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Journal of Virology, May 2009, p. 4508-4519, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02429-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Marburg Virus 3' Noncoding Region Structurally and Functionally Differs from That of Ebola Virus{triangledown}

Sven Enterlein,1,{dagger} Kristina M. Schmidt,1,2,3 Michael Schümann,1 Dominik Conrad,1,2,3 Verena Krähling,1 Judith Olejnik,1,2,3 and Elke Mühlberger1,2,3*

Institute of Virology, Philipps University Marburg, Hans-Meerwein-Strasse 2, 35043 Marburg, Germany,1 National Emerging Infectious Diseases Laboratories,2 Boston University School of Medicine, Department of Microbiology, 72 East Concord Street, Boston, Massachusetts 021183

Received 25 November 2008/ Accepted 9 February 2009

We have previously shown that the first transcription start signal (TSS) of Zaire Ebola virus (ZEBOV) is involved in formation of an RNA secondary structure regulating VP30-dependent transcription activation. Interestingly, transcription of Marburg virus (MARV) minigenomes occurs independently of VP30. In this study, we analyzed the structure of the MARV 3' noncoding region and its influence on VP30 necessity. Secondary structure formation of the TSS of the first gene was experimentally determined and showed substantial differences from the structure formed by the ZEBOV TSS. Chimeric MARV minigenomes mimicking the ZEBOV-specific RNA secondary structure were neither transcribed nor replicated. Mapping of the MARV genomic replication promoter revealed that the region homologous to the sequence involved in formation of the regulatory ZEBOV RNA structure is part of the MARV promoter. The MARV promoter is contained within the first 70 nucleotides of the genome and consists of two elements separated by a spacer region, comprising the TSS of the first gene. Mutations within the spacer abolished transcription activity and led to increased replication, indicating competitive transcription and replication initiation. The second promoter element is located within the nontranslated region of the first gene and consists of a stretch of three UN5 hexamers. Recombinant full-length MARV clones, in which the three conserved U residues were substituted, could not be rescued, underlining the importance of the UN5 hexamers for replication activity. Our data suggest that differences in the structure of the genomic replication promoters might account for the different transcription strategies of Marburg and Ebola viruses.

* Corresponding author. Mailing address: Boston University School of Medicine, Department of Microbiology, 72 East Concord Street, Boston, MA 02118. Phone: (617) 638-0336. Fax: (617) 638-4286. E-mail: muehlber{at}bu.edu

{triangledown} Published ahead of print on 18 February 2009.

{dagger} Present address: Integrated BioTherapeutics, Inc., 20358 Seneca Meadows Pkwy., Germantown, MD 20876.

Journal of Virology, May 2009, p. 4508-4519, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02429-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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