The distribution of antibodies to HHV-6 compared with other herpesviruses in young children

Farr, T. J.; Harnett, Gerald B.; Pietroboni, Glenys R.; Bucens, Marion R.

doi:10.1017/s095026880004824x

Cited by 24 publications

(14 citation statements)

References 15 publications

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“…HHV-6 also has a neurotropic property (3) and was found to cause subacute leukoencephalitis, manifesting as MS and demyelination of the central nervous system (8,19). Epidemiologic studies have shown that the vast majority of primary HHV-6 infections occur within the first year of life (13,50). Common to other herpesviruses, latency of HHV-6 is established after primary infection, and its genomic material can be found in T cells of healthy adults.…”

mentioning

confidence: 99%

Detection of Viral DNA and Immune Responses to the Human Herpesvirus 6 101-Kilodalton Virion Protein in Patients with Multiple Sclerosis and in Controls

Tejada‐Simon

Zang

Hong

et al. 2002

J Virol

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Human herpesvirus 6 (HHV-6), a latent lymphotropic and neurotropic virus, has been suspected as an etiologic agent in multiple sclerosis (MS). The study was undertaken to correlate virologic evidence for HHV-6 activity with the state of host immunity to HHV-6 in MS patients and control subjects. The study revealed that cell-free DNA of HHV-6 was detected more frequently in both serum and cerebrospinal fluid of MS patients than in those of control subjects. T cells recognizing the recombinant 101-kDa protein (101K) corresponding to the major immunoreactive region unique to HHV-6 occurred at significantly lower precursor frequency in MS patients than in control subjects. The resulting HHV-6-specific T-cell lines obtained from MS patients exhibited skewed cytokine profiles characterized by the inability to produce interleukin-4 (IL-4) and IL-10. The decreased T-cell responses to HHV-6 and the altered cytokine profile were consistent with significantly declined serum immunoglobulin G (IgG) titers for HHV-6 of MS patients compared to those of control subjects. In contrast, elevated serum IgM titers for HHV-6 were detected in the majority of MS patients, which may reflect frequent exposure of B cells to HHV-6. The findings suggest that the decreased immune responses to HHV-6 may be responsible for ineffective clearance of HHV-6 in MS patients.

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confidence: 99%

Detection of Viral DNA and Immune Responses to the Human Herpesvirus 6 101-Kilodalton Virion Protein in Patients with Multiple Sclerosis and in Controls

Tejada‐Simon

Zang

Hong

et al. 2002

J Virol

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“…With rare exceptions (Yadav et al, 1990), the prevalence of antibodies to HHV-6 is high among populations throughout the world. Epidemiologic studies in normal children have shown that the vast majority of primary HHV-6 infections occur within the ®rst year of life Farr et al, 1990). Human herpesvirus-6 IgG can be detected in more than 90% of neonates (Knowles and Gardner, 1988;Leach et al, 1992), re¯ecting both the high seroprevalence of HHV-6 among adults (Brown et al, 1988b;Ranger et al, 1991;Leach et al, 1992) and the active transport of HHV-6 IgG across the placenta .…”

Section: Epidemiologymentioning

confidence: 99%

“…Human herpesvirus-6 IgG can be detected in more than 90% of neonates (Knowles and Gardner, 1988;Leach et al, 1992), re¯ecting both the high seroprevalence of HHV-6 among adults (Brown et al, 1988b;Ranger et al, 1991;Leach et al, 1992) and the active transport of HHV-6 IgG across the placenta . The prevalence of HHV-6 IgG drops signi®cantly by 4 ± 6 months of life as maternal antibodies decline, then increases through the third year of life and remains high into adulthood Farr et al, 1990). More than 90% of immunocompetent children become infected with HHV-6 by 12 months of life (Leach et al, 1992), and virtually 100% acquire infection by 3 years of age (Brown et al, 1988b).…”

Section: Epidemiologymentioning

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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“…Seroepidemiology. The serological studies on HHV-6 infection were performed in various countries by immunofluorescence test (indirect or anticomplement test), ELBA and neutralizing antibody test (16,17,26,45,64,71,75,94,96). Great differences were not seen in the prevalence of antibody to HHV-6 in the world, but it was reported that low prevalence of the antibody was found in a few areas (71).…”

mentioning

confidence: 99%

“…There are two possibilities in the mode of transmission of HHV-6, i.e., vertical (transplacental) and horizontal transmission. Since Farr et al (1990) reported that IgM antibody to HHV-6 was not found in peripheral blood of newborn babies (26), and HHV-6 DNA was not detectable by PCR in umbilical cord blood cells so far (Yamanishi et al, unpublished data), it is unlikely that HHV-6 is transmitted through placenta. Recently Okuno et al (1991) reported that an outbreak of ES was found in a nursery in our area (67).…”

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confidence: 99%

Human Herpesvirus 6

Yamanishi

1992

Microbiology and Immunology

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551 552K. YAMANISHI balloon-like cells could be observed. When the cells were fixed and stained with the sera of acute and convalescent phase of ES, positive staining was observed only with the convalescent sera. Next, the cultured cells were observed by electron microscopy (EM) as reported elsewhere (74). The typical herpesvirus particles were found in the nucleus and cytoplasm of the cultured cells. Thus, the diameter of virion was 90-110 nm in the nucleus and 150-170 nm in the cytoplasm (91, 95), suggesting that this virus resembles a herpesvirus. Next, sera, which were specific for 5 human pathogenic herpesviruses described above, were tested for the reactivity to this viral antigen in the cultured cells, and no positive staining was observed. These results suggested that a new herpesvirus was isolated from ES patients. Then this viral antigen and HHV-6 antigen (55) were reacted with paired sera from ES patients. No antibody to both antigens was detected in the sera during the acute phase and the antibody titers to both antigens increased during the convalescent phase. This result indicated that the virus isolated from ES patients was HHV-6. Thereafter this result was confirmed by other groups, and the virus isolation rate from ES patients was shown to be high at the febrile phase of ES (6, 13). Furthermore, it was reported that HHV-6 infection without clinical symptoms of rash or fever, or even without any clinical symptoms could be seen in some individuals as the primary infection of 81,83).3. Other diseases associated with HHV-6 infection. Although the symptoms of ES are relatively mild, liver dysfunction and neurological symptoms such as convulsion are seen during ES (62). Recently it has been reported that HHV-6 caused the liver dysfunction in the patients who were in the primary infection of HHV-6 (9, 82, 88), and that unfortunately one patient died from fulminant hepatitis (9).A case that was diagnosed as encephalitis during HHV-6 infection was also reported (36). In order to detect HHV-6 in the central nervous system, we tried to detect HHV-6 DNA in the cerebrospinal fluid (CSF) from ES patients (93). CSF was obtained from patients showing the neurological symptoms, such as convulsion, vomiting, irritability and bulging of anterior fontanel, during febrile phase of ES. Since patients had high fever (more than 39 C) and the appearance of rash after subsidence of the fever, they were clinically diagnosed as ES. When cell counts in CSF were performed at the time of sample collection, they ranged in normal in each sample. CSF samples as controls were collected from patients who were admitted in the hospital and suspected as having neurological symptoms or lasting high fever by unknown causes. Sixteen specimens including 6 control samples of CSF were collected from the patients, and DNA was extracted and amplified by PCR using HHV-6 specific primers. The band specific for HHV-6 DNA could be detected by ethidium bromide staining in 5 of the 10 ES patients, CSF (50%), and this was confirmed by Southern blot...

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The distribution of antibodies to HHV-6 compared with other herpesviruses in young children

Cited by 24 publications

References 15 publications

Detection of Viral DNA and Immune Responses to the Human Herpesvirus 6 101-Kilodalton Virion Protein in Patients with Multiple Sclerosis and in Controls

Detection of Viral DNA and Immune Responses to the Human Herpesvirus 6 101-Kilodalton Virion Protein in Patients with Multiple Sclerosis and in Controls

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

Human Herpesvirus 6

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