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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.009688-0
Journal of General Virology 2009;90:1408.

A more recent version of this article appeared on June 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.009688-0
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Fusion protein is the main determinant of metapneumovirus host tropism

Miranda de Graaf, Eefje J.A. Schrauwen, Sander Herfst, Geert van Amerongen, Albert D.M.E. Osterhaus and Ron A.M. Fouchier1

Erasmus MC Dept Virology

1 E-mail: r.fouchier{at}erasmusmc.nl

Human metapneumovirus (HMPV) and avian metapneumovirus subgroup C (AMPV-C) infect humans and birds, respectively. We here confirmed the difference in host range in turkey poults, and analyzed the contribution of the individual metapneumovirus genes to host range in an in vitro cell culture model. Mammalian Vero-118 cells supported replication of both HMPV and AMPV-C in contrast to avian QT6 cells in which only AMPV-C replicated to high titers. Inoculation of Vero-118 and QT6 cells with recombinant HMPV in which genes were exchanged with those of AMPV-C revealed that the metapneumovirus F protein is the main determinant for host tropism. Chimeric viruses in which polymerase complex proteins were exchanged between HMPV and AMPV-C replicated less efficiently compared to HMPV in QT6 cells. Using minigenome systems it was shown that exchanging these polymerase proteins resulted in reduced replication and transcription efficiency in QT6 cells. Examination of infected Vero-118 and QT6 cells revealed that viruses containing the F protein of AMPV-C yielded larger syncytia compared to viruses with the HMPV F protein. Cell content mixing assays revealed that the F protein of AMPV-C was more fusogenic compared to the F protein of HMPV, and that the F2 region is responsible for the difference observed between AMPV-C and HMPV F promoted fusion in QT6 and Vero-118 cells. This study provides insight into the determinants of host tropism and membrane fusion of metapneumoviruses.

Received 19 December 2008; accepted 23 February 2009.




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