Absence of Epstein-Barr virus RNA in multiple sclerosis as assessed by in situ hybridisation.
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Abstract:
Epidemiological and serological evidence has suggested a role for Epstein-Barr virus infection in the aetiology of multiple sclerosis. Epstein-Barr virus-specific RNA was looked for in the brains of 10 patients with multiple sclerosis by in situ hybridisation. A total of 21 plaques was examined. In all of these preservation of RNA was shown by hybridisation of control probes to mitochondrial rRNA but no signal was detected with the Epstein-Barr virus probes. It is unlikely that persistent or latent Epstein-Barr virus infection of the CNS occurs in multiple sclerosis, although present findings do not exclude a role for Epstein-Barr virus in the initiation of this disorder.Keywords:
Epstein–Barr virus infection
Etiology
Gammaherpesvirinae
RNA virus
In a previous report we demonstrated Epstein-Barr virus expression in cutaneous squamous cell carcinomas from heart transplant recipients. In a comparative study, skin lesions from renal allograft recipients were investigated for the presence of Epstein-Barr virus. Thirty cutaneous squamoproliferative lesions from 10 kidney transplant recipients were examined for Epstein-Barr virus-specific gene expression. The techniques used for detection were polymerase chain reaction, in situ hybridization and immunohistochemistry. Epstein-Barr virus DNA was not detected by polymerase chain reaction in the neoplasias, and only single Epstein-Barr virus-positive carcinoma cells were shown by in situ hybridization in three cases of infiltrative squamous cell carcinomas. Immunohistochemistry for Epstein-Barr virus latent membrane protein 1 showed a negative result in all samples. These findings differ from our earlier investigations of cutaneous squamous cell carcinomas from heart transplant recipients where Epstein-Barr virus expressions were common. This may indicate that the part Epstein-Barr virus plays in the development of post-transplant, cutaneous squamoproliferative disorders is related to type of organ transplantation and/or grade of immunosuppression.
Gammaherpesvirinae
Immunosuppression
Epstein–Barr virus infection
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Gammaherpesvirinae
Cytomegalovirus
Alphaherpesvirinae
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Objective To test the hypothesis that Epstein-Barr virus (EBV) infection of cells within the synovial membrane contributes to the pathogenesis of rheumatoid arthritis (RA). Methods Biopsy samples of synovial membrane from 37 patients with RA and from 51 patients with other joint diseases were studied for evidence of EBV infection using in situ hybridization specific for the EBV-encoded RNAs (EBERs). Latent membrane protein 1 (LMP1) and the lytic-cycle BZLF1 protein were detected by immunohistochemistry. Results Rare EBER-positive B lymphocytes were detected in 7 RA biopsy samples. EBV was not detectable in any other cells. Expression of the LMP1 and BZLF1 proteins of EBV was not observed in any of the samples. No EBV infection was detected in synovial membranes from patients with other joint diseases. Conclusion Our data indicate that EBV infection is not directly involved in the pathogenesis of RA. Any contribution of EBV to the pathogenic process leading to RA is likely to be indirect.
BZLF1
Pathogenesis
Lytic cycle
Epstein–Barr virus infection
Gammaherpesvirinae
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Proliferating B cell lesions developing in a series of immunosuppressed organ transplant recipients and patients with X-linked lymphoproliferative syndrome were examined for Epstein-Barr virus and cellular gene expression using immunocytochemistry and immunoblotting techniques. Results indicate that all the lesions examined from the patients in this series expressed Epstein-Barr virus gene products that were consistent with a latent, nonproductive type of infection. No lytic cycle antigens associated with productive viral infection were detected. This pattern is similar to the viral gene expression in normal B cells immortalized by Epstein-Barr virus in vitro. The demonstration in this study of Epstein-Barr virus viral gene expression in posttransplant and X-linked proliferative syndrome B cell disorders provides important new evidence for the primary role of Epstein-Barr virus in the development of these lesions. This is in contrast to the subsidiary role that the Epstein-Barr virus has in the etiology of Burkitt's lymphoma.
Lymphoproliferative Disorders
Lytic cycle
Gammaherpesvirinae
Epstein–Barr virus infection
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Primary Sjogren′s syndrome (pSS) is a kind of chronic autoimmune disease affecting many organs of the body. The pathogenesis of pSS is still debated. Epstein-Barr virus(EBV), also called human herpesvirus-4, belongs to the herpesviridae family. Researchers have found that EBV is associated with pSS. With the deepening of researches, more evidences and opinions about the participation of EBV in the pathogenesis of pSS have emerged. EBV can cause the development of pSS in multiple ways. In this review, we summarize the roles of EBV in the pathogenesis of pSS.
Key words:
Sjogren′s syndrome; Epstein-Barr virus; Interferon; Lymphoma
Pathogenesis
Gammaherpesvirinae
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Epstein–Barr virus infection
Gammaherpesvirinae
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Although the Epstein-Barr virus (EBV) is associated with malignant and nonmalignant diseases, its lytic replication is predominantly associated with nonmalignant diseases such as acute infectious mononucleosis (IM) or chronic active EBV infection. Lytic replication is also associated with type B EBV more than with type A EBV. Sustained lytic replication, however, is not compatible with tumor growth. We investigated whether control of an EBV lytic regulatory gene, BZLF1, differed in these diseases.Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct DNA sequence analyses were used to characterize the promoter sequence of BZLF1 (Zp) in 52 tumors (34 non-Hodgkin's lymphomas, 13 post-transplant lymphoproliferative disease samples, and five nasopharyngeal carcinomas), and in peripheral blood lymphocytes from seven patients with chronic active EBV, six with IM, and 40 healthy, EBV-seropositive individuals. All sequences were compared with the prototype EBV strain B95.8 sequence. All statistical tests were two-sided.Three polymorphic Zp sequences were detected. Among the malignant samples, sequence Zp-P, associated with 84% of type A EBV, was identical to that of EBV strain B95.8, whereas a second sequence (Zp-V3), associated exclusively with type B EBV (P<.001), contained three base substitutions. Among the nonmalignant samples, a distinct polymorphism, Zp-V4, containing the substitutions detected in Zp-V3 and an additional base change, was identified in all samples from chronic active EBV, IM, and healthy individuals, but in none of the malignant samples (P<.001). Zp-V4 was independent of the EBV type.Polymorphisms in the regulatory sequences of BZLF1 are differentially distributed among malignant and nonmalignant cells and may identify EBV subtypes with various lytic activities, including those not associated with malignancies.
BZLF1
Lytic cycle
Gammaherpesvirinae
Mononucleosis
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Lymphoproliferative Disorders
Gammaherpesvirinae
Epstein–Barr virus infection
Pathogenesis
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Gammaherpesvirinae
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Summary An accumulating body of data suggests that the Epstein–Barr virus (EBV), a lymphotropic herpesvirus, is involved in the pathogenesis of a proportion of cases of Hodgkin lymphoma (HL). In this study, we showed that the frequency of circulating EBV‐infected cells was significantly higher ( P < 0·001) in pretreatment blood samples from EBV‐associated cases when compared with non‐EBV‐associated cases. We further showed that in patients with EBV‐associated disease, the virus persisted in the peripheral blood in memory B cells. This phenotype is consistent with that seen in healthy seropositive controls, post‐transplant patients and patients with acute infectious mononucleosis. The data suggest that an increased frequency of EBV carrying B cells in peripheral blood is associated with EBV‐associated HL.
Mononucleosis
Pathogenesis
Gammaherpesvirinae
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