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Koichi Yamanishi - One of the best experts on this subject based on the ideXlab platform.

  • epidemiological study of Human Herpesvirus 6 and Human Herpesvirus 7 in pityriasis rosea
    British Journal of Dermatology, 2000
    Co-Authors: H Kosuge, Koichi Yamanishi, K Tanakataya, H Miyoshi, K Amo, Reiko Harada, T Ebihara, Y Kawahara, T Nishikawa
    Abstract:

    Background Pityriasis rosea (PR) is a common papulosquamous skin disorder that is suspected to have an infectious aetiology. Objectives We aimed to study the role of Human Herpesvirus (HHV)-7 and HHV-6 in the pathogenesis of PR. Methods We performed seroepidemiological studies (indirect immunofluorescence test) and polymerase chain reaction (PCR) analysis for HHV-6 and HHV-7 in patients with PR. Seventy-two serum samples and 37 samples of peripheral blood mononuclear cells (PBMC) from 44 patients with PR were obtained. Twenty-five patients with other skin disorders such as drug eruption, urticaria or herpes zoster were studied as controls in the PCR analysis. Results HHV-7 DNA was detected in 13 of 30 (43%) samples of PBMC of the patients with PR and 14 of 25 (56%) samples of PBMC of controls. HHV-6 DNA was detected in six of 29 (21%) patients with PR and nine of 23 (39%) controls. Thus there was no difference in the prevalence of HHV-6 or HHV-7 in PBMC between patients with PR and those with other skin disorders. In the seroepidemiological study, two cases of at least a fourfold rise in titre and five cases of a fourfold decrease in titre to HHV-7 antibody, and two cases of a fourfold rise in titre and two cases of a fourfold decrease in titre to HHV-6 antibody, were observed in 24 patients with PR. This seroepidemiological study revealed antibody responses consistent with active infection in several PR patients, but the greater proportion of the patients had no definite increase in the antibody titres. Conclusions We conclude that HHV-7 and HHV-6 may play a part in some patients with PR, but that other causative agents may exist. Further analyses are needed to determine the causative agents of PR.

  • Human Herpesvirus 6 infection as a risk factor for the development of severe drug induced hypersensitivity syndrome
    Archives of Dermatology, 1998
    Co-Authors: Yosuke Suzuki, Koichi Yamanishi, Reiko Inagi, Toshiya Aono, Tetsuo Shiohara
    Abstract:

    Background Drug-induced hypersensitivity syndrome is characterized by a severe, potentially fatal, multiorgan hypersensitivity reaction that usually appears after prolonged exposure to certain drugs. Its delayed onset and clinical resemblance to infectious mononucleosis suggest that underlying viral infections may trigger and activate the disease in susceptible individuals receiving these drugs. Observations A 60-year-old woman developed an itchy, generalized, erythematous, confluent rash on the 39th day of receiving allopurinol therapy. Even after she discontinued treatment with allopurinol, her skin lesions progressed to a severe blistering skin eruption. After the patient started oral prednisone therapy, her skin lesions resolved with desquamation. After complete resolution, rechallenge with allopurinol led to the development of an erythematous eruption. Titers of Human Herpesvirus 6 IgG antibodies dramatically increased with the development of the eruption. The results of a polymerase chain reaction and in situ hybridization indicated the presence of Human Herpesvirus 6 in the skin lesions, although Human Herpesvirus 7 DNA was detected only by in situ hybridization. Conclusion Reactivation of Human Herpesvirus 6, possibly in concert with Human Herpesvirus 7, can contribute to the development of a severe drug-induced hypersensitivity syndrome.

  • Human Herpesvirus 6 and Human Herpesvirus 7 infections in renal transplant recipients and healthy adults in turkey
    Archives of Virology, 1994
    Co-Authors: Safak Yalcin, T Karpuzglu, G Suleymanlar, G Mutlu, Tetsu Mukai, Takeshi Yamamoto, Yuji Isegawa, Koichi Yamanishi
    Abstract:

    We explored the prevalence of Human Herpesvirus 6 (HHV-6) and Human Herpesvirus 7 (HHV-7) infections in 16 renal transplant recipients and 16 healthy controls by virus isolation, serology, polymerase chain reaction (PCR) followed by dot blot hybridization. HHV-6 variant A was isolated from one renal transplant recipient. Seven patients (44%) and six controls (38%) had HHV-6 variant B DNA in their peripheral blood mononuclear cells. The prevalence of HHV-7 DNA was found to be the same in patients and controls (19%).

Sara R Rashkin - One of the best experts on this subject based on the ideXlab platform.

  • the landscape of host genetic factors involved in immune response to common viral infections
    Genome Medicine, 2020
    Co-Authors: Linda Kachuri, Stephen S Francis, Maike Morrison, George A Wendt, Yohan Bosse, Taylor B Cavazos, Sara R Rashkin
    Abstract:

    Author(s): Kachuri, Linda; Francis, Stephen S; Morrison, Maike L; Wendt, George A; Bosse, Yohan; Cavazos, Taylor B; Rashkin, Sara R; Ziv, Elad; Witte, John S | Abstract: BackgroundHumans and viruses have co-evolved for millennia resulting in a complex host genetic architecture. Understanding the genetic mechanisms of immune response to viral infection provides insight into disease etiology and therapeutic opportunities.MethodsWe conducted a comprehensive study including genome-wide and transcriptome-wide association analyses to identify genetic loci associated with immunoglobulin G antibody response to 28 antigens for 16 viruses using serological data from 7924 European ancestry participants in the UK Biobank cohort.ResultsSignals in Human leukocyte antigen (HLA) class II region dominated the landscape of viral antibody response, with 40 independent loci and 14 independent classical alleles, 7 of which exhibited pleiotropic effects across viral families. We identified specific amino acid (AA) residues that are associated with seroreactivity, the strongest associations presented in a range of AA positions within DRβ1 at positions 11, 13, 71, and 74 for Epstein-Barr virus (EBV), Varicella zoster virus (VZV), Human Herpesvirus 7, (HHV7), and Merkel cell polyomavirus (MCV). Genome-wide association analyses discovered 7 novel genetic loci outside the HLA associated with viral antibody response (P l 5.0 × 10-8), including FUT2 (19q13.33) for Human polyomavirus BK (BKV), STING1 (5q31.2) for MCV, and CXCR5 (11q23.3) and TBKBP1 (17q21.32) for HHV7. Transcriptome-wide association analyses identified 114 genes associated with response to viral infection, 12 outside of the HLA region, including ECSCR: P = 5.0 × 10-15 (MCV), NTN5: P = 1.1 × 10-9 (BKV), and P2RY13: P = 1.1 × 10-8 EBV nuclear antigen. We also demonstrated pleiotropy between viral response genes and complex diseases, from autoimmune disorders to cancer to neurodegenerative and psychiatric conditions.ConclusionsOur study confirms the importance of the HLA region in host response to viral infection and elucidates novel genetic determinants beyond the HLA that contribute to host-virus interaction.

Ari Bitnun - One of the best experts on this subject based on the ideXlab platform.

  • delayed primary hhv 7 infection and neurologic disease
    Pediatrics, 2014
    Co-Authors: Kevin L Schwartz, Katherine N Ward, Susan E Richardson, Callum Donaldson, Daune Macgregor, Brenda Banwell, Sanjay Mahant, Ari Bitnun
    Abstract:

    BACKGROUND: Primary Human Herpesvirus 7 (HHV-7) infection occurs almost universally during the first 5 years of life and is rarely accompanied by central nervous system (CNS) symptoms such as febrile seizures. The present retrospective study investigated the role of primary HHV-7 infection in CNS disease in children, including adolescents. METHODS: The study included all children who had neurologic disease aged younger than 18 years seen at the Hospital for Sick Children, Toronto, Canada, between April 1, 1998 and December 31, 2011, whose cerebrospinal fluid (CSF) was found by polymerase chain reaction to contain HHV-7 DNA. Where sera were available, HHV-7 IgG antibody titers and avidity were measured to differentiate primary from past infection. RESULTS: HHV-7 DNA was detected in the CSF of 57 (1.9%) of the 2972 children tested. In 3 adolescents primary HHV-7 infection (low avidity IgG) was confirmed as the cause of neurologic disease, 2 who had encephalitis and 1 who had Guillain-Barre syndrome. Eighteen children had possible HHV-7 disease (no alternative cause identified and indeterminate antibody result or serum not available), 7 encephalitis, 8 meningitis, and 3 demyelinating disorders. HHV-7 disease was excluded in 36 children on the basis of past infection (high IgG avidity) and/or an alternative cause. CONCLUSIONS: Primary HHV-7 infection delayed into adolescence can cause serious neurologic disease. HHV-7 DNA in CSF alone is insufficient to prove an etiologic association. Combining CSF polymerase chain reaction with serology is essential to prove primary infection when investigating HHV-7 CNS disease.

T Riordan - One of the best experts on this subject based on the ideXlab platform.

  • neuroinvasion during delayed primary hhv 7 infection in an immunocompetent adult with encephalitis and flaccid paralysis
    Journal of Medical Virology, 2002
    Co-Authors: K N Ward, P Kalima, K M Macleod, T Riordan
    Abstract:

    Antibody avidity tests have been used to detect primary Human Herpesvirus-7 (HHV-7) infection in an immunocompetent 19-year-old man with encephalitis and flaccid paralysis for which all other suspected causes had been excluded. The finding of the viral DNA in the cerebrospinal fluid (CSF) but not in serum samples suggests that primary HHV-7 infection with invasion of the central nervous system and consequential disease had occurred. As almost all adults are infected with HHV-7 in early childhood, the present case of delayed primary infection with serious symptoms must be exceptionally rare and no cases of such late acquisition of the virus have been documented in the literature. This report of HHV-7 DNA in the CSF of an immunocompetent adult is also unique. J. Med. Virol. 67:538–541, 2002. © 2002 Wiley-Liss, Inc.

Katherine N Ward - One of the best experts on this subject based on the ideXlab platform.

  • delayed primary hhv 7 infection and neurologic disease
    Pediatrics, 2014
    Co-Authors: Kevin L Schwartz, Katherine N Ward, Susan E Richardson, Callum Donaldson, Daune Macgregor, Brenda Banwell, Sanjay Mahant, Ari Bitnun
    Abstract:

    BACKGROUND: Primary Human Herpesvirus 7 (HHV-7) infection occurs almost universally during the first 5 years of life and is rarely accompanied by central nervous system (CNS) symptoms such as febrile seizures. The present retrospective study investigated the role of primary HHV-7 infection in CNS disease in children, including adolescents. METHODS: The study included all children who had neurologic disease aged younger than 18 years seen at the Hospital for Sick Children, Toronto, Canada, between April 1, 1998 and December 31, 2011, whose cerebrospinal fluid (CSF) was found by polymerase chain reaction to contain HHV-7 DNA. Where sera were available, HHV-7 IgG antibody titers and avidity were measured to differentiate primary from past infection. RESULTS: HHV-7 DNA was detected in the CSF of 57 (1.9%) of the 2972 children tested. In 3 adolescents primary HHV-7 infection (low avidity IgG) was confirmed as the cause of neurologic disease, 2 who had encephalitis and 1 who had Guillain-Barre syndrome. Eighteen children had possible HHV-7 disease (no alternative cause identified and indeterminate antibody result or serum not available), 7 encephalitis, 8 meningitis, and 3 demyelinating disorders. HHV-7 disease was excluded in 36 children on the basis of past infection (high IgG avidity) and/or an alternative cause. CONCLUSIONS: Primary HHV-7 infection delayed into adolescence can cause serious neurologic disease. HHV-7 DNA in CSF alone is insufficient to prove an etiologic association. Combining CSF polymerase chain reaction with serology is essential to prove primary infection when investigating HHV-7 CNS disease.

  • use of immunoglobulin g antibody avidity for differentiation of primary Human Herpesvirus 6 and 7 infections
    Journal of Clinical Microbiology, 2001
    Co-Authors: Katherine N Ward, D J Turner, Couto X Parada, A D Thiruchelvam
    Abstract:

    A Human Herpesvirus 7 (HHV-7) indirect immunofluorescence antibody avidity test was developed and used with an existing Human Herpesvirus 6 (HHV-6) antibody avidity test to detect and distinguish low-avidity antibodies to HHV-6 and HHV-7 and hence the respective primary infections. With sera from 269 British children aged 0 to 179 weeks, the tests showed that most (10 of 98 serum samples [13%]) HHV-6 low-avidity antibody was found in the first year of life, whereas for HHV-7, most (18 of 101 serum samples [20%]) HHV-7 low-avidity antibody was found in the second year of life. Five children had low-avidity antibodies to both viruses. Of nine Japanese children with previously serologically proven primary HHV-6 or HHV-7 infections, eight had low-avidity antibody only to the relevant virus, but one child had low-avidity antibodies to HHV-6 and HHV-7. The avidity tests were applied to five British children and further proof of viral infection was sought by the detection of specific DNA in serum or plasma, and saliva or cerebrospinal fluid. In two children who had low-avidity antibody to HHV-7 but who were seronegative for HHV-6, only HHV-7 was found. Both viruses were detected in one child with low-avidity HHV-7 antibody and high-avidity HHV-6 antibody. In two children with low-avidity antibodies to both viruses, HHV-6 and HHV-7 DNAs were found, confirming dual primary infections and excluding antibody cross-reactivity.