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PubMed2003

Adenovirus infection in pediatric liver and intestinal transplant recipients: utility of DNA detection by PCR.

To evaluate the incidence of adenovirus (AdV) infection in pediatric liver and intestinal transplant recipients, the records of patients with possible AdV infection were reviewed for demographic data, symptomatology, methods of diagnosis, treatment and outcome. To evaluate the impact of polymerase chain reaction (PCR) amplification and identification of AdV DNA as a diagnostic test, the incidence and outcome of AdV before and after the introduction of PCR were compared. Adenovirus infection was identified in 4.1% of liver recipients and 20.8% of intestinal transplant recipients. The overall incidence of AdV did not increase over time, even following the introduction of PCR for virus detection. The higher incidence of AdV in the pediatric intestinal transplant recipients may be attributed to the frequent application of PCR methodology to intestinal biopsy material. Detection of AdV by PCR was associated with reduced mortality compared with detection by culture, either because of earlier detection of invasive disease or because PCR detects the presence of latent as well as active AdV.

Adenoviridae↗
PubMed1985

Adenovirus infection elevates levels of cellular topoisomerase I.

We have developed a specific, sensitive, and quantitative assay for topoisomerase I, which is based on the formation of a covalent enzyme-DNA intermediate. Our assay measures the quantitative transfer of 32P radioactivity from 32P-labeled DNA to topoisomerase I. Since 32P-labeled topoisomerase molecules are resolved by NaDodSO4/PAGE, HeLa topoisomerase I (100 kDa) and calf thymus topoisomerase I (82 kDa) can be quantitatively assayed in the same reaction mixture. The assay can detect at least 0.3 ng (3 fmol) of topoisomerase I. We have used our assay to measure the levels of topoisomerase I activity in crude extracts of nuclei prepared from uninfected, adenovirus-infected, and adenovirus-transformed human cells. The evidence suggests that an adenovirus early gene product, presumably a protein encoded in early region 1A (E1A), increases cellular topoisomerase I activity at least 10-fold. Immunoblotting analysis with antiserum against calf thymus topoisomerase I shows that the increase in activity is due to an increase in the amount of enzyme.

Adenoviridae↗
PubMed1994

Rearrangements of intranuclear structures involved in RNA processing in response to adenovirus infection.

We have studied in HeLa cells at the electron microscope level the response to adenovirus infection of the RNA processing machinery. Components of the spliceosomes were localized by in situ hybridization with biotinylated U1 and U2 DNA probes and by immunolabeling with Y12 anti-Sm monoclonal antibody, whereas poly(A)+ RNAs were localized by specific binding of biotinylated poly(dT) probe. At early stages of nuclear transformation, the distribution of small nuclear RNPs was similar to that previously described in non-infected nuclei (Visa, N., Puvion-Dutilleul, F., Bachellerie, J.P. and Puvion, E., Eur. J. Cell Biol. 60, 308-321, 1993; Visa, N., Puvion-Dutilleul, F., Harper, F., Bachellerie, J. P. and Puvion, E., Exp. Cell Res. 208, 19-34, 1993). As the infection progresses, the large virus-induced inclusion body consists of a central storage site of functionally inactive viral genomes surrounded by a peripheral shell formed by clusters of interchromatin granules, compact rings and a fibrillogranular network in which are embedded the viral single-stranded DNA accumulation sites. Spliceosome components and poly(A)+ RNAs were then exclusively detected over the clusters of interchromatin granules and the fibrillogranular network whereas the viral single-stranded DNA accumulation sites and compact rings remained unlabeled, thus appearing to not be directly involved in splicing. Our data, therefore, suggest that the fibrillogranular network, in addition to being the site of viral transcription, is also a major site of viral RNA splicing. Like the clusters of interchromatin granules, which had been already involved in spliceosome assembly, they could also have a role in the sorting of viral spliced polyadenylated mRNAs before export to the cytoplasm. The compact rings, which contain non-polyadenylated viral RNA, might accumulate the non-used portions of the viral transcripts resulting from differential poly(A)+ site selection.

Adenoviruses, Human↗
PubMed1977

Virus-Induced Specific Cell Surface Antigen(s) on Mouse Adenovirus-Infected Cells.

A virus-specific cell surface antigen(s) was detected on mouse adenovirus-infected cells by the immunofluorescent antibody technique. It was demonstrated in infected cells regardless of the mouse strain or animal species used. It became detectable on the cell surface about 6 h postinfection and was demonstrated in 90% of infected cells at 24 to 36 h postinfection. On the other hand, intracellular capsid antigens became detectable by the immunofluorescent antibody technique at about 24 h postinfection. Since it was also detected on virus-infected cells treated with 5'-fluorodeoxyuridine to block viral deoxyribonucleic acid synthesis, it was synthesized at the early stage of infection and may not be a virus structural component. The relationship between this serologically detectable cell surface antigen(s) and cell-mediated immune response to virus infections is discussed.

Journal Article↗
PubMed1997

Adenovirus infection of the cornea causes histopathologic changes in the lacrimal gland.

PURPOSE: To explore the effects on the lacrimal gland of adenovirus infection of the cornea. METHODS: Rabbit corneas were inoculated with human adenoviruses Ad5, Ad14, or a rabbit adapted form of Ad 5, and in some instances booster inoculations were given. Sections of lacrimal glands removed 21-59 days post-inoculation were immunostained using antibodies against rabbit Class I and Class II MHC molecules, CD4, CD8, CD18, and rabbit thymic lymphocyte antigen (RTLA). Relative numbers of positively stained cells were quantified with a Metamorph image analysis system. RESULTS: RTLA and CD18 antigens were expressed on many interstitial cells in the normal lacrimal gland, but few expressed CD4 or CD8. The number of RTLA+ cells increased by 60-100% after inoculation of Ad5 and after boosting, and CD18+ cells increased from 33-100% after inoculation of Ad5 and after boosting. Booster inoculations also caused focal lymphocytic infiltration. MHC Class I was expressed on interstitial cells and duct epithelium, but not acinar cells, and there was no detectable difference after viral infection. In controls, MHC Class II was localized to a population of interstitial cells and a few acinar cells. A single inoculation of the Ad5 virus did not result in an increase in the total number of MHC Class II-positive cells at 21 days, but inoculation with the rabbit-adapted Ad 5 and booster inoculations caused a 30% increase. CONCLUSIONS: Ad5 and rabbit-adapted Ad5 infection of the cornea induce lymphocytic infiltration in the lacrimal gland, and the effect is enhanced by boosting. There is also an increase in expression of MHC Class II after inoculation with rabbit-adapted Ad5 and with booster inoculations.

Adenoviridae↗
PubMed1977

Polypeptide phosphorylation in adenovirus-infected cells.

Cells infected with human adenovirus type 5 have been labelled with 32P-orthophosphate under various conditions and extracts examined, after denaturation in sodium dodecyl sulphate (SDS), by polyacrylamide gel electrophoresis (PAGE) followed by autoradiography. A number of polypeptides appear to be phosphorylated specifically as a result of infection. Early in infection, phosphorylation of a polypeptide of apparent mol. wt. 26 K associated with ribosomes can be detected. Two other phosphorylated polypeptides of apparent mol. wt. 72 K and 18 K can also be seen, the former being mainly confined to the nucleus and capable of being precipitated by the previously described virus-specific P antiserum. The 18 K phosphorylated polypeptide is found mainly in association with membrane fractions. Later in infection phosphorylated polypeptides of apparent mol. wt. 100 K and 39 K can be recognized, the former being associated with ribosomes but removed, however, with a high salt wash; the latter component is mainly detected in the nucleus. Analysis of the purified 32P-labelled virus by the SDS PAGE technique indicated that a structural polypeptide of apparent mol. wt. 66 K (IIIa) was also phosphorylated.

Adenoviruses, Human↗
PubMed2001

Lethal adenovirus infection in a patient who had undergone nonmyeloablative stem cell transplantation.

We present a case of adenovirus (ADV) infection in a patient who had undergone nonmyeloablative stem cell transplantation (NST). A 50-year-old man with chronic myelogenous leukemia in the second chronic phase underwent NST from an HLA 2-loci-mismatched sibling. ADV hemorrhagic cystitis developed and progressed to lethal pneumonia. ADV was isolated from urine, bronchoalveolar lavage fluid, and postmortem specimens of kidney and liver. Because there are few reports of lethal pneumonia associated with ADV in Japan, we present the case and discuss the cause of and therapy for the infection.

Adenoviridae Infections↗
PubMed1990

Adenovirus infection induces amplification of persistent viral DNA sequences (simian virus 40, hepatitis B virus, bovine papillomavirus) in human and rodent cells.

Adenoviruses, types 2 and 12 induce amplification of SV40 DNA sequences in cells of the SV40-transformed human newborn kidney cell line, NB-E. Similarly, integrated hepatitis B virus DNA sequences in the human hepatoma cell line, PLC/*PRF/5, and bovine papillomavirus (BPV) DNA sequences in BPV-transformed mouse cells (ID13) are amplified by adenovirus infection. Thus, similar to herpes group or vaccinia viruses or DNA damaging agents, adenoviruses are able to mediate selective DNA amplification in addition to their reported mutagenic and chromosome damaging effects. The role of amplification of integrated viral DNA sequences in development and progression of specific tumors (e.g. hepatocellular carcinoma) remains to be determined.

Adenoviruses, Human↗
PubMed1998

Inhibition of ICE-like proteases inhibits apoptosis and increases virus production during adenovirus infection.

Interleukin-1b converting enzyme (ICE)-related cysteine proteases are required for E1A-induced, p53-dependent apoptosis in baby rat kidney (BRK) cells. Adenovirus E1B 19K protein, which is a potent inhibitor of apoptosis, inhibits activation of these proteases in BRK cells. E1A expression induces apoptosis during infection of human cells by mutant adenoviruses which contain nonfunctional E1B 19K. The question arises as to whether ICE-related proteases are involved in E1A-induced apoptosis during mutant adenovirus infection of human cells. To test the involvement of the cysteine proteases in E1A-induced apoptosis during productive adenovirus infection of HeLa cells, we examined whether Z-VAD-FMK, an inhibitor of ICE-related proteases, can inhibit apoptosis induced by mutant adenovirus which lacks functional E1B 19K. Z-VAD-FMK inhibited E1A-induced apoptosis in adenovirus-infected Hela cells, suggesting that the ICE family proteases are involved in this apoptosis pathway. Z-VAD-FMK also inhibited cleavage of substrates such as cysteine protease CPP32 and nuclear lamins, whereas cleavage of poly(ADP-ribose) polymerase was partially inhibited during infection with an E1B 19K mutant. Inhibition of apoptosis by Z-VAD-FMK significantly enhanced production of infectious adenovirus and attenuated virus release. Thus apoptosis may be a method for the host cell to limit virus production and release at the end of the infection cycle.

Adenovirus E1A Proteins↗
PubMed2002

Release of snRNP and RNA from transcription sites in adenovirus-infected cells.

Small nuclear ribonucleoprotein (snRNP) splicing factors colocalize with nascent RNA in the nucleus of adenovirus-infected cells in a pattern that appears as a series of rings surrounding viral replication centers. We have studied the release of snRNP and RNA from transcription sites following transcription inhibition by actinomycin D. SnRNP, poly(A) RNA, and viral RNA were no longer detected in the ring pattern following transcription inhibition and were instead detected in nuclear clusters. Release of snRNP from transcription sites was blocked when transcription was inhibited at 4 degrees C, suggesting that release requires temperature-dependent processes. Release of snRNP was also inhibited when transcription was blocked in the presence of 9-beta-D-arabinofuranosyladenine, to inhibit 3'-end cleavage and polyadenylation, or staurosporine, to inhibit kinases. By contrast, release of snRNP was not inhibited when transcription was blocked in the presence of cordycepin, to inhibit RNA polyadenylation without affecting 3'-end cleavage, or okadaic acid, to inhibit phosphatase activity. Our results suggest that temperature-dependent processes involved in the release of splicing factors from transcription sites could include 3'-end cleavage of pre-mRNA and phosphorylation events inhibited by stauropsorine.

Adenoviridae↗
PubMed1978

Microcalorimetric measurement of normal and adenovirus infected HeLa cells.

The use of a simple microcalorimetric technique for the study of HeLa cells and adenovirus infected HeLa cells has been investigated. The calorimetric curves obtained with these two cellular systems showed characteristic differences. It is concluded that the method can serve as a useful analytical technique for the monitoring of the overall metabolic activity of tissue cells attached to a solid support.

Adenoviridae↗
PubMed1993

Seroepidemiologic survey for adenovirus infection in lambs.

A serologic survey was conducted to determine the prevalence and seroconversion rates for ovine adenovirus (OAV) serotypes 1-4 and bovine adenovirus (BAV) serotypes 2, 3, and 7 in sheep in Iowa and in surrounding states. For 2 consecutive years, paired serum samples were obtained from 1- to 2-month-old lambs as they entered a ram test station and, again, 2 months later. Sera were tested for adenovirus antibodies by use of a microtitration serum virus-neutralization test. At the time of entry, high prevalence of antibody (titer > or = 2) was detected to all tested adenoviruses except BAV-3. All adenoviruses were active in the ram test station both years, as indicated by > or = fourfold increase in adenovirus antibody titer (seroconversion) in some of the lambs. The prevalence and seroconversion rate for OAV-1 was 94.0 and 7.2%, respectively; for OAV-2, 98.6 and 15.1%; for OAV-3, 86.5 and 11.0%; for OAV-4, 98.4 and 13.2%; for BAV-2, 97.6 and 22.4%; for BAV-3, 11.4 and 3.8%; and for BAV-7, 81.6 and 4.5%. The results indicate that adenovirus infections were widespread in the sheep population and that the prevalence of active infection based on seroconversion rates was approximately 45%.

Adenoviridae Infections↗
PubMed1996

Previous enteric adenovirus infection does not protect against subsequent symptomatic infection: longitudinal follow-up of eight infants.

Eight infants followed longitudinally were found to have enteric adenovirus (EAdv) infections: in 5 infants with diarrhea and in 3 with no accompanying diarrhea. Sequential stool samples prior to EAdv infections were tested for adenovirus antigen, anti-adenoviral IgA and neutralizing antibodies to serotypes 40, 41 and 2 in order to ascertain whether protection from symptoms was due to prior infection. No difference was found in the number of adenoviral infections among infants prior to their EAdv infections with or without accompanying diarrhea. However, in 3 of the 5 infants in whom EAdv infection was accompanied by diarrhea and 2 of 3 control infants, previous EAdv infections had occurred as detected by serotype-specific antibody rises.

Adenoviridae Infections↗
PubMed1992

Adenovirus infection and specific secretory IgA responses in the intestine of infants.

We investigated adenovirus (Ad) infection of the intestine and Ad group-specific fecal IgA antibody responses in seven infants who were followed up from birth to 16 months to seven years of age. We isolated in tissue culture from fecal samples not only enteric Ad type 41 but also other Ads (types 2, 3, 5, 6, and 12). We also detected Ad antigens in the feces by ELISA at the times of infection with even non-enteric Ads, suggesting that a large amount of antigens were produced in the intestine. We found that repeated Ad infections with different serotypes were occurring and there were good fecal IgA antibody responses at each time. The infection seemed usually mild or asymptomatic: only one out of 23 occasions of the detected infections required hospitalization.

Adenovirus Infections, Human↗
PubMed2003

Acute inflammatory response and remodeling of airway epithelium after subspecies B1 human adenovirus infection of the mouse lower respiratory tract.

Despite the well-recognized role of adenoviruses of species B in the etiology of severe respiratory disease, the lack of an experimental in vivo model system has limited the understanding of the molecular pathogenesis of species B adenovirus-induced pneumonia. Intratracheal instillation of 5 x 10(8) plaque-forming units (pfu) of adenoviruses 3p and 7h resulted in a robust inflammatory response in the lungs of infected mice. A marked infiltration of neutrophils into the lung air spaces was observed at 1 and 2 days postinfection (dpi), with a concomitant increase in the levels of neutrophil chemokines MIP-2 and KC. The overall histological severity scores were significantly higher for Ad3p-infected mice at 2 dpi, but similar between the two viruses at other time points. Remodeling of the airway epithelia and mucous cell metaplasia were noted in the proximal airways of infected mice, indicating marked epithelial differentiation and/or injury. The proinflammatory cytokines interleukin-beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma [see symbol in text]), and interleukin-12 (IL-12) were induced by viral infection. Expression of the early viral immunomodulatory genes E3-15.3K and E3gp19K mRNA was readily detectable in the lungs of infected mice by reverse transcription-polymerase chain reaction (RT-PCR) at 1 and 2 dpi, coinciding with the peak levels of TNF-alpha. While the detection of gp19K mRNA declined thereafter, 15.3K mRNA was detectable up to 6 dpi. Our results indicate that human Ad3 and Ad7 cause marked pulmonary pathology, inducing similar host responses in the respiratory tract, thus validating the use of the mouse model for the study of early virus-host interactions during lung infection by adenoviruses of subspecies B1.

Acute Disease↗
PubMed1989

Modification of protein synthesis initiation factors and the shut-off of host protein synthesis in adenovirus-infected cells.

A substantial body of data, largely derived from study of cell extracts, indicates that protein synthesis in adenovirus-infected cells requires VA RNAI at late times of infection to prevent the activation of a protein kinase known as DAI, and the consequent phosphorylation of the alpha-subunit of initiation factor eIF-2. To verify this conclusion, we have measured the steady-state levels of eIF-2 alpha phosphorylation in cells infected with wild-type virus (Ad2) and a mutant that produces no VA RNAI (Ad5dl331). Consistent with the proposed mechanism, the alpha-subunit was very highly phosphorylated (approximately 90%) at late times of infection with Ad5dl331. Surprisingly, eIF-2 alpha phosphorylation also increased (to approximately 30%) at late times of infection with Ad2, suggesting that VA RNA and DAI might be involved in the selective translation of viral mRNA and the shut-off of host cell protein synthesis during the late phase. In agreement with this model, host protein synthesis shut-off is defective in cells expressing low levels of DAI.

Adenoviruses, Human↗
PubMed1988

Aplastic anaemia complicating adenovirus infection in DiGeorge syndrome.

An 18-month-old child with partial DiGeorge syndrome developed aplastic anaemia during an acute adenovirus infection. Assessment of the child's immune system revealed T-cell subset abnormalities consistent with DiGeorge syndrome. A possible link between the underlying immune deficiency and the observed complication is suggested.

Adenoviridae Infections↗