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PubMed articles by:
Jääskeläinen, K.
Plyusnina, A.
Lundkvist, Å.
Plyusnin, A.
Virol J. 2008; 5: 3.
Published online 2008 January 11. doi: 10.1186/1743-422X-5-3.
PMCID: PMC2253529
Copyright © 2008 Jääskeläinen et al; licensee BioMed Central Ltd.
Tula hantavirus isolate with the full-length ORF for nonstructural protein NSs survives for more consequent passages in interferon-competent cells than the isolate having truncated NSs ORF
Kirsi M Jääskeläinen,corresponding author1 Angelina Plyusnina,1 Åke Lundkvist,2,3 Antti Vaheri,1 and Alexander Plyusnin1,2
1Department of Virology, Haartman Institute, PO Box 21, FIN-00014 University of Helsinki, Helsinki, Finland
2Swedish Institute for Infectious Disease Control, S-171 82 Stockholm, Sweden
3Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden
corresponding authorCorresponding author.
Kirsi M Jääskeläinen: Kirsi.M.Jaaskelainen/at/helsinki.fi; Angelina Plyusnina: Anguelina.Pljusnina/at/helsinki.fi; Åke Lundkvist: Ake.Lundkvist/at/smi.ki.se; Antti Vaheri: Antti.Vaheri/at/helsinki.fi; Alexander Plyusnin: Alexander.Plyusnin/at/helsinki.fi
Received October 19, 2007; Accepted January 11, 2008.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Abstract

Background
The competitiveness of two Tula hantavirus (TULV) isolates, TULV/Lodz and TULV/Moravia, was evaluated in interferon (IFN) -competent and IFN-deficient cells. The two isolates differ in the length of the open reading frame (ORF) encoding the nonstructural protein NSs, which has previously been shown to inhibit IFN response in infected cells.

Results
In IFN-deficient Vero E6 cells both TULV isolates survived equally well. In contrast, in IFN-competent MRC5 cells TULV/Lodz isolate, that possesses the NSs ORF for the full-length protein of 90 aa, survived for more consequent passages than TULV/Moravia isolate, which contains the ORF for truncated NSs protein (66–67 aa).

Conclusion
Our data show that expression of a full-length NSs protein is beneficial for the virus survival and competitiveness in IFN-competent cells and not essential in IFN-deficient cells. These results suggest that the N-terminal aa residues are important for the full activity of the NSs protein.

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