Arch Virol (2000) 145: 1671–1683
Pathogenic avian adenovirus type II induces apoptosis
in turkey spleen cells
, M. Suresh
, and J. M. Sharma
Department of Veterinary PathoBiology, University of Minnesota,
St. Paul, Minnesota, U.S.A.
Department of Veterinary Pathobiology, College of Veterinary Medicine,
University of Wisconsin, Madison, Wisconsin, U.S.A.
Accepted February 16, 2000
Summary.Wild-type mammalianadenovirusesare known toinhibit programmed
cells death in infected cells. This study demonstrated for the ﬁrst time that an
avian type II adenovirus, the hemorrhagic enteritis virus (HEV) of turkeys, in-
duced apoptosis in turkey spleen cells at 3 and 4 days post infection. The increased
apoptosis rate in spleens of HEV-infected turkeys was associated with increased
virus replication. Increased apoptosis preceded extensive virus-induced cellular
necrosis. At 3 days post infection, spleen cells from HEV-infected turkeys re-
leased tumor necrosis like factor and nitric oxide inducing factors after ex vivo
stimulation with concanavalin A. Spleen cells from HEV-exposed turkeys also
secreted an interleukin 6-like factor when cultured in vitro. These cytokines may
have contributed to HEV-pathogenesis and HEV-induced apoptosis and necrosis
in the spleen. Induction of apoptosis by an avian adenovirus but not by wild-type
mammalian adenoviruses indicates that evolutionarily distant adenoviruses may
have different pathogenic mechanisms.
Apoptosis and necrosis are two main mechanisms of cell death, and the char-
acteristics of these modes are both morphologically and biochemically distinct.
Necrosis is a pathological response involving a dramatic increase in cell vol-
ume that leads to death and does not occur in a development context that re-
quires the expression of new proteins . Apoptosis, a form of programmed cell
death, can be induced by a number of different factors and has been implicated in
pathogenicity related to infection with certain viruses [10, 17, 19, 21, 22, 24, 36].
This type of cell death is characterized morphologically by cell shrinkage and hy-