Primary human herpesvirus‐6 associated with an afebrile seizure in a 3‐week‐old infant

Zerr, Danielle M.; Yeung, Laurence C.; Obrigewitch, Rose M.; Huang, Meei‐Li; Frenkel, Lisa M.; Corey, Lawrence

doi:10.1002/jmv.2156

Cited by 28 publications

(18 citation statements)

References 27 publications

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“…The occurrence of encephalitis and febrile or afebrile seizures as complications of primary infection has been described previously (41,43), suggesting that HHV-6 has neuropathogenic potential. In addition, HHV-6 has also been demonstrated to be the causative agent of encephalitis in adult immunosuppressed patients such as bone marrow transplant recipients (40).…”

mentioning

confidence: 71%

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Donati

Martinelli

Cassiani-Ingoni

et al. 2005

J Virol

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Though first described as a lymphotropic virus, human herpesvirus 6 (HHV-6) is highly neuropathogenic. Two viral variants are known: HHV-6A and HHV-6B. Both variants can infect glial cells and have been differentially associated with central nervous system diseases, suggesting an HHV-6 variant-specific tropism for glial cell subtypes. We have performed infections with both viral variants in human progenitor-derived astrocytes (HPDA) and monitored infected cell cultures for cytopathic effect (CPE), intra-and extracellular viral DNA load, the presence of viral particles by electronic microscopy, mRNA transcription, and viral protein expression. HHV-6A established a productive infection with CPE, visible intracellular virions, and high virus DNA loads. HHV-6B-infected HPDA showed no morphological changes, intracellular viral particles, and decreasing intra-and extracellular viral DNA over time. After long-term passage, HHV-6B-infected HPDA had stable but low levels of intracellular viral DNA load with no detectable viral mRNA. Our results demonstrate that HHV-6A and HHV-6B have differential tropisms and patterns of infection for HPDA in vitro, where HHV-6A results in a productive lytic infection. In contrast, HHV-6B was associated with a nonproductive infection. These findings suggest that HHV-6 variants might be responsible for specific infection patterns in glial cells in vivo. Astrocytes may be an important reservoir for this virus in which differential tropism of HHV-6A and HHV-6B may be associated with different disease outcomes.

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confidence: 71%

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Donati

Martinelli

Cassiani-Ingoni

et al. 2005

J Virol

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“…Febrile seizures were reported in approximately 10% of children with primary HHV-6 infection, representing 10 to 20% of febrile seizure cases in children under 2 years old (22,29,154,218,426 (185,196,202,278,378,445). One case report describing an infant with afebrile convulsions due to primary infection with HHV-6B demonstrated that HHV-6 infection can have a direct effect on the brain, causing convulsions in the absence of fever (459). HHV-6 DNA has been detected in cerebrospinal fluid (CSF) of children with convulsions during primary infection or reactivation (218,378).…”

Section: Clinical Manifestations Of Hhv-6 Infectionmentioning

confidence: 99%

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

2005

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Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular receptor for HHV-6, CD46, has shed a new light on HHV-6 cell tropism. Furthermore, the in vitro interactions between HHV-6 and other viruses, particularly human immunodeficiency virus, and their relevance for the in vivo situation are discussed, as well as the transactivating capacities of several HHV-6 proteins. The insight into the clinical spectrum of HHV-6 is still evolving and, apart from being recognized as a major pathogen in transplant recipients (as exemplified by the rising number of prospective clinical studies), its role in central nervous system disease has become increasingly apparent. Finally, we present an overview of therapeutic options for HHV-6 therapy (including modes of action and resistance mechanisms)

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“…The role of HHV-6 in neurological disease is poorly understood. Neurological complications such as febrile and afebrile seizures, encephalitis, and meningitis sometimes occur after primary HHV-6 infection Hall et al, 1994;Jones et al, 1994;Suga et al, 1993;Yanagihara et al, 1995;Zerr et al, 2002). Reactivation of HHV-6 in adults is believed to be responsible for encephalitis in immunocompromized hosts such as bone marrow transplant, organ transplant, and stem cell recipients (Drobyski et al, 1994;Wainwright et al, 2001;Zerr et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Differential tropism of human herpesvirus 6 (HHV-6) variants and induction of latency by HHV-6A in oligodendrocytes

et al. 2005

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Human herpesvirus 6 (HHV-6) is a ubiquitous beta -herpesvirus associated with a number of clinical disorders. Two closely but biologically distinct variants have been described. HHV-6 variant B causes the common childhood disease exhanthem subitum, and although the pathologic characteristics for HHV-6 variant A are less well defined, HHV-6A has been suggested to be more neurotropic. We studied the effect of both HHV-6 variants in an oligodendrocyte cell line (MO3.13). Infection of M03.13 was monitored by cytopathic effect (CPE), quantitative TaqMan PCR for viral DNA in cells and supernatant, reverse transcriptase-polymerase chain reaction (RT-PCR) to detect viral RNA, and indirect immunofluorescence (IFA) to detect viral protein expression. HHV-6A infection induced significantly more CPE than infection with HHV-6B. HHV-6B induced an abortive infection associated with a decrease of the initial viral DNA load over time, early RNA expression, and no expression of viral antigen. In contrast, infection with HHV-6A DNA persisted in cells for at least 62 days. During the acute phase of infection with HHV-6A, intracellular and extracellular viral load increased and cells expressed the viral protein IE-2 and gp116/54/64. No HHV-6A RNA or protein was expressed after 30 days post infection, suggesting that HHV-6A formed a latent infection. These studies provide in vitro support to the hypothesis that HHV-6 can actively infect oligodendrocytes. Our results suggest that HHV-6A and HHV-6B have different tropism in MO3.13 cells and that an initially active HHV-6A infection can develop latency. Differences between HHV-6A and -6B infection in different neural cell types may be associated with different neurological diseases.

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Primary human herpesvirus‐6 associated with an afebrile seizure in a 3‐week‐old infant

Cited by 28 publications

References 27 publications

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

Differential tropism of human herpesvirus 6 (HHV-6) variants and induction of latency by HHV-6A in oligodendrocytes

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