Meningoencephalitis caused by human herpesvirus-6 in an immunocompetent adult patient: Case report and review of the literature

Torre, Donato; Speranza, Filippo; Martegani, Roberto; Ferrante, Pasquale; Omodeo-Zorini, Elisabetta; Mancuso, Roberta; Fiori, G P

doi:10.1007/bf02770845

Cited by 27 publications

(21 citation statements)

References 25 publications

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“…There are a remarkable number of cases of encephalitis in immunocompetent adults attributed to variant A, 6 in all (4,13,26,29,30,39), as opposed to one attributed to variant B (5,28). As previously discussed, HHV-6B, not HHV-6A, is responsible for primary infection in childhood, whereas either variant A or B can be integrated into human chromosomes.…”

Section: Discussionmentioning

confidence: 88%

“…Turning to older individuals in whom primary infection is extremely unlikely, there are a few case reports describing, in all, 11 immunocompetent adults and 1 teenager. All had clinically defined encephalitis and HHV-6 DNA in their CSF (4,5,13,21,26,29,30,33,39), and in each case, the diagnosis was given as HHV-6 encephalitis but viral integration had not been considered. Viral DNA load in CSF was measured in 7 patients; low level HHV-6 DNA was found in 2 of these but in both primary infection was excluded (29,30) suggesting viral reactivation.…”

Section: Discussionmentioning

confidence: 99%

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Human Herpesvirus 6 DNA Levels in Cerebrospinal Fluid Due to Primary Infection Differ from Those Due to Chromosomal Viral Integration and Have Implications for Diagnosis of Encephalitis

et al. 2007

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The prevalence and concentration of human herpesvirus 6 (HHV-6) DNA in the cerebrospinal fluid (CSF) of the immunocompetent in primary infection was compared with that in viral chromosomal integration. Samples from 510 individuals with suspected encephalitis, 200 young children and 310 older children and/or adults, and 12 other patients were tested. HHV-6 DNA concentration (log 10 copies/ml) was measured in CSF, serum, and whole blood using PCR. Serum HHV-6 immunoglobulin G antibody was measured by indirect immunofluorescence. Primary infection was defined by antibody seroconversion and/or a low concentration of HHV-6 DNA (<3.0 log 10 copies/ml) in a seronegative serum. Chromosomal integration was defined by a high concentration of viral DNA in serum (>3.5 log 10 copies/ml) or whole blood (>6.0 log 10 copies/ml). The prevalences of CSF HHV-6 DNA in primary infection and chromosomal integration were 2.5% and 2.0%, respectively, in the young children (<2 years) and 0% and 1.3%, respectively, in the older children and/or adults. The mean concentration of CSF HHV-6 DNA in 9 children with primary infection (2.4 log 10 copies/ml) was significantly lower than that of 21 patients with viral chromosomal integration (4.0 log 10 copies/ml). Only HHV-6B DNA was found in primary infection, whereas in viral integration, 4 patients had HHV-6A and 17 patients HHV-6B. Apart from primary infection, chromosomal integration is the most likely cause of HHV-6 DNA in the CSF of the immunocompetent. Our results show that any diagnosis of HHV-6 encephalitis or other type of active central nervous system infection should not be made without first excluding chromosomal HHV-6 integration by measuring DNA load in CSF, serum, and/or whole blood.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Human Herpesvirus 6 DNA Levels in Cerebrospinal Fluid Due to Primary Infection Differ from Those Due to Chromosomal Viral Integration and Have Implications for Diagnosis of Encephalitis

et al. 2007

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“…The high fever, characteristic of HHV-6 primary infection, is often accompanied by seizures, and HHV-6 reactivation in immunocompromised patients is associated with severe encephalitis and/or encephalopathy. There have been case reports on immunocompetent and immunocompromised adults with severe CNS disease due to HHV-6 active infection, which was characterized by a fulminant multifocal demyelinating disease (32,115,262,313,329,410). The neuroinvasiveness of the virus is proven by the fact that HHV-6 DNA is frequently detected in specimens from divergent regions of the brain (incidence rate of individuals with positive HHV-6 PCR on brain tissue, 32 to 85%) (60,61,83,110,249).…”

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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“…HHV-6A has been implicated in the etiology of several other pathologies (4,42), but this remains to be confirmed. Reports suggest a role of this variant in multiple sclerosis (36) as well as encephalitis (28,39). Importantly, several lines of experimental and clinical evidence suggest that HHV-6A might accelerate AIDS progression (24).…”

Section: Human Herpesvirus 6 (Hhv-6) Is a Ubiquitous Pathogen Of The mentioning

confidence: 99%

Downregulation of the T-Cell Receptor Complex and Impairment of T-Cell Activation by Human Herpesvirus 6 U24 Protein

Sullivan

Coscoy

2008

J Virol

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We have performed a screen aimed at identifying human herpesvirus 6 (HHV-6)-encoded proteins that modulate immune recognition. Here we show that the U24 protein encoded by HHV-6 variant A downregulates cell surface expression of the T-cell receptor (TCR)/CD3 complex, a complex essential to T-cell activation and the generation of an immune adaptive response. In the presence of U24, the TCR/CD3 complex is endocytosed but is not recycled back to the plasma membrane. Instead, it accumulates in early and late endosomes. Interestingly, whereas CD3 downregulation from the cell surface is normally associated with T-cell activation, U24 downregulates CD3 independently of T-cell activation. Moreover, we found that U24-expressing T cells are resistant to activation by antigen-presenting cells. HHV-6 has evolved a unique mechanism of inhibition of T-cell activation that may impair the establishment of an adaptive immune response. Furthermore, lymphocyte activation creates an environment favorable to the reactivation and replication of lymphotropic herpesviruses. Thus, by inhibiting T-cell activation, HHV-6 might limit its reactivation and thus minimize immune recognition.

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Meningoencephalitis caused by human herpesvirus-6 in an immunocompetent adult patient: Case report and review of the literature

Cited by 27 publications

References 25 publications

Human Herpesvirus 6 DNA Levels in Cerebrospinal Fluid Due to Primary Infection Differ from Those Due to Chromosomal Viral Integration and Have Implications for Diagnosis of Encephalitis

Human Herpesvirus 6 DNA Levels in Cerebrospinal Fluid Due to Primary Infection Differ from Those Due to Chromosomal Viral Integration and Have Implications for Diagnosis of Encephalitis

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

Downregulation of the T-Cell Receptor Complex and Impairment of T-Cell Activation by Human Herpesvirus 6 U24 Protein

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