Studies on Cell Lines Derived From Burkitt's Lymphoma*,†

Henle, Gertrude; Henle, Werner

doi:10.1111/j.2164-0947.1966.tb02253.x

Cited by 219 publications

(203 citation statements)

References 22 publications

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“…Patients sera were tested for antibodies to structural antigens (virus capsid antigen) and for antibodies to the early antigen complex of EBV by immunofluorescence according to the method described by Henle and Henle [1966]. In addition, antibodies to the recombinant protein Epstein-Barr nuclear antigen 1 rp72 were detected by ELISA (Biotest).…”

Section: Antibody Detectionmentioning

confidence: 99%

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Meerbach

Wutzler

Häfer

et al. 2008

Journal of Medical Virology

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Epstein-Barr virus (EBV)-associated post-transplant lymphoproliferative disease is a lifethreatening complication following hematopoietic stem cell transplantation. A quantitative polymerase chain reaction to evaluate EBV-genome copy numbers based on a nested polymerase chain reaction and an end-point dilution was used. Applying this assay EBV load was prospectively screened weekly in 123 patients after transplantation. The results demonstrate that EBV reactivations with more than 1,000 EBV-genome copies measured in 10(5) peripheral blood mononuclear cells were observed in 31 patients (25.2%). Three patients developed lymphoproliferative disease with extremely high EBV-genome copies in peripheral blood mononuclear cells (>100,000 copies/10(5) cells) and plasma. After combined antiviral and immune therapy two of three patients showed a dramatic decrease of EBV load and survived, while the third patient died of lymphoma. A subclinical EBV reactivation was observed in 24 cases (19.5%) with EBV-genome copies in 10(5) peripheral blood mononuclear cells ranging between 2,500 and mostly 10,000. After reduction of immunosuppression the EBV levels normalized. In four patients, the high copy number of > or =80,000 copies/10(5) peripheral blood mononuclear cells and plasma positivity prompted us to start pre-emptive therapy with rituximab and cidofovir for prevention of lymphoproliferative disease. After drug administration the high EBV load was reduced remarkably. Ninety-two patients (74.8%) who had < or =1,000 copies/10(5) peripheral blood mononuclear cells did not develop EBV-associated lymphoproliferative disease. In conclusion, monitoring of EBV load is a sensitive and useful parameter in the surveillance of EBV reactivation for early intervention in EBV-associated lymphoproliferative disease as well as for follow-up of the efficacy of therapy. Applying this assay EBV load was prospectively screened weekly in 123 patients after transplantation. The results demonstrate that EBV reactivations with more than

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Section: Antibody Detectionmentioning

confidence: 99%

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Meerbach

Wutzler

Häfer

et al. 2008

Journal of Medical Virology

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“…Titers of IgM and IgG antibodies to VCA were determined on acetone-fixed HR1-K cells by using fluorescein isothiocyanate (FITC)-labeled antibody to IgM and antibody to IgG, according to Schmitz and Scherer [9] and Henle and Henle [10], respectively. In order to eliminate rheumatoid factor as a cause of a false-positive IgM test, we adsorbed some sera with heat-aggregated human gammaglobulin, according to Shirodaria et al [11].…”

Section: Ebv Serology and Serological Diagnosismentioning

confidence: 99%

Epstein-Barr Virus Infections and DNA Hybridization Studies in Posttransplantation Lymphoma and Lymphoproliferative Lesions: The Role of Primary Infection

Ho¹,

Miller²,

Atchison³

et al. 1985

Journal of Infectious Diseases

420

161

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Fourteen patients who developed B cell lymphomas or lymphoproliferative lesions after kidney, liver, heart, or heart-lung transplantation in Pittsburgh during [1981][1982][1983] had active infection with Epstein-Barr virus (EBV) of the primary (six patients), reactivated (seven patients), or chronic (one patient) type. In transplant patients without tumors, the incidence of EBV infection was 30% (39 of 128). Only three of these patients had primary infections. Thus the frequency of active infection was significantly higher in patients with tumors, and patients with primary infections were at greater risk of developing tumors. Five of 13 tumors tested contained EBV nuclear antigen (EBNA) and nine of 11 contained EBV genomes detected by DNA-DNA hybridization with BamHI K, BamHI W, or EcoRI B cloned probes. All EBNA-positive tumors, except one, were also positive by hybridization. Only one tumor was negative for both EBNA and EBV DNA. These data suggest that EBV plays an etiologic role in the development of these lesions.Epstein-Barr virus (EBV) is a human herpesvirus associated with an array of conditions that range from inapparent infection and infectious mononucleosis to lethal lymphoproliferative syndromes, nasopharyngeal carcinoma, Burkitt's lymphoma, and B cell lymphomas in immunocompromised patients [1]. The precise role of the virus in carcinogenesis is unclear, although in Burkitt's lymphoma the importance of viral transformation of infected B lymphocytes and chromosomal translocations has been emphasized [2]. It is even less clear in lymphomas and lymphoproliferative lesions arising in immuno-compromised patients, where the immunopathology may not be uniform and where chromosomal studies are largely lacking.Recently, we reported on the reversibility of lymphomas and lymphoproliferative lesions in a series of 17 transplant patients after reduction of cyclosporine and steroid immunosuppression [3]. In that preliminary report we noted that seven of these patients had evidence of primary EBV infections and eight had evidence of reactivated infection. Six tumors had evidence of EBV nuclear antigen (EBNA) and seven had evidence of EBV DNA by nucleic acid hybridization. [6] reported the results of studies on 19 renal transplant patients who developed lymphoproliferative disorders and lymphomas after transplantation. All the patients except one were receiving azathioprine, prednisone, and antithymocyte globulin. Two of their patients developed primary EBV infection, in six the infection reactivated, and 12 had evidence of EBV DNA in their tumors by hybridization studies. Bieber et al. [7] reported that five of 39 heart transplant recipients receiving cyclosporine, prednisone, and antithymocyte globulin developed lymphomas. Four tumors were positive for EBV DNA by cRNA-DNA filter hybridization, and three patients had serological evidence of EBV infection.We report here evidence for active EBV infection in all of our patients with tumors and a significantly higher frequency of primary infection than found i...

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“…Serum IgA concentration was found to be significantly higher in NPC patients than in control subjects (Wara et al, 1975;Ho et al, 1976). Henle and Henle (1976) reported that NPC patients have high titres of IgA antibody against viral capsid antigen (VCA) (Henle and Henle, 1966) and early antigens (EA) (Henle et al, 1970). These reactivities are detected less frequently and occur at lower titres in sera from patients with Burkitt's lymphoma (BL) and infectious mononucleosis (IM).…”

mentioning

confidence: 99%

Factors affecting serum IgA antibody to Epstein-Barr viral capsid antigens in nasopharyngeal carcinoma

Ho¹,

Ng²,

Kwan³

1978

Br J Cancer

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Summary.-Irrespective of the ethnic origin of the patient, nasopharyngeal carcinoma (NPC), appears to stimulate the production of IgA antibodies against VCA. These antibodies are detected at high frequency and titres in sera from NPC patients but only rarely from control subjects. A majority of relapse-free survivors tested 1-12 years after radiotherapy (RT) sustain a detectable level of IgA anti-VCA. Serum titres of IgA anti-VCA remain relatively unchanged in individual NPC patients after RT, regardless of the disease evolution. These antibodies were detected in serum from one individual 9 months before NPC and the titre rose concomitantly with its clinical onset.

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Studies on Cell Lines Derived From Burkitt's Lymphoma*,†

Cited by 219 publications

References 22 publications

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Monitoring of Epstein‐Barr virus load after hematopoietic stem cell transplantation for early intervention in post‐transplant lymphoproliferative disease

Epstein-Barr Virus Infections and DNA Hybridization Studies in Posttransplantation Lymphoma and Lymphoproliferative Lesions: The Role of Primary Infection

Factors affecting serum IgA antibody to Epstein-Barr viral capsid antigens in nasopharyngeal carcinoma

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