Reovirus-induced apoptosis of MDCK cells is not linked to viral yield and is blocked by Bcl-2

S. E. Rodgers, E. S. Barton, S. M. Oberhaus, B. Pike, C. A. Gibson, K. L. Tyler, T. S. Dermody

Research output: Contribution to journalArticlepeer-review

105 Scopus citations


In this study, we investigated the relationship between reovirus- induced apoptosis and viral growth. Madin-Darby canine kidney (MDCK) epithelial cells infected with prototype reovirus strains type 1 Lang (T1L) or type 3 Dearing (T3D) were found to undergo apoptosis, and T3D induced apoptosis of MDCK cells to a substantially greater extent than T1L. By using T1L x T3D reassortant viruses, we found that differences in the capacities of these strains to induce apoptosis are determined by the viral S1 and M2 gene segments. These genes encode viral outer-capsid proteins that play important roles in viral entry into cells. T1L grew significantly better in MDCK cells than T3D, and these differences in growth segregated with the vital L1 and M1 gene segments. The L1 and M1 genes encode viral core proteins involved in vital RNA synthesis. Bcl-2 nverexpression in MDCK cells inhibited reovirus- induced apoptosis but did not substantially affect reovirus growth. These findings indicate that differences in the capacities of reovirus strains to induce apoptosis and grow in MDCK cells are determined by different vital genes and that premature cell death by apoptosis does not limit reovirus growth in MDCK cells.

Original languageEnglish (US)
Pages (from-to)2540-2546
Number of pages7
JournalJournal of virology
Issue number3
StatePublished - 1997
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology


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