Human herpesvirus 7 infection associated with central nervous system manifestations

Torigoe, Sadayoshi; Koide, Waka; Yamada, Masao; Miyashiro, Eikichi; Tanaka‐Taya, Keiko; Yamanishi, Koichi

doi:10.1016/s0022-3476(96)70259-7

Cited by 121 publications

(67 citation statements)

References 12 publications

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“…tuberculosis detected in CSF by PCR N. meningitidis (1) N. meningitidis isolated from blood culture Demyelinating disorders (8) ADEM (4) Multiple sclerosis (1) None None identified (3) Influenza vaccine 3 weeks before neurologic symptom onset in 1 case; none (2) Optic neuritis (2) None identified (2) None Transverse myelitis (1) None identified (1) Upper respiratory tract infection 2 weeks before neurologic symptom onset Cranial nerve VI palsy (1) Multiple sclerosis (1) None Other conditions (6) Fever, lymphadenopathy (1) EBV-associated PTLD (1) c Post cardiac transplant; high EBV load in peripheral blood (.1000 cells/10 6 PBMCs) Fever, weakness, paresthesias (1) EBV-associated HLH (1) EBV DNA detected by PCR in blood Fever, rash, arthralgia (1) Parvovirus B19 (1) Parvovirus B19 DNA detected in skin biopsy Fever, myalgia, headache (1) Benign intracranial hypertension (1 shown). Indeed HHV-7 reactivation has never been causally associated with any disease.…”

Section: Discussionmentioning

confidence: 99%

“…Primary HHV-7 infection occurs predominantly in young children; ∼65% have evidence of infection by 2 years of age 2,3 and .90% are seropositive at age 5 years. 3,4 Primary HHV-7 infection is causally associated with several clinical entities in early childhood including exanthem subitum, 5,6 febrile illness without a rash, 3 febrile seizures, 7 and febrile status epilepticus. 8,9 The possibility of HHV-7 encephalitis in young children was first invoked by a description of 2 cases of exanthem subitum accompanied by encephalopathy and hemiplegia.…”

mentioning

confidence: 99%

“…8,9 The possibility of HHV-7 encephalitis in young children was first invoked by a description of 2 cases of exanthem subitum accompanied by encephalopathy and hemiplegia. 6 The consequences of delayed primary HHV-7 infection in older children are unknown. However, a single case of encephalitis in a 19-year-old man has been reported in whom primary HHV-7 infection was established on the basis of low IgG avidity in acute serum together with HHV-7 DNA in the cerebrospinal fluid (CSF).…”

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confidence: 99%

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Delayed Primary HHV-7 Infection and Neurologic Disease

Schwartz

Richardson²,

Ward

et al. 2014

Pediatrics

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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-Barré 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.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Delayed Primary HHV-7 Infection and Neurologic Disease

Schwartz

Richardson²,

Ward

et al. 2014

Pediatrics

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“…Soon after the discovery of the virus, HHV-7, in addition to HHV-6, was reported to be a causative agent in exanthem subitum (14,15). Primary HHV-7 infection usually has a benign and self-limited clinical course but can in rare instances cause several severe complications (16,18). Furthermore, although the clinical features of HHV-7 reactivation remain obscure, several manifestations, including fatality due to viral reactivation, have been reported for organ transplant recipients (3,5,8,12,17,21).…”

Section: Human Herpesvirus 7 (Hhv-7) Was Originally Isolated In 1990 mentioning

confidence: 99%

Detection of Human Herpesvirus 7 DNA by Loop-Mediated Isothermal Amplification

et al. 2004

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The reliability of loop-mediated isothermal amplification (LAMP), initially developed for the detection of human herpesvirus 7 (HHV-7), was evaluated in this study. Although a LAMP product was detected in HHV-7 DNA, neither HHV-6 nor human cytomegalovirus DNA produced a product. When agarose gel electrophoresis was used for the detection of LAMP products, the sensitivity of a 30-min HHV-7 LAMP reaction reached 250 copies/tube. The use of turbidity for the detection of the LAMP products gave a sensitivity of 500 and 250 copies/tube for 30-and 60-min reactions, respectively. Following these initial validation studies, clinical samples collected from two patients with primary HHV-7 infections were examined by HHV-7 LAMP. By use of agarose gel electrophoresis, HHV-7 LAMP products could be detected in acute-phase plasma samples but no LAMP product was detectable in convalescent-phase plasma samples from either patient. Since a turbidity assay is less sensitive than agarose gel electrophoresis, no HHV-7 LAMP product could be detected in plasma samples after a 30-min LAMP reaction. After a 60-min LAMP reaction, HHV-7 LAMP product could be detected in acute-phase plasma samples.

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“…Both viruses belong to the Roseolovirus genus of the betaherpesvirus subfamily of herpesviruses and show very similar biological behaviors: (i) after primary infection they are shed in saliva throughout life (14,16,18,26,33); (ii) primary infection with either virus causes exanthem subitum (roseola infantum) (25,35), a classical exanthematous disease of childhood; and (iii) primary infection with either virus has been associated with childhood neurological illness, particularly febrile convulsions (12,27,28,32), and the DNAs of both HHV-6 (12) and HHV-7 (20) have been detected in cerebrospinal fluid. Any study of the relationship between the two viruses and disease must therefore use diagnostic methods able to distinguish between primary HHV-6 and primary HHV-7 antibody responses.…”

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confidence: 99%

Use of Immunoglobulin G Antibody Avidity for Differentiation of Primary Human Herpesvirus 6 and 7 Infections

et al. 2001

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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.

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Human herpesvirus 7 infection associated with central nervous system manifestations

Cited by 121 publications

References 12 publications

Delayed Primary HHV-7 Infection and Neurologic Disease

Delayed Primary HHV-7 Infection and Neurologic Disease

Detection of Human Herpesvirus 7 DNA by Loop-Mediated Isothermal Amplification

Use of Immunoglobulin G Antibody Avidity for Differentiation of Primary Human Herpesvirus 6 and 7 Infections

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