalovirus, 14 Epstein-Barr virus, 15 influenza virus A and B, 16 herpes simplex virus 1 and 2, 17 and hepatitis virus C. 18 In addition, DNA was extracted from peripheral blood cells (PBLs) to exclude a systemic infection with PVB19, EBV, and HHV6. As a control for successful extraction of DNA and RNA from heart muscle tissue, oligonucleotide sequences were chosen from the DNA sequence of the GAPDH gene.…”

Molecular phenotypes of human parvovirus B19 in patients with myocarditis

“…B19V-coinfection with other cardiotropic viruses like EV, ADV and HHV6 may contribute to the severity of B19V-myocarditis [4,7,8,20] , possibly by reactivating B19V replication and thereby enhancing virus specific host immune responses, tissue inflammation and the progression to chronic heart failure [37] . This is reminiscent of the increased replication of HIV caused by coinfection with HHV6 and HHV8 [21,38] .…”

“…Recent reports have indicated that coinfection with different cardiotropic viruses of the human heart is common [7,8,18,19] . Human herpes virus 6 (HHV6) has been identified as an important coinfecting pathogen with B19V of the myocardium and resulting in fatal myocarditis in infants [1,20] . It has been reported that HHV6 is able to transactivate human immunodeficiency virus (HIV) and human cytomegalovirus (HCMV) [19,21] .…”