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PubMedDate not supplied

[Development of PCR-test system for the detection of human adenovirus infection].

The paper deals with the development of the PCR-test system that allows the greatest possible number of human adenovirus (AdV) serotypes in the clinical samples to be tested by polymerase chain reaction. Primers have been selected on the basis of analysis of 3'-end sequences of hexon genes of 48 AdV serotypes. Five laboratory human AdV strains of different serotypes and some other DNA viruses were used to show the high sensitivity and specificity of AdV DNA detection. The proposed test system was not inferior to the Russian available analogues in sensitivity and specificity.

Adenoviridae↗
PubMed1981

Nuclear ribonucleoprotein particles from adenovirus infected Hela cells.

Heterogenous nuclear RNA-protein complexes (hnRNP) from adenovirus-2 (Ad-2) infected Hela cells contain most of the virus-specific RNA which is labeled in the nucleus during periods lasting from 45 seconds to 2 hours. Moreover, the percentage of RNA which is Ad-2 specific as monitored by filter hybridization increases progressively from early to late period where it accounts for as much as 50-60% of the labeled RNA. The Ad-2 sequences are found in heterogenous complexes sedimenting between 30 and 200 S the density of which in CsCl (rho approximately 1.39) as well as metrizamide (rho approximately 1.29) seems to be the same as that of the bulk particles. A more detailed analysis with restriction fragments shows that all regions of the Ad-2 genome are represented in these particles.

Adenoviridae↗
PubMed2003

Intestinal intussusception associated with adenovirus infection in Mexican children.

Formalin-fixed intestinal tissue specimens from 12 Mexican pediatric patients with intussusception were examined for the presence of adenovirus. Four patients (33%) had detectable adenovirus antigen in epithelial cells as determined by using immunohistochemical analysis. Two of the patients with positive immunohistochemical results had antigens in dendritic and mononuclear inflammatory cells, and 3 patients had positive results for species C adenovirus by in situ hybridization using adenovirus species-specific probes (A-F). A real-time polymerase chain reaction assay specific for species C (nonenteric) adenoviruses was used to confirm immunohistochemical results and to amplify adenovirus DNA for sequencing. A sequence similar to that for adenovirus serotype 1 was found in 1 patient, serotype 2 in another, and serotype 6 in a third; in the fourth patient, the sequence was indeterminate between serotypes 2 and 6. The assays used in this study proved useful for the identification of species C adenoviruses in formalin-fixed specimens from Mexican pediatric patients with intussusception.

Adenoviridae Infections↗
PubMed1995

Mitotic cycle reactivation in terminally differentiated cells by adenovirus infection.

Different cell types (e.g., neurons, skeletal and heart myocytes, adipocytes, keratinocytes) undergo terminal differentiation, in which acquisition of specialized functions entails definitive withdrawal from the cell cycle. Such cells are distinct from quiescent (reversibly growth-arrested) cells, such as contact-inhibited fibroblasts. Terminally differentiated cells can not be induced to proliferate by means of growth factor stimulation or transduction of cellular oncogenes. An important first step toward defining the molecular basis for such unresponsiveness is to find a practical means to overcome the proliferative block. Furthermore, determining whether terminally differentiated, postmitotic cells still retain a potential competence for proliferation that can be reactivated would have important theoretical and practical implications. To address these questions, we exploited the properties of adenoviruses. These viruses can infect postmitotic cells and express E1A, a powerful activator of proliferation in reversibly growth-arrested cells. We infected terminally differentiated skeletal muscle cells and adipocytes with human adenovirus type 5 or 12, obtaining full reentry into the cell cycle, including DNA synthesis, mitosis, cytokinesis, and extended proliferation. Similar results were obtained with established cell lines and primary cells belonging to several species, from quail to humans. Genetic analysis indicated that the smaller splice product of E1A, E1A 12S, is sufficient to induce cell cycle reactivation in otherwise permanently nonmitotic cells. These results demonstrate that terminally differentiated cells retain proliferative potential and establish adenovirus as a convenient and powerful means to force such cells to reenter the cell cycle.

Adenovirus E1A Proteins↗
PubMed1978

Cell-mediated immunity to mouse adenovirus infection. Macrophage migration inhibition test.

Cell-mediated immunity (CMI) to mouse adenovirus (M-Ad) infection was studied by macrophage migration inhibition test (MMI) as one of in vitro correlates of CMI. Both direct and indirect tests showed clearly that migration of packed peritoneal exudate cells (PEC) (immune mouse or nonimmune guinea pig) was remarkably inhibited; MIF was produced by interactions between immune PEC and infected cell extracts and between immune spleen cells and infected cells or their extracts. The antigen(s) responsible for the above MMI was demonstrated in 6- to 12-hour infected ME cells, and FUdR-treated infected ME cells. Since under these conditions there is S antigen(s) synthesis but not capsid antigen synthesis, the antigen(s) concerned must be an S antigen(s). T cells sensitized to infected cells were shown to be required to induce MMI. The MMI is specific for M-Ad, since no cross MMI was observed between M-Ad and SV40 systems. Time course study of the development of CMI to M-Ad by MMI tests showed that CMI became detectable 4 days post-infection (pi), reached its peak level about 10 days pi, and faded away rapidly in about 10 days thereafter.

Adenoviridae Infections↗
PubMed1977

Immunization of chickens against adenovirus infection.

Chickens were vaccinated with monovalent and polyvalent adenovirus vaccines using three different serotypes, types 1, 2, and 3. No cross-protection was elicited by the heterologous serotypes but satisfactory protection from lesions and the shedding of challenge virus was induced by the homologous serotypes in the monovalent and polyvalent vaccines. The virus neutralizing (VN) titers were occasionally lower where the polyvalent vaccines were used when compared to those from chickens given the monovalent vaccines. This suggested possible interference though protection did exist against the appearance of lesions. Where chickens were vaccinated at an early age and in the presence of congenital homologous VN antibodies, protection against the effects of infection was satisfactory whereas the VN antibody titers were low or insignificant by the assay methods employed. The vaccine virus was not shed beyond 28 days after vaccination. No physical effects of vaccination were noted in any of the chickens during the post-vaccination period.

Adenoviridae Infections↗
PubMed1996

Selective translation initiation by ribosome jumping in adenovirus-infected and heat-shocked cells.

Translation initiation on eukaryotic mRNAs usually occurs by 5'-processive scanning of 40S ribosome subunits from the m7GTP-cap to the initiating AUG. In contrast, picornavirus and some specialized mRNAS initiate translation by internally binding ribosomes. A poorly described third mechanism of initiation, referred to as ribosome shunting or jumping, involves discontinuous scanning by 40S ribosome subunits, in which large segments of the 5' noncoding region are bypassed. Ribosome shunting has only been observed to date on a cauliflower mosaic virus mRNA. In this report we show that the family of adenovirus late mRNAs, which are preferentially translated during infection, use a ribosome jumping mechanism to initiate protein synthesis. Late adenovirus mRNAs contain a common 5'-noncoding region known as the tripartite leader, which confers preferential translation by reducing the requirement for the rate-limiting initiation factor eIF-4F (cap-binding protein complex). Adenovirus inhibits cell protein synthesis largely by inactivating eIF-4F. We show that the tripartite leader directs both 5' linear ribosome scanning and ribosome jumping when eIF-4F is abundant but exclusively uses a ribosome jumping mechanism during late adenovirus infection or heat shock (stress) of mammalian cells, when eIF-4F is altered or inactivated. Shunting is directed by a complex group of secondary structures in the tripartite leader and is facilitated by one or more unidentified viral late gene products. We propose that shunting may represent a widespread mechanism to facilitate selective translation of specialized classes of capped mRNAs, including some stress and developmentally regulated mRNAs, which possess little requirement for eIF-4F but do not initiate by internal ribosome binding.

Adenoviridae↗