A total of 115 potential open reading frames (ORFs) were identified within the 161 573-bp contiguous sequence of the entire HHV-6B genome (HST) (Isegawa et al., 1999). All experiments were performed in compliance with relevant laws and institutional guidelines and in accordance with the ethical standards of the Declaration of Helsinki. Viral culture for HHV was negative in all patients. The 10 patients and seven control subjects tested for enteroviral RNA were negative. HHV-7 has also been associated with febrile illness in children and is another etiologic agent of exanthem subitum . Together, they account for one third of FSE, a condition associated with an increased risk of both hippocampal injury and subsequent temporal lobe epilepsy.
1990). HHV-6 was recently recognized as an opportunistic pathogen in transplant recipients. By contrast, infection with HHV-6A is generally symptomless and appears to be unrelated to any specific pathology (8). By contrast, infection with HHV-6A is generally symptomless and appears to be unrelated to any specific pathology (8). Honma, K. Antibody titers decline sharply from birth to a nadir at 3 to 6 months of age (Fig.
We explored a potential interaction between HHV-6 and primary CMV infection in solid organ transplantation, which previously demonstrated a significant reduction in CMV disease using CMV immune globulin (CMVIG) prophylaxis in kidney transplant recipients at risk for primary CMV infection . With the exception of a few genes or regions, the coding sequences of HHV-6A and HHV-6B are >90% identical (14, 27). Major histocompatibility complex (MHC) tetramers generated with these epitopes were able to detect HHV-6-specific T cell populations. The integration of the viral genome into human chromosomes is a unique mode of congenital infection, and little information exists about the biological characteristics and clinical importance of the integrated virus. In all, 33 peripheral FP patients (26 idiopathic, 5 with herpesvirus infection, 1 puerperal, 1 Melkersson-Rosenthal syndrome) (34 CSF samples) and 36 controls (16 nonidiopathic FP, 7 hearing loss, 6 vertigo, 5 headache, 2 other) previously tested for HSV-1, VZV, and HHV-6 DNA by polymerase chain reaction (PCR) were tested with highly sensitive multiplex-PCR and an oligonucleotide microarray method. Human herpesvirus 6 (HHV-6) causes life-long persistent infection in over 90% of persons before age 2 years [1, 2].
HHV-6 belongs to the Betaherpesvirinae subfamily and to the Roseolovirus genus. The tropism of HHV-6 for thyroid cells was verified by infection of Nthy-ori3-1, a thyroid follicular epithelial cell line, showing that thyrocytes are permissive to HHV-6 replication, which induces de novo expression of HLA class II antigens. In this regard, PCR of serum DNA extracts may be used as a sensitive indicator of active HHV-6 infection in infants prior to their seroconversion. HHV-6 was able to infect these cells, but viral replication was restricted. Corresponding figures for HHV7 were 28 and 6.2/7, and 5/6 with CSF viral DNA also had it in PBMC, respectively. Subsequent investigation revealed a broader cell tropism, with notable T-cell lymphotropism.
After primary infection, HHV-6 is characterized by life-long latency in PBMCs, salivary glands, and brain tissue [1, 3]. Thus, attributing a pathological role to the virus in diseases of the central nervous system (CNS) can be challenging. The book examines the role of HHV-6 in myriad diseases, including cognitive disorders following bone marrow transplant, mesial temporal lobe epilepsy, multiple sclerosis, autoimmune disease, encephalitis, Hodgkin’s disease lymphoma (HHV-6B), and glioma (HHV-6A). HHV-6 exists as two variants; HHV-6A and HHV-6B. To determine the effect of U94/REP upon viral replication, the protein was produced. Human herpes virus-6 (HHV-6) and HHV-7 are newly discovered members of herpesviridae family.
Over 95% of people older than 2 years of age are seropositive for either or both HHV-6 variants, and current serologic methods are incapable of discriminating infection with one variant from infection with the other. Platelet-associated antibodies (PAIg) were measured by competitive ELISA in 66 ITP patients. HHV-6 isolates can be classified into at least two variants, variant A (HHV-6A) and variant B (HHV-6B), based on their genetic, antigenic, and growth characteristics (1, 2). Both intrauterine and sexual transmission of human herpesvirus (HHV)-6 and HHV-7 have been suggested, and congenital HHV-6 infection does occur. A follow up study was undertaken of patients with multiple sclerosis, searching peripheral blood mononuclear cells for molecular markers associated with HHV-6 latency and lytic replication.