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Primary EBV Infection (primary + ebv_infection)
Selected AbstractsHypothesis: Could Epstein-Barr virus play a role in the development of gastroschisis?BIRTH DEFECTS RESEARCH, Issue 2 2010Martha M. Werler BACKGROUND: The strong inverse association between maternal age and risk of gastroschisis in offspring has spurred many investigators to hypothesize that behaviors among younger females are the cause. Examples include cigarette smoking, illicit drugs, genitourinary infections, and sexually transmitted diseases, each of which has been reported to be associated with gastroschisis. Although these exposures are more common in young women, recent studies have shown that cigarette smoking, genitourinary infections, and sexually transmitted diseases are most strongly associated with gastroschisis in older women. There is both anecdotal and published evidence showing that gastroschisis sometimes (but not always) occurs in clusters, raising the possibility that an infectious agent might be involved in its pathogenesis. RESULTS: One such agent whose epidemiologic characteristics parallel those of gastroschisis is Epstein-Barr virus (EBV). Primary EBV infection in early childhood has been decreasing over time, leaving a greater proportion of adolescents at risk, as reflected by increased rates of infectious mononucleosis over time. During the childbearing years, risk of primary EBV infection decreases dramatically, as does risk of gastroschisis. The stronger risks of gastroschisis associated with cigarette smoking, genitourinary infections, and sexually transmitted diseases in older women might be explained by EBV reactivation resulting from multiple challenges to immune response such as pregnancy, age, toxic exposures, and genitourinary and sexually transmitted infections. CONCLUSION: EBV and other herpes viruses should be added to the research agenda for gastroschisis. Birth Defects Research (Part A) 2010. © 2009 Wiley-Liss, Inc. [source] Reed-Sternberg cells in atypical primary EBV infectionACTA PAEDIATRICA, Issue 2 2001M Bitsori The presence of Epstein-Barr virus (EBV) in the Hodgkin's/Reed-Sternberg (HRS) cells of a significant proportion of cases of Hodgkin's lymphoma (HL) is a matter of consideration when a case of presumptive HL has to be differentiated from infectious mononucleosis (IM). A 15-y-old boy was admitted with a presumptive diagnosis of extranodal HL, based on the biopsy of a painless ulcer on the right mandibular alveolar crest. Histologic examination of the lesion was consistent with mixed cellularity HL. The patient additionally presented with hepatosplenomegaly and regional lymphadenopathy. Serology for EBV was indicative of acute infection. Histological examination of regional lymphoid tissue was consistent with immunologic activation due to primary EBV infection. The patient was left untreated, under close observation. All clinical findings resolved within 3 mo and EBV viral capsid antigen (VCA) IgM antibodies converted to negative after 6 mo. A 3-y follow-up period was uneventful. [source] Regulatory T cell activity in primary and persistent Epstein,Barr virus infectionJOURNAL OF MEDICAL VIROLOGY, Issue 5 2009P.J. Wingate Abstract Regulatory T cells (Treg) provide a balance to immune T cell activation thereby protecting the body from pathogen-induced immunopathology. Several persistent viruses induce Treg that subvert protective immune mechanisms and promote viral persistence. Epstein,Barr virus (EBV) generally infects children subclinically and persists thereafter, but primary infection in early adulthood may cause immunopathological damage manifest as infectious mononucleosis. In this study the role of Treg was investigated in acute infectious mononucleosis and healthy EBV seropositive donors. The proportion of CD4+CD25high T cells in blood from infectious mononucleosis patients was significantly lower than in seropositive donors (P,=,0.05). Using the FOXP3 marker for Treg the same frequency and extra-follicular distribution of Treg was noted in infectious mononucleosis and control tonsils. Regulatory cytokines, interleukin (IL)-10 and transforming growth factor (TGF)-,, were significantly raised in infectious mononucleosis compared to seropositive donor plasma (P,=,0.0001, P,=,0.0004 respectively) although levels of IL-10 peaked earlier in infectious mononucleosis than TGF-,. Previous studies identified EBV latent membrane protein (LMP)-1-induced Treg activity [Marshall et al. (2003): J Immunol 170:6183,6189; Marshall et al. (2007): Brit J Haematol 139:81,89], and in this study a significant reduction in interferon-, production was found from infectious mononucleosis but not seropositive donor lymphocytes after stimulation with a recall antigen when LMP-1 peptide PRG was added (P,=,0.03). It is possible that Treg are important in controlling primary EBV infection to a subclinical level in most cases and that infectious mononucleosis represents a failure of this protective mechanism. J. Med. Virol. 81:870,877, 2009. © 2009 Wiley-Liss, Inc. [source] Quantitative Epstein-Barr virus (EBV) serology in lung transplant recipients with primary EBV infection and/or post-transplant lymphoproliferative diseaseJOURNAL OF MEDICAL VIROLOGY, Issue 2 2003Erik Verschuuren Abstract The Epstein-Barr virus (EBV)-specific antibody response was studied in lung transplant patients to assess their value in the diagnosis and prognosis of post-transplant lymphoproliferative disease. Recently developed synthetic peptides representing Epstein-Barr nuclear antigen-1 (EBNA-1), diffuse early antigen (EA(D)), and virus capsid antigen (VCA) were studied in a semiquantitative enzyme-linked immunosorbent assay (ELISA) to study antibody patterns in 12 seronegative lung transplant patients, of whom four developed a post-transplant lymphoproliferative disease, and seven seropositive lung transplant patients, all of whom developed a post-transplant lymphoproliferative disease. Immunoblot technique was used as a control. All 12 EBV-seronegative patients had a very limited antibody response that was restricted mainly to VCA antibodies. EA(D) antibodies became detectable in only two patients. Antibody response never preceded clinical diagnosis of post-transplant lymphoproliferative disease in the four EBV-seronegative patients who developed post-transplant lymphoproliferative disease. In the seven seropositive lung transplant patients with post-transplant lymphoproliferative disease, we found a rise in antibody titer in only two patients. Immunoblot analysis confirmed the serological results. In conclusion, EBV-specific antibody patterns after lung transplantation are highly restricted and variable and of limited value for the diagnosis or prognosis of post-transplant lymphoproliferative disease. J. Med. Virol. 69:258,266, 2003. © 2003 Wiley-Liss, Inc. [source] The changing face of post-transplant lymphoproliferative disease in the era of molecular EBV monitoringPEDIATRIC TRANSPLANTATION, Issue 4 2010Nanda Kerkar Kerkar N, Morotti RA, Madan RP, Shneider B, Herold BC, Dugan C, Miloh T, Karabicak I, Strauchen JA, Emre S. The changing face of post-transplant lymphoproliferative disease in the era of molecular EBV monitoring. Pediatr Transplantation 2010: 14:504,511. © 2010 John Wiley & Sons A/S. Abstract:, Pediatric PTLD is often associated with primary EBV infection and immunosuppression. The aim was to retrospectively review the spectrum of histologically documented PTLD for two time intervals differentiated by changes in use of molecular EBV monitoring. Eleven of 146 patients (7.5%) in 2001,2005 (Era A) and 10 of 92 (10.9%) in 1993,1997 (Era B) were diagnosed with PTLD. The median age at liver transplantation (0.8 and 0.9 yr, respectively) and the median duration between liver transplant and diagnosis of PTLD (0.6 and 0.7 yr, respectively) were similar in both eras. However, patients in Era A presented with significantly less advanced histological disease compared to patients in Era B (p = 0.03). Specifically, nine patients (82%) in Era A had Pl hyperplasia/polymorphic PTLD, whereas in Era B, six had advanced histological disease (five monomorphic and one unclassified). Three transplant recipients in Era B died secondary to PTLD, whereas there were no PTLD-related deaths in Era A (p = 0.03). Heightened awareness of risk for PTLD, alterations in baseline immunosuppression regimens, implementation of molecular EBV monitoring, pre-emptive reduction in immunosuppression and improved therapeutic options may have all contributed to a milder PTLD phenotype and improved clinical outcomes. [source] Hypothesis: Could Epstein-Barr virus play a role in the development of gastroschisis?BIRTH DEFECTS RESEARCH, Issue 2 2010Martha M. Werler BACKGROUND: The strong inverse association between maternal age and risk of gastroschisis in offspring has spurred many investigators to hypothesize that behaviors among younger females are the cause. Examples include cigarette smoking, illicit drugs, genitourinary infections, and sexually transmitted diseases, each of which has been reported to be associated with gastroschisis. Although these exposures are more common in young women, recent studies have shown that cigarette smoking, genitourinary infections, and sexually transmitted diseases are most strongly associated with gastroschisis in older women. There is both anecdotal and published evidence showing that gastroschisis sometimes (but not always) occurs in clusters, raising the possibility that an infectious agent might be involved in its pathogenesis. RESULTS: One such agent whose epidemiologic characteristics parallel those of gastroschisis is Epstein-Barr virus (EBV). Primary EBV infection in early childhood has been decreasing over time, leaving a greater proportion of adolescents at risk, as reflected by increased rates of infectious mononucleosis over time. During the childbearing years, risk of primary EBV infection decreases dramatically, as does risk of gastroschisis. The stronger risks of gastroschisis associated with cigarette smoking, genitourinary infections, and sexually transmitted diseases in older women might be explained by EBV reactivation resulting from multiple challenges to immune response such as pregnancy, age, toxic exposures, and genitourinary and sexually transmitted infections. CONCLUSION: EBV and other herpes viruses should be added to the research agenda for gastroschisis. Birth Defects Research (Part A) 2010. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||