This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Horga, M.-A.
Right arrow Articles by Moscona, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Horga, M.-A.
Right arrow Articles by Moscona, A.

 Previous Article  |  Next Article 

Journal of Virology, December 2000, p. 11792-11799, Vol. 74, No. 24
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Mechanism of Interference Mediated by Human Parainfluenza Virus Type 3 Infection

Maria-Arantxa Horga,1 G. Luca Gusella,2 Olga Greengard,1 Natalia Poltoratskaia,1 Matteo Porotto,1 and Anne Moscona1,*

Department of Pediatrics1 and Department of Medicine,2 Mount Sinai School of Medicine, New York, New York 10029-6574

Received 8 August 2000/Accepted 13 September 2000

Viral interference is characterized by the resistance of infected cells to infection by a challenge virus. Mechanisms of viral interference have not been characterized for human parainfluenza virus type 3 (HPF3), and the possible role of the neuraminidase (receptor-destroying) enzyme of the hemagglutinin-neuraminidase (HN) glycoprotein has not been assessed. To determine whether continual HN expression results in depletion of the viral receptors and thus prevents entry and cell fusion, we tested whether cells expressing wild-type HPF3 HN are resistant to viral infection. Stable expression of wild-type HN-green fluorescent protein (GFP) on cell membranes in different amounts allowed us to establish a correlation between the level of HN expression, the level of neuraminidase activity, and the level of protection from HPF3 infection. Cells with the highest levels of HN expression and neuraminidase activity on the cell surface were most resistant to infection by HPF3. To determine whether this resistance is attributable to the viral neuraminidase, we used a cloned variant HPF3 HN that has two amino acid alterations in HN leading to the loss of detectable neuraminidase activity. Cells expressing the neuraminidase-deficient variant HN-GFP were not protected from infection, despite expressing HN on their surface at levels even higher than the wild-type cell clones. Our results demonstrate that the HPF3 HN-mediated interference effect can be attributed to the presence of an active neuraminidase enzyme activity and provide the first definitive evidence that the mechanism for attachment interference by a paramyxovirus is attributable to the viral neuraminidase.

* Corresponding author. Mailing address: Department of Pediatrics, Mount Sinai School of Medicine, 1 Gustave Levy Pl., Box 1657, New York, NY 10029-6574. Phone: (212) 241-6930. Fax (212) 426-4813. E-mail: anne.moscona{at}mssm.edu.

Journal of Virology, December 2000, p. 11792-11799, Vol. 74, No. 24
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Huang, I-C., Li, W., Sui, J., Marasco, W., Choe, H., Farzan, M. (2008). Influenza A Virus Neuraminidase Limits Viral Superinfection. J. Virol. 82: 4834-4843 [Abstract] [Full Text]  
  • Sawatsky, B., Grolla, A., Kuzenko, N., Weingartl, H., Czub, M. (2007). Inhibition of henipavirus infection by Nipah virus attachment glycoprotein occurs without cell-surface downregulation of ephrin-B2 or ephrin-B3. J. Gen. Virol. 88: 582-591 [Abstract] [Full Text]  
  • Ludlow, M., McQuaid, S., Cosby, S. L., Cattaneo, R., Rima, B. K., Duprex, W. P. (2005). Measles virus superinfection immunity and receptor redistribution in persistently infected NT2 cells. J. Gen. Virol. 86: 2291-2303 [Abstract] [Full Text]  
  • Bose, S., Basu, M., Banerjee, A. K. (2004). Role of Nucleolin in Human Parainfluenza Virus Type 3 Infection of Human Lung Epithelial Cells. J. Virol. 78: 8146-8158 [Abstract] [Full Text]  
  • Henrickson, K. J. (2003). Parainfluenza Viruses. Clin. Microbiol. Rev. 16: 242-264 [Abstract] [Full Text]  
  • Murrell, M., Porotto, M., Weber, T., Greengard, O., Moscona, A. (2002). Mutations in Human Parainfluenza Virus Type 3 Hemagglutinin-Neuraminidase Causing Increased Receptor Binding Activity and Resistance to the Transition State Sialic Acid Analog 4-GU-DANA (Zanamivir). J. Virol. 77: 309-317 [Abstract] [Full Text]  
  • Greco, G., Pal, S., Pasqualini, R., Schnapp, L. M. (2002). Matrix Fibronectin Increases HIV Stability and Infectivity. J. Immunol. 168: 5722-5729 [Abstract] [Full Text]  
  • Porotto, M., Greengard, O., Poltoratskaia, N., Horga, M.-A., Moscona, A. (2001). Human Parainfluenza Virus Type 3 HN-Receptor Interaction: Effect of 4-Guanidino-Neu5Ac2en on a Neuraminidase-Deficient Variant. J. Virol. 75: 7481-7488 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»