Guest guest Posted April 29, 2002 Report Share Posted April 29, 2002 J Virol 2001 Dec;75(23):11641-50 Related Articles, Books, LinkOut Gene expression profile of herpesvirus-infected T cells obtained using immunomicroarrays: induction of proinflammatory mechanisms. Mayne M, Cheadle C, Soldan SS, Cermelli C, Yamano Y, Akhyani N, Nagel JE, Taub DD, Becker KG, son S. Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada. mmayne@... Herpesvirus infections can frequently lead to acute inflammation, yet the mechanisms regulating this event remain poorly understood. In order to determine some of the immunological mechanisms regulated by human herpesvirus infections, we studied the gene expression profile of lymphocytes infected with human herpesvirus 6 (HHV-6) by using a novel immunomicroarray. Our nylon-based immunomicroarray contained more than 1,150 immune response-related genes and was highly consistent between experiments. Experimentally, we found that independently of the HHV-6 strain used to infect T cells, multiple proinflammatory genes were increased and anti-inflammatory genes were decreased at the mRNA and protein levels. HHV-6 strains A and B increased expression of the genes for interleukin-18 (IL-18), the IL-2 receptor, members of the tumor necrosis factor alpha superfamily receptors, mitogen-activated protein kinase, and Janus kinase signaling proteins. As reported previously, CD4 protein levels were also increased significantly. Specific type 2 cytokines, including IL-10, its receptor, and IL-14, were downregulated by HHV-6 infection and, interestingly, amyloid precursor proteins and type 1 and 2 presenilins. Thus, T cells respond to HHV-6 infection by inducing a type 1 immune response that may play a significant role in the development and progression of diseases associated with HHV-6, including pediatric, hematologic, transplant, and neurologic disorders. PMID: 11689646 [PubMed - indexed for MEDLINE] ----------------------------------------------------------------------- Am J Clin Pathol 2001 Nov;116(5):648-54 Related Articles, Books, LinkOut Prevalence and cellular reservoir of latent human herpesvirus 6 in tonsillar lymphoid tissue. Roush KS, Domiati-Saad RK, Margraf LR, Krisher K, Scheuermann RH, BB, Dawson DB. Department of Pathology, University of Texas Southwestern Medical Center at Dallas, USA. There are few studies that examine prevalence, quantity, and cellular proclivity of latent human herpesvirus 6 (HHV-6) in healthy populations. We examined 69 tonsils with paired blood specimens from children without evidence of acute infection. By polymerase chain reaction (PCR), HHV-6 was detected at low levels in 100% of tonsils and 39% of blood samples (n = 27), suggesting that prevalence of latent HHV-6 infection is high in children and may be underestimated by PCR analysis of blood. Although HHV-6A and HHV-6B were detected, HHV-6B predominated, being found in 97% of samples (n = 67). Tonsil sections from 7 cases were examined by in situ hybridization using 2 HHV-6 probes and immunohistochemical analysis. Using both in situ hybridization and immunohistochemical analysis, all tissues revealed marked HHV-6-specific staining in the squamous epithelium of the tonsillar crypts and rare positive lymphocytes. We conclude that HHV-6 is present universally in tonsils of children, and tonsillar epithelium may be an important viral reservoir in latent infection. PMID: 11710680 [PubMed - indexed for MEDLINE] ---------------------------------------------------------------------- Blood 2001 Dec 15;98(13):3739-44 Related Articles, Books, LinkOut Asymptomatic primary Epstein-Barr virus infection occurs in the absence of blood T-cell repertoire perturbations despite high levels of systemic viral load. Silins SL, Sherritt MA, Silleri JM, Cross SM, Elliott SL, Bharadwaj M, Le TT, on LE, Khanna R, Moss DJ, Suhrbier A, Misko IS. Infectious Disease and Immunology Division, Queensland Institute of Medical Research, Herston, Australia. sharons@... Primary infection with the human herpesvirus, Epstein-Barr virus (EBV), may result in subclinical seroconversion or may appear as infectious mononucleosis (IM), a lymphoproliferative disease of variable severity. Why primary infection manifests differently between patients is unknown, and, given the difficulties in identifying donors undergoing silent seroconversion, little information has been reported. However, a longstanding assumption has been held that IM represents an exaggerated form of the virologic and immunologic events of asymptomatic infection. T-cell receptor (TCR) repertoires of a unique cohort of subclinically infected patients undergoing silent infection were studied, and the results highlight a fundamental difference between the 2 forms of infection. In contrast to the massive T-cell expansions mobilized during the acute symptomatic phase of IM, asymptomatic donors largely maintain homeostatic T-cell control and peripheral blood repertoire diversity. This disparity cannot simply be linked to severity or spread of the infection because high levels of EBV DNA were found in the blood from both types of acute infection. The results suggest that large expansions of T cells within the blood during IM may not always be associated with the control of primary EBV infection and that they may represent an overreaction that exacerbates disease. PMID: 11739180 [PubMed - indexed for MEDLINE] --------------------------------------------------------------------- Med Virol 2002 Mar;66(3):384-7 Related Articles, Books, LinkOut Primary human herpesvirus-6 associated with an afebrile seizure in a 3-week-old infant. Zerr DM, Yeung LC, Obrigewitch RM, Huang ML, Frenkel LM, Corey L. Department of Pediatrics, University of Washington, Seattle, Washington. We describe a 3-week-old male infant with an afebrile seizure in whom serologic and polymerase chain reaction (PCR) findings support concomitant primary human herpesvirus 6 (HHV-6) infection. Although HHV-6 infection has been associated with first-time febrile seizures and encephalitis in both immunocompetent and immunocompromised hosts, it has not been associated previously with afebrile seizures in healthy infants. This report provides additional evidence of the neuropathogenic potential of HHV-6. Copyright 2002 Wiley-Liss, Inc. PMID: 11793391 [PubMed - in process] --------------------------------------------------------------------- J Med Virol 2002 Apr;66(4):497-505 Related Articles, Books, LinkOut Latent infection of human herpesvirus 6 in astrocytoma cell line and alteration of cytokine synthesis. Yoshikawa T, Asano Y, Akimoto S, Ozaki T, Iwasaki T, Kurata T, Goshima F, Nishiyama Y. Laboratory of Virology, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Aichi, Japan. In order to study the pathogenesis of HHV-6 infection in central nervous system disorders, U251 cell line was infected with freshly isolated variant B HHV-6. Although IEA/ex 3 antigen (immediate early protein) was detected in infected cell nuclei, neither the presence of OHV-3 antigen (late antigen) nor production of infectious virus was demonstrated. These results indicate that abortive infection was established in the cells. After viral infection, the viral genome copy in the infected cells gradually decreased and became stable after 6 cell passages. At that point, HHV-6 gene expression was restricted to only 2 immediate early genes (U90 and U94). However, 12-O-tetra-decanoyl (TPA) treatment induced transcription of other genes (U31 and U39) by the 10th cell passage, indicating HHV-6 reactivation. Moreover, production of two proinflamatory cytokines (IL-6 and IL-1[beta]) was up-regulated by the presence of the HHV-6 genome and TPA-induced activation of the viral transcripts. Copyright 2002 Wiley-Liss, Inc. PMID: 11857528 [PubMed - as supplied by publisher] ----------------------------------------------------------------------- Clin Infect Dis 2002 Feb 15;34(4):461-6 Related Articles, Books, LinkOut Influenza Encephalopathy Associated with Infection with Human Herpesvirus 6 and/or Human Herpesvirus 7. Sugaya N, Yoshikawa T, Miura M, Ishizuka T, Kawakami C, Asano Y. Department of Pediatrics, Nippon Kokan Hospital, Kawasaki, Kanagawa 210-0852, Japan. sugaya-n@... Influenza-associated encephalopathy is often reported in young Japanese children, but its pathogenesis is unknown. Although influenza virus can be demonstrated by throat culture for patients with encephalopathy, cultures of samples of cerebrospinal fluids (CSF) do not yield the virus. Eight patients with encephalopathy or complicated febrile convulsions had influenza virus infection diagnosed by means of culture, polymerase chain reaction (PCR), or rapid diagnosis using throat swabs. In all 8 cases, the results of PCR testing of CSF specimens for influenza virus were negative. On the other hand, human herpesvirus 6 (HHV-6) DNA was demonstrated in CSF specimens obtained from 2 of 8 patients. In 3 of 8 patients, the presence of human herpesvirus 7 (HHV-7) DNA was demonstrated in CSF specimens. Some cases of influenza-associated encephalopathy reported in Japan may be attributable to a dual infection with influenza virus and HHV-6, -7, or both. Another possibility is that latent HHV-6 or HHV-7 in the brain is reactivated by influenza, causing encephalopathy or febrile convulsions. PMID: 11797172 [PubMed - in process] ---------------------------------------------------------------------- Nippon Rinsho 2001 Nov;59(11):2285-92 Related Articles, Books, LinkOut [Hypersensitivity syndrome and HHV-6] [Article in Japanese] Tohyama M, Hashimoto K. Department of Dermatology, Ehime University School of Medicice. Hypersensitivity syndrome (HS) has been recognized as one of severe adverse drug eruptions. HS has several characteristic features as follows. First, the clinical symptoms are high fever, multiple lymphadenopathy, severe skin rash, mononucleosis and multiple visceral involvement. Secondly, those symptoms appear two to six weeks after the initiation of drug administration. Thirdly, HS is induced by the specific drugs, carbamazepine, phenytoin, salazosulfapyridine, allopurinol, diaphenylsulphone, and mexiletine. Recently, we reported the association of HS with reactivation of HHV-6, the causative virus for exanthem subitum. We propose the new disease entity of HHV-6-associated drug eruption (HADE) because HS is composed of two clinical phases, drug allergic reaction in the early phase and HHV-6 reactivation in the late phase. Publication Types: Review Review, Tutorial PMID: 11712420 [PubMed - indexed for MEDLINE] ----------------------------------------------------------------------- Scand J Infect Dis 2001;33(9):648-58 Related Articles, Books, LinkOut Multiple sclerosis and Kaposi's sarcoma--chronic diseases associated with new human herpesviruses? Enbom M. Department of Virology, Swedish Institute for Infectious Disease Control, Solna. Two diseases that for many years have been suspected to be of viral origin are multiple sclerosis (MS) and Kaposi's sarcoma (KS). With the use of a new technique called representational difference analysis both these diseases have recently been associated with new lymphotropic herpesviruses, i.e. human herpesviruses (HHV) 6 and 8. HHV-6 is a ubiquitous virus and the etiological agent of exanthema subitum. Viral neuroinvasion occurs frequently in primary HHV-6 infection, and meningitis, encephalitis and demyelination have been described as rare complications. A relation with MS has been suggested for HHV-6, as the virus has been detected in MS plaques in the brain. Data from different studies are, however, conflicting and a definitive role for HHV-6 in MS pathogenesis has not been established. HHV-8 is believed to be the causative agent of KS, and is also associated with some rare hematological malignancies. The viral genome contains several potential oncogenes that are believed to have been picked up from the human genome during evolution. The role of HHV-8 in healthy, immunocompetent individuals is however uncertain. In conclusion, the full spectrum of human diseases associated with these new viruses is not yet understood, and rapid developments in molecular biology will continue to shed new light on the interactions between herpesviruses and their hosts. Publication Types: Review Review, Tutorial PMID: 11669221 [PubMed - indexed for MEDLINE] ----------------------------------------------------------------------- J Med Virol 2001 Nov;65(3):576-83 Related Articles, Books, LinkOut Human herpesvirus 6 downregulates major histocompatibility complex class I in dendritic cells. Hirata Y, Kondo K, Yamanishi K. Department of Microbiology, Osaka University Medical School, Yamada-oka, Suita, Osaka 565-0871, Japan. The expression of major histocompatibility complex (MHC) class I, class II, CD1a, and CD 83 in dendritic cells (DCs) after infection with human herpesvirus 6 (HHV-6) was examined. Whereas there was no significant change in the expression of CD1a, CD83, and MHC class II in infected DCs, MHC class I expression was downregulated after infection with HHV-6 variant A but not HHV-6B. The expression of HHV-6 immediate-early or early genes was required for the downregulation of MHC class I. The de novo synthesis of MHC class I was greatly suppressed by infection with HHV-6A in DCs, while its rate of degradation was only slightly elevated. These results suggest that HHV-6A may escape from the host immune system in DCs by causing the downregulation of MHC class I synthesis. Copyright 2001 Wiley-Liss, Inc. PMID: 11596096 [PubMed - indexed for MEDLINE] ----------------------------------------------------------------------- Herpes 2001 Nov;8(3):64-8 Related Articles, Books The association of herpes simplex virus and Alzheimer's disease: a potential synthesis of genetic and environmental factors. Pyles RB. Department of Pediatrics and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX, USA. The chronic and sporadic nature of Alzheimer's disease (AD), in which the majority of presenting cases are over 65 years of age, suggests that compounded injury or long-term exposure to environmental factors is involved in the aetiology, rather than inherited genetic alterations. Great hope has been placed on identifying a causative infectious agent that would present the potential for therapeutic or preventative vaccines or drugs. Although not the sole causative agent, herpes simplex virus type 1 has been the most clearly established pathogen to be associated with AD development to date. Recent advances have begun to suggest mechanisms by which this ubiquitous, neurotropic pathogen may predispose an individual to the development of AD. Such progress should ultimately lead to therapeutic strategies that limit predisposing neurological damage and potentially reverse the process, increasing the quality and quantity of life in this patient population. PMID: 11867022 [PubMed - in process] ----------------------------------------------------------------------- Arch Neurol 2001 Oct;58(10):1580-3 Related Articles, Books, LinkOut Increase in peripheral CD4 bright+ CD8 dull+ T cells in Parkinson disease. Hisanaga K, Asagi M, Itoyama Y, Iwasaki Y. Department of Neurology, Miyagi National Hospital, 100 Kassenhara, Takase, Yamamoto, Watari, Miyagi 989-2202, Japan. BACKGROUND: Immune abnormalities are known to be involved in the pathogenesis of sporadic Parkinson disease. OBJECTIVE: To examine whether abnormalities in peripheral lymphocytes exist in Parkinson disease. METHODS: Immune mediators, including CD1a, CD3, CD4, CD8, CD45RO, and Fas (CD95), were examined in peripheral lymphocytes of patients by 3-color flow cytometry. RESULTS: Patients with Parkinson disease displayed a significantly greater population of circulating CD3+ CD4 bright+ CD8 dull+ lymphocytes than age-matched control subjects (P =.005) and patients with cerebrovascular disease (P =.002). The increase in these cells appeared to continue for at least 17 months. These T cells also expressed CD45RO and Fas, markers for activated T cells, while CD1a, a marker for thymic T cells, was negative, suggesting that these cells are mature T cells with immune activities. CONCLUSIONS: As CD4+ CD8+ T cells are known to increase after some specific viral infections, the continuous increase in CD4 bright+ CD8 dull+ T cells shown here may indicate postinfectious immune abnormalities that are possibly associated with the pathogenesis of this slowly progressive, multifactorial neurodegenerative disease. PMID: 11594915 [PubMed - indexed for MEDLINE] ---------------------------------------------------------------------- Microb Pathog 2002 Feb;32(2):49-60 Related Articles, Books, LinkOut Pathogenesis of transplacental virus infection: pestivirus replication in the placenta and fetus following respiratory infection. Swasdipan S, McGowan M, N, Bielefeldt-Ohmann H. School of Veterinary Science, University of Queensland, Brisbane, North Mymms, Qld 4072, Australia Although transplacental virus infections account for considerable morbidity and mortality in both animals and humans, very little is so far known about the pathways whereby virus reaches the conceptus, the subsequent virus-host interactions in the early phases of the infections, and the establishment of persistent non-lethal infection. Using a natural animal model we recently demonstrated that bovine pestivirus can spread from the site of infection to the ovine fetus within 72 h, despite the expression of interferon in the reproductive tract [1]. In the present study we demonstrate that pestivirus first establishes infection and spread within the allantoic and amniotic membranes and then the fetus, followed several days later by infection of the uterine glands. However, virus replication and spread within the fetus is, at least in part, controlled by fetal developmental factors. In fetuses less than 25 days of gestational age, the virus remains restricted to the bulbis cordis, the first brachial pouch and occasionally the aorta. Over the next few days the virus spreads to multiple tissues, in addition to becoming more widespread and pronounced within the initially infected tissues. A potential role for the binucleated cells of the allantochorion in the spread of the virus from the fetal to the maternal tissues was also found. These cells expressed high levels of viral antigen just prior to and during the time period in which virus antigen became detectable in the epithelial cells of the uterine glands, in endothelial cells of uterine vessels and in scattered macrophage-like cells in the uterine stroma. Most likely this relatively late virus transfer is inconsequential for the mother, since it occurs at a time when a maternal virus-specific antibody response is becoming measurable. This is in contrast to the fetus, where the infection will have established itself widely prior to the development of lymphoid tissues and a functional immune response, thus setting the scenario for development of specific tolerance to the persisting virus. Copyright 2002 Academic Press. PMID: 11812211 [PubMed - in process] _________________________________________________________________ Chat with friends online, try MSN Messenger: http://messenger.msn.com Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.