Distribution of human herpesvirus 6 and varicella‐zoster virus in organs of a fatal case with exanthem subitum and varicella
Takeshi UedaYoko MiyakeKoji ImotoShigenori HattoriSusumu MiyakeT. ISHIZAKIAkira YamadaTakeshi KurataTakao NagaiSadao SugaYoshizo Asano
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Abstract The distribution of human herpesvirus 6 (HHV‐6) and varicella‐zoster virus (VZV) was examined in autopsy samples from a fatal case with both virus infections. A 9‐month‐old boy developed convulsive seizures followed by macular skin rashes, rapidly progressed to brain death, and died 15 days after the onset, when signs of varicella were noted. An isolation of HHV‐6 from blood and evaluation of antibody activities to various viral agents including HHV‐6 were performed before his death. Postmortem examinations included: (i) isolation of HHV‐6 and VZV from tissues or organs; (ii) detection of both virus antigens in tissues or organs by an indirect immunofluorescent assay using monoclonal antibodies to both viruses; (iii) amplification of both viruses and human herpesvirus 7 DNA sequences by a nested polymerase chain reaction assay; and (iv) endonuclease digestion of amplified products of HHV‐6 DNA for differentation of variants A and B. Human herpesvirus 6 DNA was detected in peripheral blood mononuclear cells (PBMC) and plasma obtained at the eruptive stage but present only in PBMC 15 days after, indicating the primary infection with HHV‐6, although the virus was not isolated from the same blood sample and a significant rise in the antibody titers to HHV‐6 was not observed. Both virus antigens and DNA were detected in various tissues or organs obtained at autopsy, but only VZV was isolated from these samples, suggesting disseminated infection with both viruses in an infant. All the amplified products of HHV‐6 DNA were variant B. Among the findings for the distribution of virus antigens, it was noteworthy that HHV‐6 antigen was demonstrated in the endothelial cells of small vessels in the frontal lobe of the brain. There was no evidence of HHV‐7 infection. These data indicate that the primary HHV‐6 infection closely followed by the primary VZV infection had the potential hazard of an unexpected and apparently life‐threatening event, in which disseminated infections with both viruses were noted in multiple tissues or organs including the brain.Keywords:
Varicella zoster virus
Human herpesvirus 6
Exanthem
Exanthem
Human herpesvirus 6
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Twenty two cases of human herpesvirus 7 (HHV-7) infection are described. HHV-7 infection occurred later than human herpesvirus 6 (HHV-6) infection and induced exanthem subitum in 47.1% of the children. HHV-7 infection was associated with exanthem subitum and the other symptoms that were observed in HHV-6 infection.
Human herpesvirus 6
Exanthem
Herpesviridae Infections
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This chapter focuses on the varicella-zoster virus (VZV), a member of the herpesviruses family and the etiologic agent of varicella and varicella-zoster. Varicella is the exanthem caused by primary infection with VZV, and shingles is the clinical syndrome of segmental, unilateral exanthem and neuralgic pain due to reactivation of latent VZV infection. Both primary and reactivated VZV infection can lead to severe generalized virus dissemination in an immunodeficient person. The chapter discusses the availability of antiviral agents for management of VZV infection, which has raised the importance of recognizing this infection in high-risk groups. It analyzes the association between aging and VZV vulnerability that is apparent in the epidemiology of the disease.
Exanthem
Shingles
Varicella zoster virus
Chicken Pox
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Exanthem
Human herpesvirus 6
Antibody titer
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Shingles
Exanthem
Varicella zoster virus
Chicken Pox
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Human herpesvirus 6
Varicella zoster virus
Etiology
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Abstract Several studies have suggested an association between human herpesvirus 6 (HHV‐6) infection and multiple sclerosis. As HHV‐6 is predominantly a T‐cell tropic virus, we examined the frequency of detection of HHV‐6 genome in peripheral blood mononuclear cells from relapsing–remitting (n = 32) and chronic progressive (n = 14) patients and from healthy (n = 17) and neurological (n = 7) controls. Two sensitive polymerase chain reaction assays were used to target different regions within the HHV‐6 genome. Depending on the polymerase chain reaction assay used, the detection of HHV‐6 genome ranged from 11.7 to 23.5% (controls), 3.1 to 23.0% (relapsing–remitting), and 14.2 to 28.5% (chronic progressive). Although these observations do not exclude a pathogenic role for HHV‐6 in multiple sclerosis, they indicate a lack of correlation between HHV‐6 infection of peripheral blood mononuclear cells and the development of multiple sclerosis.
Human herpesvirus 6
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A provisional clinical diagnosis of exanthem subitum was made in six febrile infants seen in the Paediatric Unit of Assunta Hospital, Petaling Jaya, Malaysia with uvulo-palatoglossal junctional ulcers prior to the eruption of maculopapular rash. On follow-up, all six infants developed maculopapular rash with the subsidence of fever at the end of the fourth febrile day. Human herpesvirus 6 was isolated from the peripheral blood mononuclear cells during the acute phase of the illness and HHV 6 specific genome was also detected in these cells by nested polymerase chain reaction. All the six infants showed seroconversion for both specific IgG and IgM to the isolated virus. This study suggests that the presence of uvulo-palatoglossal junctional ulcers could be a useful early clinical sign of exanthem subitum due to human herpesvirus 6.
Exanthem
Maculopapular rash
Seroconversion
Human herpesvirus 6
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ABSTRACT. We report a 10‐month‐old boy with acute meningo‐encephalitis associated with exanthem subitum. It has recently been reported that human herpesvirus‐6 is the causative agent of exanthem subitum, and to our knowledge our case is the first report of meningo‐encephalitis associated with HHV‐6 infection.
Exanthem
Human herpesvirus 6
Herpesviridae Infections
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Interferon (IFN) production after inoculation with human herpesvirus 6 (HHV-6) was studied in peripheral blood mononuclear cells from 10 HHV-6-seropositive healthy adults and five samples of cord blood mononuclear cells. When the cells were exposed to HHV-6 at a multiplicity of infection of 10−2 50% tissue culture infectious doses/cell, IFN activity was detected as early as 12 h after exposure to HHV-6, plateaued at days 2–5, and gradually decreased thereafter. IFN was also induced by ultraviolet-inactivated but not heat-inactivated HHV-6. The response ofcord blood mononuclear cells was lower than that of the cells from healthy adults. The activity of all IFN samples was stable to acid and exclusively neutralized by anti-human IFN-α. The IFNproducing cell population was mainly non-T cells and monocytes. Furthermore, exogenous IFN suppressed HHV-6 replication. Production of IFN-α may be an important part of the host response to HHV-6.
Human herpesvirus 6
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Multiplicity of infection
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