Se. Rodgers et al., REOVIRUS-INDUCED APOPTOSIS OF MDCK CELLS IS NOT LINKED TO VIRAL YIELDAND IS BLACKED BY BCL-2, Journal of virology, 71(3), 1997, pp. 2540-2546
In this study, we investigated the relationship between reovirus-induc
ed apoptosis and viral growth. Madin-Darby canine kidney (MDCK) epithe
lial cells infected with prototype reovirus strains type 1 Lang (T1L)
or type 3 Dearing (T3D) were found to undergo apoptosis, and no induce
d apoptosis of MDCK cells to a substantially greater extent than T1L.
By using T1L x T3D reassortant viruses, we found that differences in t
he capacities of these strains to induce apoptosis are determined by t
he viral S1 and M2 gene segments. These genes encode viral outer-capsi
d proteins that play important roles in viral entry into cells. T1L gr
ew significantly better in MDCK cells than T3D, and these differences
in growth segregated with the viral L1 and M1 gene segments. The L1 an
d M1 genes encode viral core proteins involved in viral RNA synthesis.
Bcl-2 overexpression in MDCK cells inhibited reovirus-induced apoptos
is but did not substantially affect reovirus growth. These findings in
dicate that differences in the capacities of reovirus strains to induc
e apoptosis and grow in MDCK cells are determined by different viral g
enes and that premature cell death by apoptosis does not limit reoviru
s growth in MDCK cells.