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Upregulation of Epstein‐Barr virus‐encoded latent membrane protein by human herpesvirus 6 superinfection of EBV‐carrying Burkitt lymphoma cells
Author(s) -
Cuomo Laura,
Trivedi Pankaj,
de Grazia Ugo,
Calogero Antonella,
D'Onofrio Mara,
Yang Weiwen,
Frati Luigi,
Faggioni Alberto,
Rymo Lars,
Ragona Giuseppe
Publication year - 1998
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199807)55:3<219::aid-jmv7>3.0.co;2-4
Subject(s) - epstein–barr virus , virology , biology , virus , transfection , cell culture , plasmid , downregulation and upregulation , herpesviridae , microbiology and biotechnology , gene , lymphoma , immunology , genetics , viral disease
The effect of HHV‐6 strain A infection on the expression of Epstein‐Barr virus‐ (EBV‐) encoded growth transformation‐associated genes in two EBV‐positive Burkitt lymphoma cell lines, Akata and P3HR‐3, was investigated. The results indicate that HHV‐6A upregulates the expression of the latent membrane protein LMP‐1 in both cell lines. Expression of EBNA‐2 was also upregulated in Akata cells following HHV‐6A infection. Transfection of reporter constructs carrying the LMP‐1 regulatory sequences (LRS; −634/+40) or its 5′ deleted derivatives in Akata and in a T‐lymphoblastoid cell line, J‐Jhan, confirmed the presence of positive and negative regulatory elements responsive to HHV‐6A infection in LMP‐1 regulatory sequence (LRS). The majority of LRS constructs were under the influence of dominant negative factors. HHV‐6A was able to override the effect of such factors acting on reporter plasmids containing the −634/−54, −324/−54, −214/−54, and −106/−54 parts of LRS. The plasmid that carried only the −54/'40 LRS region was constitutively active in both Akata and J‐Jhan cells; in Akata, its activity was influenced by HHV‐6A. The finding that HHV‐6A infection may activate LMP‐1 and EBNA‐2 expression, which is essential for the immortalization of B‐lymphocytes by EBV, shows a novel aspect of the interaction between these two herpesviruses. J. Med. Virol. 55:219–226, 1998 . © 1998 Wiley‐Liss, Inc.