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At least 505 records · Page 28Linked to original sources
PubMed1991

Clinical features of enteric adenovirus infection in infants.

During the period December 1984 to October 1988, adenoviruses (Ads) were isolated on 119 occasions (1.6%) from stool samples of patients with gastroenteritis. By DNA restriction analysis, 85 enteric adenoviruses (EAds) were identified. Sixty-seven patients with these infections were studied, of whom 18 had Ad40, 30 had Ad41 and 19 had untyped Ad infections. The incidence of Ad infection was high in children between 6 and 11 months of age. The illness was characterized by watery diarrhea (whitish in one third of patients), continuing for a mean of 4.5 days, and vomiting, which occurred more often in patients with EAds than in other types of infection. Diarrhea, fever and vomiting were seen significantly more frequently in patients with Ad40 than in Ad41 infection. Diarrhea and vomiting were also seen significantly more frequently in patients with EAds than in Ads infection. Diarrhea, fever and vomiting were observed more frequently in patients with rotavirus than EAds infection.

Acute Disease↗
PubMed1996

Pathogenesis of type II avian adenovirus infection in turkeys: in vivo immune cell tropism and tissue distribution of the virus.

Hemorrhagic enteritis virus (HEV), a type II avian adenovirus, causes intestinal hemorrhages and immunosuppression in turkeys. In this study, we exposed turkeys to virulent HEV and examined fractionated spleen cells for the presence of viral DNA by in situ hybridization and amplification of DNA extracted from virus-infected cells by PCR. HEV replication was detected only in the immunoglobulin M-bearing B lymphocytes and macrophage-like cells but not in the CD4+ or CD8+ T lymphocytes. The inability to infect T cells distinguishes type II avian adenoviruses from lymphotropic mammalian adenoviruses which infect and replicate in T cells. Furthermore, these data suggested that HEV-induced immunosuppression in turkeys may be due to the effect of the virus on B lymphocytes and macrophages. We also examined tissue tropism of HEV by in situ hybridization conducted on sections of lymphoid and nonlymphoid tissues. Large numbers of HEV-positive cells were detected in spleen and cecal tonsils. Diminutive viral activity was present in the intestines, the principal site of HEV-induced pathology. Thus, intestinal pathology was not associated with local cytopathic viral replication. This result and our previous observation that cyclosporin A abrogated intestinal hemorrhaging in HEV-infected turkeys strongly suggested that intestinal lesion induced by this virus may be immune system mediated.

Adenoviridae Infections↗
PubMed1991

Murine adenovirus infection of SCID mice induces hepatic lesions that resemble human Reye syndrome.

Murine adenovirus type 1 (MAV-1) infection of CB-17 SCID mice (which are homozygous for the severe combined immunodeficiency mutation) induces hepatic histopathologic and ultrastructural features that are strikingly similar to human Reye syndrome. Gross pathologic examination of MAV-1-infected mice revealed only pale yellow liver tissue. Histopathologic studies of tissue from MAV-1-infected mice revealed diffuse hepatic injury manifested by microvesicular fatty degenerative changes of hepatocytes and electron microscopic evidence of focal mitochondrial swelling with disruption of cristae and depletion of glycogen. Serum aminotransferase activities increased markedly in the infected animals; however, plasma ammonia levels were not elevated at the times assayed. Although all mice infected with MAV-1 died, neutralizing anti-MAV-1 monoclonal antibodies provided a dose-dependent delay in the appearance of clinical disease and hepatic histopathologic findings. Other findings included rare viral inclusions with only minimal inflammation in spleen, adrenal, and liver of infected mice. Our findings indicate that MAV-1 infection of SCID mice may provide important insights into the pathogenesis of the hepatic lesions of Reye syndrome.

Adenoviridae↗
PubMed1994

High resolution localization of replicating viral genome in adenovirus-infected HeLa cells.

Previous autoradiographical and in situ hybridization experiments have revealed that the replication of viral genomes in adenovirus type 5 infected HeLa cells induces changes in nuclear structure of which one of the more striking is the formation of distinctive replicative foci. The latter consist of a viral ssDNA accumulation site and a surrounding fibrillogranular network. We have reexamined these structures and processes by a more direct and higher resolution approach, that is, incorporation of bromodeoxyuridine (BrdU) by the infected cells and subsequent immunogold detection of the BrdU incorporated into DNA. Short pulses with BrdU in pulse-chase experiments confirmed that viral DNA replication at the early stage of nuclear transformation was confined within small virus-induced structures, the so-called early replicative sites, and revealed the persistence of the newly synthesized viral DNA at those sites for at least 2 h. At intermediate and late stages of nuclear transformation, the intensity of viral DNA replication, which varies from one type of replicative focus to another, was most intense in that layer of the fibrillogranular network which was in closest proximity to the viral single-stranded DNA (ssDNA) accumulation sites, whereas replication was weakest over the latter. Subsequently, BrdU-containing viral DNA molecules became more widely distributed in the viral ssDNA accumulation sites and the fibrillogranular network, the two constituents of the viral replicative machinery. Two hours later, some labeled molecules attained the viral genome storage site and/or became encapsulated. The most striking observation is the presence of a limited region in the replicative focus which is the preferential site for viral genome replication. The data also indicated that viral DNA molecules which were labeled during the short pulses remained in the replicative foci themselves, to be replicated and transcribed prior to attaining the pool of inactive genomes and/or becoming encapsulated.

Adenoviruses, Human↗