Clinical and virological analyses of 21 infants with exanthem subitum (roseola infantum) and central nervous system complications

Suga, S.; Yoshikawa, Tetsushi; Asano, Yoshizo; Kozawa, Toru; Nakashima, Toshihiko; Kobayashi, Ikuko; Yazaki, Takehiko; Yamamoto, Hiroko; Kajita, Yaji; Ozaki, Takao; Nishimura, Yataka; Yamanaka, Tarsuhiro; Yamada, Akira; Imanishi, Jirô

doi:10.1002/ana.410330607

Cited by 162 publications

(85 citation statements)

References 33 publications

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“…This presumably reflects the concurrent and similarly brief low-level HHV-6 DNA in serum or plasma seen in the first few days of primary infection (6,36,47). Indeed, it has been previously reported that HHV-6 DNA appears transiently in CSF at this time (35).…”

Section: Discussionmentioning

confidence: 72%

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: 72%

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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“…In the present study, 1 patient (7% of the 15) had a convulsive seizure during the febrile phase of the disease, as observed in primary HHV-6 infection. 17,21 It is not known whether HHV-7 invades the central nervous system, although reports of complications linked to primary HHV-7 infection are increasing. 13,25 As reported elsewhere, 9 -11,13 at least 53% of the 15 showed a significant simultaneous rise in antibody titers to HHV-6 during primary HHV-7 infection.…”

Section: Discussionmentioning

confidence: 99%

“…12,17 The extracted HHV-6 DNA was amplified by the nested double PCR, as described previously. 17 The outer and inner primers were made following the nucleotide sequences reported elsewhere. 18,19 The primers amplify a DNA fragment of 751 base pairs (bp) of putative large tegument protein gene.…”

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confidence: 99%

“…The extracted HHV-7 DNA was amplified according to procedures reported elsewhere. 2,12,17 The outer (HV7 and HV8) and inner (HV10 and HV11) primers were made following the nucleotide sequences reported by Berneman et al 2 These primers amplify a DNA fragment of 124 bp. The specific amplification was confirmed by using proven HHV-7 strains RK 1 and JI 2 and our own isolates.…”

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confidence: 99%

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Clinical Features and Virological Findings in Children With Primary Human Herpesvirus 7 Infection

Suga

Yoshikawa

Nagai³

et al. 1997

Pediatrics

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ABSTRACT. Objective. To elucidate clinical features of patients with primary human herpesvirus 7 (HHV-7) infection and serologic and virologic findings between HHV-7 and human herpesvirus 6 (HHV-6).Materials and Methods. During a 19-month observation period, 71 infants and children (35 boys and 36 girls with a mean age of 14.5 months [range, 1 month to 48 months]) who had acute febrile respiratory illness with or without skin rash were examined clinically and virologically. Heparinized blood samples were used for isolation of HHV-6 and HHV-7 and detection of both virus DNA sequences by a nested polymerase chain reaction amplification. Both virus antibody activities were measured by an indirect immunofluorescent assay.Results. HHV-7 infection was observed in 15 (6 boys and 9 girls with a mean age of 12.9 months [range, 7 months to 27 months]), 1 of 10 with upper respiratory infection and 14 (28%) of 50 with febrile exanthem, whereas HHV-6 infection was in 22 (44%) of the 50. Fever (37.5°C) was observed in all 15, with an average maximum body temperature of 38.7°C (range, 37.6°C to 39.8°C), which persisted for 2.9 days (range, 1 to 5 days). Papular, macular, or maculopapular rash was observed in 14 (93%) of the 15, which appeared on day 2.9 of fever (range, days 2 to 5) on the face, trunk, and extremities and persisted for 2.7 days (range, 1 to 5 days). A convulsive seizure that persisted for a few minutes developed in 1 patient on the first day of elevation of fever. HHV-6 antibody was demonstrated in 13 (87%), and a simultaneous significant increase to HHV-6 antibody titers was observed in 8 (53%) of the 15 during primary HHV-7 infection. HHV-7 and HHV-6 DNAs were almost always detected in mononuclear cells (MNCs) during acute and convalescent phases, whereas HHV-7 DNA was positive in some plasma samples obtained during the acute phase of the disease.Conclusions. Primary HHV-7 infection occurred somewhat later than HHV-6, which was confirmed by the isolation of HHV-7 from blood and/or seroconversion to the virus. Clinical features of a virologically confirmed patient with primary HHV-7 infection were comparable with those of primary HHV-6 infection. Preexisting HHV-6 antibody increased significantly in the half of patients with primary HHV-7 infection. HHV-7 DNA was detected in peripheral blood MNCs and plasma in the acute phase and persisted in MNCs thereafter. Pediatrics 1997;99(3). URL: http://www.pediatrics.org/cgi/ content/full/99/3/e4; human herpesvirus 7, human herpesvirus 6, exanthem subitum, roseola infantum, polymerase chain reaction.

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“…Symptoms and signs of patients in these early reports included bulging fontanels, irritability, febrile seizures, meningoencephalitis and residual encephalopathy (Berenberg et al, 1949;Posson, 1949;Moller, 1956;Burnstine and Paine, 1959). Following the identi®cation of HHV-6 as the causative agent of exanthem subitum, many additional instances of CNS involvement in primary HHV-6 infection have been reported (Ishiguro et al, 1990;Asano et al, 1991a;Huang et al, 1991;Asano et al, 1992;Segondy et al, 1992;Yoshikawa et al, 1992b;Kondo et al, 1993;Suga et al, 1993;Caserta et al, 1994;Hall et al, 1994;Ward and Gray, 1994;McCullers et al, 1995). Association of such neurologic ®ndings with HHV-6 is suggested by the concomitant identi®cation of virus by culture from PBMCs, by seroconversion, or, less commonly, by detection of the viral genome in CSF by PCR (Ishiguro et al, 1990;Asano et al, 1992;Yamanishi et al, 1992;Yoshikawa et al, 1992b;Caserta et al, 1994;Ward and Gray, 1994).…”

Section: Central Nervous System (Cns) Involvementmentioning

confidence: 99%

Human Herpesvirus-6: Neurologic Implications of a Newly-Described Viral Pathogen

Kimberlin

Whitley

1998

J Neurovirol

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Discovered only 12 years ago, human herpesvirus-6 (HHV-6) has been associated with central nervous system (CNS) ®ndings such as febrile seizures, encephalitis, meningitis, and possibly multiple sclerosis. These manifestations have been reported in both immunocompetent and immunocompromised individuals. The applications of such sophisticated laboratory tools as polymerase chain reaction, in situ hybridization, immunohistochemical staining, and representational difference analysis have expanded knowledge of the spectrum of CNS disease attributable to HHV-6 while delineating pathogenic mechanisms of both primary HHV-6 infection and reactivation from latency. This article reviews existing knowledge of the CNS manifestations of HHV-6, focusing on both clinical aspects of HHV-6 infection and its pathogenesis on neurologic diseases.

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Clinical and virological analyses of 21 infants with exanthem subitum (roseola infantum) and central nervous system complications

Cited by 162 publications

References 33 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

Clinical Features and Virological Findings in Children With Primary Human Herpesvirus 7 Infection

Human Herpesvirus-6: Neurologic Implications of a Newly-Described Viral Pathogen

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