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H W Kreth

Publications and source records attributed to H W Kreth.

78 records · Page 5Linked to original sources
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Limited sequence heterogeneity of Epstein-Barr virus nuclear antigen 1 in benign and malignant EBV-associated disorders.

BACKGROUND: The Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is essential for replication and maintenance of circular EBV genomes in latently infected B lymphocytes and is the only EBV protein expressed in nearly all cells carrying the virus. EBNA-1 is suggested to be oncogenic in vivo since its expression induces B-cell neoplasia in transgenic mice. PATIENTS, MATERIALS AND METHODS: EBV wild-type isolates from ten malignant tumors and from 15 children with various benign EBV-associated disorders were examined for the presence of EBNA-1 variant strains by PCR and sequencing. RESULTS: One isolate harbored both the B95-8-like and a variant sequence within the C-terminus of the EBNA-1 gene. All other isolates (n = 24) revealed clustered nucleic acid sequence alterations within the EBNA-1 gene, which led to amino acid exchanges at positions 524, 563, 574, 585, 594 and 595. Few isolates exhibited additional amino acid exchanges at positions 564, 571 or 588. CONCLUSIONS: The observed EBNA-1 sequence variation pattern seems not to be restricted to a certain EBV-associated disease or tumor type. The EBNA-1 variant strains reported here may reflect the most prevalent EBV strains in the exposed population. In none of all the cases studied so far did the sequence alteration affect any known functionally crucial amino acids in the core domain of EBNA-1. This suggests that strict conservation of most of the C-terminal portion of EBNA-1 sequence may be essential for survival of EBV in the infected host.

Base Sequence↗
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[X-chromosome recessive lymphoproliferative disease (XLP): molecular genetic studies].

X-linked lymphoproliferative disease (XLP) is a rare worldwide occurring inherited immunodeficiency which is triggered by Epstein-Barr virus infection. Clinical phenotypes in 21 affected males from 5 German families with XLP ranged from severe and fatal infectious mononucleosis (57%) to acquired hypogammaglobulinaemia (28%), malignant lymphoma (28%), aplastic anaemia (19%) and hypergammaglobulinaemia M (19%). Molecular genetic studies with various polymorphic X-chromosomal DNA markers in 14 XLP families mapped the XLP gene locus to Xq25-q26. Haplotype analysis enables detection of XLP-positive and XLP-negative males already before EBV-infection as well as diagnosis of healthy female carriers within XLP families.

Child↗