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Journal of Virology, August 2009, p. 8122-8130, Vol. 83, No. 16
0022-538X/09/$08.00+0     doi:10.1128/JVI.02680-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Dynamics of Biologically Active Subpopulations of Influenza Virus: Plaque-Forming, Noninfectious Cell-Killing, and Defective Interfering Particles {triangledown}

Philip I. Marcus,* John M. Ngunjiri, and Margaret J. Sekellick

Department of Molecular and Cell Biology, and Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut 06269

Received 31 December 2008/ Accepted 22 May 2009

The dynamic changes in the temporal appearance and quantity of a new class of influenza virus, noninfectious cell-killing particles (niCKP), were compared to defective interfering particles (DIP). After a single high-multiplicity passage in MDCK cells of an egg-derived stock that lacked detectable niCKP or DIP, both classes of particles appeared in large numbers (>5 x 108/ml), and the plaque-forming particle (PFP) titer dropped ~60-fold. After two additional serial high-multiplicity passages the DIP remained relatively constant, the DIP/niCKP ratio reached 10:1, and the PFP had declined by about 10,000-fold. Together, the niCKP and DIP subpopulations constituted ca. 20% of the total hemagglutinating particle population in which these noninfectious biologically active particles (niBAP) were subsumed. DIP neither killed cells nor interfered with the cell-killing (apoptosis-inducing) activity of niCKP or PFP (infectious CKP), even though they blocked the replication of PFP. Relative to the UV-target of ~13,600 nucleotides (nt) for inactivation of PFP, the UV target for niCKP was ~2,400 nt, consistent with one of the polymerase subunit genes, and that for DIP was ~350 nt, consistent with the small DI-RNA responsible for DIP-mediated interference. Thus, niCKP and DIP are viewed as distinct particles with a propensity to form during infection at high multiplicities. These conditions are postulated to cause aberrations in the temporally regulated replication of virus and its packaging, leading to the production of niBAP. DIP have been implicated in the virulence of influenza virus, but the role of niCKP is yet unknown.

* Corresponding author. Mailing address: Department of Molecular and Cell Biology, University of Connecticut, U-3125, 91 North Eagleville Rd., Storrs, CT 06269. Phone: (860) 486-4254. Fax: (860) 486-5193. E-mail: philip.marcus{at}uconn.edu

{triangledown} Published ahead of print on 3 June 2009.

Journal of Virology, August 2009, p. 8122-8130, Vol. 83, No. 16
0022-538X/09/$08.00+0     doi:10.1128/JVI.02680-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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