Defining CAR as a cellular receptor for the avian adenovirus CELO using a genetic analysis of the two viral fibre proteins. (9/57)

The coxsackievirus and adenovirus receptor (CAR) is a high affinity receptor used by adenoviruses, including adenovirus type 5 (Ad5). The adenovirus fibre molecule bears the high affinity cell binding domain of Ad5, allowing virions to attach to CAR. The avian adenovirus CELO displays two fibre molecules on its capsid and it was logical to expect that the cell binding functions of CELO might also reside in one or both of these fibres. We had previously shown that the cell binding properties of CELO resemble Ad5, suggesting that the two viruses use similar receptors. Experiments with CAR-deficient CHO cells and CHO cells modified to express CAR demonstrated that CELO has CAR-dependent transduction behaviour like Ad5. Mutations were introduced into the CELO genome to disrupt either the long fibre 1 or the short fibre 2. A CELO genome with fibre 2 disrupted did not generate virus, demonstrating that fibre 2 is essential for some stage in virus growth, assembly or spread. However, a CELO genome with disrupted fibre 1 gene produced virus (CELOdF1) that was capable of entering chicken cells, but had lost both the ability to efficiently transduce human cells and the CAR-specific transduction displayed by wild-type CELO. The ability of CELOdF1 to transduce chicken cells suggests that CELOdF1 may still bind, probably via fibre 2, to a receptor expressed on avian but not mammalian cells. CELOdF1 replication was dramatically impaired in chicken embryos, demonstrating that fibre 1 is important for the in vivo biology of CELO.  (+info)

Marble spleen disease in pheasants in Korea. (10/57)

Two pheasants maintained in outdoor closed pen died within several days after having a history of depression. On necropsy, the spleens from both pheasants were enlarged about 3 times of their normal size and appeared mottled in color varying white to red. Histopathologically, there were diffuse severe follicular necrosis in the spleen and congestion and edema in the lung. Intranuclear basophilic inclusion bodies, which are strongly positive to group II avian adenovirus with immunohistochemistry, were noted in the spleen.  (+info)

Histone deacetylase 1 inactivation by an adenovirus early gene product. (11/57)

Gam1 is an early gene product of the avian adenovirus CELO and is essential for viral replication. Gam1 has no homology to any known proteins; however, its early expression and nuclear localization suggest that the protein functions to influence transcription in the infected cell. A determinant of eukaryotic gene expression is the acetylation state of chromosomal histones and other nuclear proteins. We find that Gam1 expression increases the level of transcription from a variety of eukaryotic promoters, similar to the effect of treating cells with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA ). We show that Gam1 can effectively inhibit histone deacetylation by HDAC1 and that Gam1 binds to HDAC1 both in vitro and in vivo. A CELO virus lacking Gam1 (CELOdG) is replication defective, but the defect can be overcome by either expressing an interfering HDAC1 mutant or by treating infected cells with TSA. The identification of a viral early gene product having the specific function of binding and inactivating HDAC suggests that deacetylase complexes play an important role in limiting early gene expression from invading viruses.  (+info)

Pancreatic necrosis and ventricular erosion in adenovirus-associated hydropericardium syndrome of broilers. (12/57)

Seven 19-day-old broiler chickens affected with hydropericardium syndrome (HPS) with pancreatic necrosis and gizzard erosions were investigated pathologically and virologically. Mortality increased after 13 days of age in a flock on a broiler farm. The mortality rate of the flock reached 10% by 19 days of age. Macroscopically, the chickens had hydropericardium (the characteristic gross change of HPS), pinpoint white foci in the pancreas, and ventricular erosions. Histologically, the chickens had multifocal hepatic necrosis with intranuclear inclusions in hepatocytes, a marked increase of macrophages in the spleen and lung, mild epicardial edema, multifocal necrosis of pancreatic acinar cells with intranuclear inclusions, focal necrosis of the ventricular koilin layer, and degeneration of the ventricular glandular epithelium with intranuclear inclusions. Immunohistochemically, intranuclear inclusions in the liver, pancreas, and ventriculi were stained positively against group I avian adenovirus (GIAAV) antigens. Ultrastructurally, 67-nm diameter viral particles were present in intranuclear inclusions. Virologically, serotype 4 of GIAAV was isolated from the liver, heart, and kidney of affected chickens. The pathologic changes of the present cases differ from previous cases of HPS; therefore, the present strain of GIAAV may have different pathogenicity for chickens than the previous virus strain of HPS.  (+info)

Unique features of fowl adenovirus 9 gene transcription. (13/57)

We examined the transcriptional organization of fowl adenovirus 9 (FAdV-9) and analyzed temporal transcription profiles of its early and late mRNAs. At least six early and six late transcriptional regions were identified for FAdV-9. Extensive splicing was observed in all FAdV-9 early transcripts examined. Sequence analysis of the cDNAs representing the early proteins identified untranslated leader sequences, precise locations of splice donor and acceptor sites, as well as polyadenylation signals and polyadenylation sites. A unique characteristic, compared to other adenoviruses, was the detection by RT-PCR of multiple transcripts specific for each of five late genes (protein III, pVII, pX, 100K, and fiber), suggesting that FAdV-9 late transcripts undergo more extensive splicing than reported for other adenoviruses.  (+info)

Characterization of a new species of adenovirus in falcons. (14/57)

In 1996, a disease outbreak occurred at a captive breeding facility in Idaho, causing anorexia, dehydration, and diarrhea or sudden death in 72 of 110 Northern aplomado falcons (Falco femoralis septentrionalis) from 9 to 35 days of age and in 6 of 102 peregrine falcons (Falco peregrinus) from 14 to 25 days of age. Sixty-two Northern aplomado and six peregrine falcons died. Epidemiologic analyses indicated a point source epizootic, horizontal transmission, and increased relative risk associated with cross-species brooding of eggs. Primary lesions in affected birds were inclusion body hepatitis, splenomegaly, and enteritis. The etiology in all mortalities was determined by molecular analyses to be a new species of adenovirus distantly related to the group I avian viruses, serotypes 1 and 4, Aviadenovirus. In situ hybridization and PCR demonstrated that the virus was epitheliotropic and lymphotropic and that infection was systemic in the majority of animals. Adeno-associated virus was also detected by PCR in most affected falcons, but no other infectious agents or predisposing factors were found in any birds. Subsequent to the 1996 epizootic, a similar disease caused by the same adenovirus was found over a 5-year period in orange-breasted falcons (Falco deiroleucus), teita falcons (Falco fasciinucha), a merlin (Falco columbarius), a Vanuatu peregrine falcon (Falco peregrinus nesiotes), and gyrfalcon x peregrine falcon hybrids (Falco rusticolus/peregrinus) that died in Wyoming, Oklahoma, Minnesota, and California. These findings indicate that this newly recognized adenovirus is widespread in western and midwestern North America and can be a primary pathogen in different falcon species.  (+info)

Isolation and epidemiology of falcon adenovirus. (15/57)

An adenovirus was detected by electron microscopy in tissues from falcons that died during an outbreak of inclusion body hepatitis and enteritis that affected neonatal Northern aplomado (Falco femoralis septentrionalis) and peregrine (Falco peregrinus anatum) falcons. Molecular characterization has identified the falcon virus as a new member of the aviadenovirus group (M. Schrenzel, J. L. Oaks, D. Rotstein, G. Maalouf, E. Snook, C. Sandfort, and B. Rideout, J. Clin. Microbiol. 43:3402-3413, 2005). In this study, the virus was successfully isolated and propagated in peregrine falcon embryo fibroblasts, in which it caused visible and reproducible cytopathology. Testing for serum neutralizing antibodies found that infection with this virus was limited almost exclusively to falcons. Serology also found that wild and captive peregrine falcons had high seropositivity rates of 80% and 100%, respectively, although clinical disease was rarely reported in this species. These data implicate peregrine falcons as the natural host and primary reservoir for the virus. Other species of North American falcons, including aplomado falcons, had lower seropositivity rates of 43 to 57%. Falcon species of tropical and/or island origin were uniformly seronegative, although deaths among adults of these species have been described, suggesting they are highly susceptible. Chickens and quail were uniformly seronegative and not susceptible to infection, indicating that fowl were not the source of infection. Based on the information from this study, the primary control of falcon adenovirus infections should be based on segregation of carrier and susceptible falcon species.  (+info)

Development of an immunocytochemical procedure to detect adenoviral antigens in chicken tissues. (16/57)

An immunocytochemical technique utilizing an avidin-biotin peroxidase complex was developed to detect viral antigens in various tissues following oral administration of a locally isolated serotype 8 avian adenovirus (AAV) in specific pathogen-free (SPF) chickens. A strong color reaction was obtained with tissues from infected birds that contained a minimal amount of AAV antigens as determined by an indirect enzyme-linked immunosorbent assay. No reaction was detected in sections of tissues obtained from SPF chickens, and the reactivity with infected tissues could be removed by prior absorption of the primary antibody with purified AAV. A group-specific antigen common to the 12 serotypes of AAV was demonstrated by this technique. Because of the high sensitivity and broad-spectrum reactivity, this technique could be useful for studying the pathogenesis and laboratory diagnosis of inclusion body hepatitis caused by several serotypes of AAV.  (+info)