This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Watanabe, N Articles by Amanuma, H Search for Related Content PubMed PubMed Citation Articles by Watanabe, N Articles by Amanuma, H

 Previous Article  |  Next Article 

J Virol. 1991 January; 65(1): 132-137

Conversion of Friend mink cell focus-forming virus to Friend spleen focus-forming virus by modification of the 3' half of the env gene.

Laboratory of Gene Technology and Safety, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.

ABSTRACT

The 3' half of the env gene of the dualtropic Friend mink cell focus-forming virus was modified by replacing the restriction enzyme fragment of the genome DNA with the corresponding fragment of the acutely leukemogenic, polycythemia-inducing strain of Friend spleen focus-forming virus (F-SFFVP) genome DNA. Replacement with the fragment of F-SFFVP env containing the 585-bp deletion, the 6-bp duplication, and the single-base insertion converted the resulting chimeric genome so that the mutant had a pathogenic activity like that of F-SFFVP. Replacement with the fragment containing only the 585-bp deletion did not result in a pathogenic virus. However, when this virus pseudotyped by Friend murine leukemia virus was passaged in newborn DBA/2 mice, we could recover weakly pathogenic viruses with a high frequency. Molecular analysis of the genome of the recovered virus revealed the presence of a single-base insertion in the same T5 stretch where the wild-type F-SFFV env has the single-base insertion. These results provided evidence that the unique genomic structures present in the 3' half of F-SFFV env are the sole determinants that distinguish the pathogenicity of F-SFFV from that of Friend mink cell focus-forming virus. The importance of the dualtropic env-specific sequence present in the 5' half of F-SFFV env for the pathogenic activity was evaluated by constructing a mutant F-SFFV genome in which this sequence was replaced by the ecotropic env sequence of Friend murine leukemia virus and by examining its pathogenicity. The results indicated that the dualtropic env-specific sequence was essential to pathogenic activity.

This article has been cited by other articles:

• Liu, W., Crocker, E., Constantinescu, S. N., Smith, S. O. (2005). Helix Packing and Orientation in the Transmembrane Dimer of gp55-P of the Spleen Focus Forming Virus. Biophys. J 89: 1194-1202 [Abstract] [Full Text]  
• Gomez-Lucia, E., Zhi, Y., Nabavi, M., Zhang, W., Kabat, D., Hoatlin, M. E. (1998). An Array of Novel Murine Spleen Focus-Forming Viruses That Activate the Erythropoietin Receptor. J. Virol. 72: 3742-3750 [Abstract] [Full Text]  
• Yugawa, T., Amanuma, H. (1998). Sequence Flexibility in the Polytropic env gp70-Derived Region of the Membrane Glycoprotein (gp55) of Friend Spleen Focus-Forming Virus Affects Its Biological Activity. J. Virol. 72: 2272-2279 [Abstract] [Full Text]  
• Gonda, T. J., D'Andrea, R. J. (1997). Activating Mutations in Cytokine Receptors: Implications for Receptor Function and Role in Disease. Blood 89: 355-369 [Full Text]