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Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs.
Mol Cell Biol. 1997 Jan; 17(1):364-77.MC

Abstract

Epstein-Barr virus (EBV) is capable of adopting three distinct forms of latency: the type III latency program, in which six EBV-encoded nuclear antigens (EBNAs) are expressed, and the type I and type II latency programs, in which only a single viral nuclear protein, EBNA1, is produced. Several groups have reported heavy CpG methylation of the EBV genome in Burkitt's lymphoma cell lines which maintain type I latency, and loss of viral genome methylation in tumor cell lines has been correlated with a switch to type III latency. Here, evidence that the type III latency program must be inactivated by methylation to allow EBV to enter the type I or type II restricted latency program is provided. The data demonstrates that the EBNA1 gene promoter, Qp, active in types I and II latency, is encompassed by a CpG island which is protected from methylation. CpG methylation inactivates the type III latency program and consequently allows the type I or II latency program to operate by alleviating EBNA1-mediated repression of Qp. Methylation of the type III latency EBNA gene promoter, Cp, appears to be essential to prevent type III latency, since EBNA1 is expressed in all latently infected cells and, as shown here, is the only viral antigen required for activation of Cp. EBV is thus a pathogen which subverts host-cell-determined methylation to regulate distinct genetic programs.

Authors+Show Affiliations

Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8972217

Citation

Schaefer, B C., et al. "Host-cell-determined Methylation of Specific Epstein-Barr Virus Promoters Regulates the Choice Between Distinct Viral Latency Programs." Molecular and Cellular Biology, vol. 17, no. 1, 1997, pp. 364-77.
Schaefer BC, Strominger JL, Speck SH. Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs. Mol Cell Biol. 1997;17(1):364-77.
Schaefer, B. C., Strominger, J. L., & Speck, S. H. (1997). Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs. Molecular and Cellular Biology, 17(1), 364-77.
Schaefer BC, Strominger JL, Speck SH. Host-cell-determined Methylation of Specific Epstein-Barr Virus Promoters Regulates the Choice Between Distinct Viral Latency Programs. Mol Cell Biol. 1997;17(1):364-77. PubMed PMID: 8972217.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs. AU - Schaefer,B C, AU - Strominger,J L, AU - Speck,S H, PY - 1997/1/1/pubmed PY - 1997/1/1/medline PY - 1997/1/1/entrez SP - 364 EP - 77 JF - Molecular and cellular biology JO - Mol. Cell. Biol. VL - 17 IS - 1 N2 - Epstein-Barr virus (EBV) is capable of adopting three distinct forms of latency: the type III latency program, in which six EBV-encoded nuclear antigens (EBNAs) are expressed, and the type I and type II latency programs, in which only a single viral nuclear protein, EBNA1, is produced. Several groups have reported heavy CpG methylation of the EBV genome in Burkitt's lymphoma cell lines which maintain type I latency, and loss of viral genome methylation in tumor cell lines has been correlated with a switch to type III latency. Here, evidence that the type III latency program must be inactivated by methylation to allow EBV to enter the type I or type II restricted latency program is provided. The data demonstrates that the EBNA1 gene promoter, Qp, active in types I and II latency, is encompassed by a CpG island which is protected from methylation. CpG methylation inactivates the type III latency program and consequently allows the type I or II latency program to operate by alleviating EBNA1-mediated repression of Qp. Methylation of the type III latency EBNA gene promoter, Cp, appears to be essential to prevent type III latency, since EBNA1 is expressed in all latently infected cells and, as shown here, is the only viral antigen required for activation of Cp. EBV is thus a pathogen which subverts host-cell-determined methylation to regulate distinct genetic programs. SN - 0270-7306 UR - https://www.unboundmedicine.com/medline/citation/8972217/Host_cell_determined_methylation_of_specific_Epstein_Barr_virus_promoters_regulates_the_choice_between_distinct_viral_latency_programs_ L2 - http://mcb.asm.org/cgi/pmidlookup?view=long&pmid=8972217 DB - PRIME DP - Unbound Medicine ER -