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PubMed1986

Control of cellular and viral transcription during adenovirus infection.

The control of transcription initiation is an issue central to the regulation of eukaryotic gene expression, and as such, the elucidation of the mechanisms of control of initiation frequency is critical. The study of adenovirus transcription control has provided insights into these mechanisms. Transcription of the early viral genes is activated by the product of the viral E1A gene. Possibly of greater importance is the fact that this activation does not appear to be "viral specific". Rather, the E1A protein effects a general activation of transcription in the cell, resulting in the stimulation of transcription of at least one cellular gene in addition to the viral genes. Furthermore, there appears to be a cellular activity that functions in a manner analogous to E1A. Recent experiments also suggest a role for E1A in negative regulation of transcription, mediated through enhancer elements, that may be one aspect of gene control during cellular differentiation. Therefore, the study of E1A action may well contribute to an understanding of cellular transcription control. Finally, other mechanisms of transcription control in adenovirus infected cells such as genome replication-dependent gene activation and transcription termination control will likely contribute to the overall understanding of the control of mammalian cell gene expression.

Adenoviridae Infections↗

PubMed1996

The dynamics of coiled bodies in the nucleus of adenovirus-infected cells.

The coiled body is a specific intranuclear structure of unknown function that is enriched in splicing small nuclear ribonucleoproteins (snRNPs). Because adenoviruses make use of the host cell-splicing machinery and subvert the normal subnuclear organization, we initially decided to investigate the effect of adenovirus infection on the coiled body. The results indicate that adenovirus infection induces the disassembly of coiled bodies and that this effect is probably secondary to the block of host protein synthesis induced by the virus. Furthermore, coiled bodies are shown to be very labile structures, with a half-life of approximately 2 h after treatment of HeLa cells with protein synthesis inhibitors. After blocking of protein synthesis, p80 coilin was detected in numerous microfoci that do not concentrate snRNP. These structures may represent precursor forms of the coiled body, which goes through a rapid cycle of assembly/disassembly in the nucleus and requires ongoing protein synthesis to reassemble.

Adenovirus Infections, Human↗

PubMed1995

E1A gene expression induces susceptibility to killing by NK cells following immortalization but not adenovirus infection of human cells.

Adenovirus (Ad) infection and E1A transfection were used to model changes in susceptibility to NK cell killing caused by transient vs stable E1A expression in human cells. Only stably transfected target cells exhibited cytolytic susceptibility, despite expression of equivalent levels of E1A proteins in Ad-infected targets. The inability of E1A gene products to induce cytolytic susceptibility during infection was not explained by an inhibitory effect of viral infection on otherwise susceptible target cells or by viral gene effects on class I MHC antigen expression on target cells. This differential effect of E1A expression on the cytolytic phenotypes of infected and stably transfected human cells suggests that human NK cells provide an effective immunologic barrier against the in vivo survival and neoplastic progression of E1A-immortalized cells that may emerge from the reservoir of persistently infected cells in the human host.

Adenovirus E1A Proteins↗

PubMed2002

Use of polymerase chain reaction for diagnosis of disseminated adenovirus infection.

We report a fatal case of disseminated adenovirus infection with fulminant hepatic failure in an 8-month-old child after peripheral blood stem cell transplantation. The virus was identified in blood, urine, respiratory aspirate and stool samples and was typed as adenovirus type 2 through PCR and sequencing of part of the hexon gene, with the use of degenerated consensus primers.

Adenoviridae Infections↗

PubMed1983

Immunoassay diagnosis of adenovirus infections in children.

Direct detection of viral antigen in nasopharyngeal secretions and stool specimens by radioimmunoassay and the determination of serum antibody responses by complement fixation and immunoglobulin class-specific enzyme immunoassay against the hexon antigen were compared for diagnostic efficacy in 52 children with acute adenovirus infections. The highest diagnosis rate (85% of the cases) was obtained by antigen detection in nasopharyngeal secretions. Adenovirus antigen was also detected in stools of 72% of the 18 patients tested. The immunoglobulin G (IgG) antibody enzyme immunoassay detected 77% of the cases, being more sensitive than the complement fixation test with a 67% detection rate. The IgM antibody response was variable with no clear correlation with the age of the patient or severity of the clinical symptoms. IgM antibody response was detected in 48% of the patients and had the normal transient course, with a persistence of the IgM antibodies of approximately 2 months. Determination of IgA antibodies gave a diagnostic increase in titer in 37% of the cases and was found less suitable for serological diagnosis. Because of the clinical importance of rapid laboratory diagnosis, the direct detection of viral antigen in nasopharyngeal secretions or stool or both should be used as the primary diagnostic test in adenovirus infections.

Adenoviridae↗

PubMed2002

Inhibition of proteolytic processing of adenoviral proteins by epsilon-aminocaproic acid and ambenum in adenovirus-infected cells.

Maturation of adenovirus particles is markedly affected by proteolytic processing. The possibility for blocking the conversion of precursor structural core protein (preVII) into mature structure protein VII by officinal drugs epsilon-aminocaproic acid and ambenum has been demonstrated in Hep-2 cells infected with adenovirus. Proteolytic processing may be regarded as one of the targets for inhibiting adenovirus reproduction.

4-Aminobenzoic Acid↗

PubMed1994

Cytolysis of adenovirus-infected murine fibroblasts by IFN-gamma-primed macrophages is TNF- and contact-dependent.

The effect of interferon-gamma (IFN-gamma) priming on macrophages for cytolysis of adenovirus-infected murine fibroblasts was examined using peritoneal macrophages and the RAW264.7 (RAW) murine macrophage cell line. Adenovirus-infected cells were lysed by IFN-gamma-primed RAW macrophages via a TNF- and contact-dependent mechanism under conditions in which little or no soluble TNF was detected in the supernatant of these effectors. TNF involvement in the lytic mechanism of IFN-gamma-primed macrophages is shown by (a) cytolysis of TNF-sensitive LM and adenovirus E1A-expressing cells, (b) protection from cytolysis by the adenovirus E3-14.7K protein and the E3-10.4/14.5K complex of proteins, and (c) inhibition of cytolysis when neutralizing anti-TNF serum is added to cocultures of macrophages and susceptible adenovirus-infected targets. Physical separation of effectors and targets prevents cytolysis, indicating that cell contact is required. Nonetheless, IFN-gamma-primed RAW macrophages are unable to lyse E8 tumor cells, which are killed by fully activated (triggered) macrophages. These findings indicate that IFN-gamma-primed macrophages are cytolytic for TNF-sensitive targets without soluble TNF release, but they lack the full cytolytic capacity of LPS-triggered macrophages.

3T3 Cells↗

PubMed1997

Regulation of p53 levels by the E1B 55-kilodalton protein and E4orf6 in adenovirus-infected cells.

The adenovirus type 5 243R E1A protein induces p53-dependent apoptosis in the absence of the 19- and 55-kDa E1B polypeptides. This effect appears to result from an accumulation of p53 protein and is unrelated to expression of E1B products. We now report that in the presence of the E1B 55-kDa polypeptide, the 289R E1A protein does not induce such p53 accumulation and, in fact, is able to block that induced by E1A 243R. This inhibition also requires the 289R-dependent transactivation of E4orf6 expression. E4orf6 is known to form complexes with the E1B 55-kDa protein and to function both in the transport and stabilization of viral mRNA and in shutoff of host cell protein synthesis. We demonstrated that the block in p53 accumulation is not due to the generalized shutoff of host cell metabolism. Rather, it appears to result from a mechanism targeted specifically to p53, most likely involving a decrease in the stability of p53 protein. The E1B 55-kDa protein is known to interact with both E4orf6 and p53, and as demonstrated recently by others, we showed that E4orf6 also binds directly to p53. Thus, multiple interactions between all three proteins may regulate p53 stability, resulting in the maintenance of low levels of p53 following virus infection.

Adenovirus E1B Proteins↗

PubMed1989

[Changes in the respiratory organs in experimental adenovirus infection].

An experiment on 6 green monkeys and on 286 cotton newly born rats was made with the aim of studying the lung during experimental adenovirus infection. All the animals during different terms of infection (from 6 hours and up to 40 days) have been studied. Several morphological changes were discovered in the lungs of monkeys and rats after 6 hours of infection and were retained up to the 10-th day of infection. All the components of air-blood barrier and basal membranes were involved in the process, but after 20 day of the experimental adenovirus infection the entire restoration of cellular structure occurred.

Adenoviridae Infections↗

PubMed1993

Alternative poly(A) site utilization during adenovirus infection coincides with a decrease in the activity of a poly(A) site processing factor.

The recognition and processing of a pre-mRNA to create a poly(A) addition site, a necessary step in mRNA biogenesis, can also be a regulatory event in instances in which the frequency of use of a poly(A) site varies. One such case is found during the course of an adenovirus infection. Five poly(A) sites are utilized within the major late transcription unit to produce more than 20 distinct mRNAs during the late phase of infection. The proximal half of the major late transcription unit is also expressed during the early phase of a viral infection. During this early phase of expression, the L1 poly(A) site is used three times more frequently than the L3 poly(A) site. In contrast, the L3 site is used three times more frequently than the L1 site during the late phase of infection. Recent experiments have suggested that the recognition of the poly(A) site GU-rich downstream element by the CF1 processing factor may be a rate-determining step in poly(A) site selection. We demonstrate that the interaction of CF1 with the L1 poly(A) site is less stable than the interaction of CF1 with the L3 poly(A) site. We also find that there is a substantial decrease in the level of CF1 activity when an adenovirus infection proceeds to the late phase. We suggest that this reduction in CF1 activity, coupled with the relative instability of the interaction with the L1 poly(A) site, contributes to the reduced use of the L1 poly(A) site during the late stage of an adenovirus infection.

Adenoviridae Infections↗

PubMed1987

Disseminated adenovirus infection in an immunocompromised host. Pitfalls in diagnosis.

In this report, a bone marrow transplant recipient with rapidly fatal gastroenteritis is presented. The presence of intranuclear inclusions on postmortem light microscopic examination of liver, lung, and small bowel tissue was considered diagnostic of cytomegalovirus infection. However, electron microscopic examination of liver tissue demonstrated adenovirus infection. This was confirmed by isolation of an adenovirus type 2 with unusual laboratory features from liver, lung, colon contents, serum, esophageal swab, and oral ulcerations. Results of a complement fixation test for antibodies to adenovirus performed on postmortem serum samples were negative, and a titer of 1:4 was noted for antibody against cytomegalovirus. This case illustrates the diagnostic pitfalls that may be encountered in establishing a specific viral diagnosis in severely ill patients.

Adenoviridae Infections↗

PubMed1988

Genomic footprinting detects factors bound to major late and IVa2 promoters in adenovirus-infected HeLa cells.

We used DNase I footprinting assays on nuclei isolated from adenovirus-infected cells to examine the nucleoprotein configuration of a 250-base-pair segment which encompasses the adenovirus type 5 major late (ML) and IVa2 promoters. At 12 and 20 h postinfection (p.i.), fine DNase I digestion mapping of wild-type adenovirus-infected cells revealed specific sequences protected from digestion which corresponded to promoter elements required for expression of the ML gene in vivo. At 12 h p.i., a G+C-rich region which lies upstream of the IVa2 cap site and is important for maximal IVa2 activity was also found masked to nuclease activity. At 20 h p.i., however, this element became more sensitive to nuclease attack, while the ML promoter elements stayed protected. No major changes in DNA-protein interactions were detected in the region spanning the ML and IVa2 cap sites upon promoter activation, suggesting that the binding properties of the cognate factors for this region are not modified during the process.

Adenoviruses, Human↗

PubMed1992

Adenovirus infection and childhood intussusception.

OBJECTIVE: To investigate the possible relationship between enteric adenovirus types 40 and 41 and intestinal intussusception in children. DESIGN: Prospective, case-control patient study. PATIENTS: Sixty-three consecutive children suspected clinically of having intestinal intussusception were enrolled in this study. Of these, 25 children (mean age, 1.4 years; range, 3 months to 5 years) had barium enema examination-proved intussusception. Age-matched normal controls (24) and controls with diarrhea (21) were obtained within 1 month of the index case. MEASUREMENTS AND RESULTS: Stools were tested for the presence of nonenteric adenovirus and enteric adenovirus using a monoclonal antibody-based enzyme immunoassay. Five (20%) of 25 children with intussusception had nonenteric adenovirus in their stools compared with one (4%) of 24 normal controls, none (0%) of 21 of the controls with diarrhea, and none (0%) of 37 patients suspected of having intussusception who had negative results on barium enema examination. However, no stool samples were positive for enteric adenovirus. CONCLUSIONS: Nonenteric adenovirus infection and intestinal intussusception may be associated. However, because enteric adenovirus was not found in any of the groups studied, no conclusions can be made regarding their possible influence on the risk for developing intussusception.

Adenovirus Infections, Human↗

PubMed1988

Adenovirus infection in families.

Eighteen families were followed up for four to six weeks after one member of each family was diagnosed as having an adenovirus infection. In 17 of 18 index cases the diagnosis was based on the rapid detection of adenovirus hexon antigen in the nasopharyngeal mucus specimens and in one case (the only adult index case) on isolation of the virus. All index cases had high temperatures associated most commonly with tonsillitis, acute otitis media, gastroenteritis, or febrile convulsions. In 14 of the 16 families with symptomatic contacts the index case was the first symptomatic case, or one of the first symptomatic cases, in that family. Fifteen (94%) of the siblings and 20 (56%) of the parents had signs and symptoms of acute infection during the follow up period. In 10 (63%) and eight (20%) of these cases, respectively, adenovirus was confirmed. The mean (SD) incubation period of confirmed adenovirus infections was 10 (3) days. The observations show that adenovirus infection spreads actively to other siblings in the family. Rapid diagnosis permits parents to be informed prospectively about the expected spread and clinical picture of the illness in the family.

Adenoviridae Infections↗

PubMed1984

Actin mRNAs in HeLa cells. Stabilization after adenovirus infection.

We have carried out a comparative analysis of the expression of the actin genes in HeLa and adenovirus-infected HeLa cells. The rate of actin gene transcription was examined in these cells by pulse-labeling of the newly synthesized RNA and/or by in vitro transcription in nuclei isolated from uninfected or infected HeLa cells. In addition, accumulation of actin-specific heterogeneous nuclear RNA, and rate of appearance of the actin mRNAs in the cytoplasm were examined by dot and Northern blot analysis. The rate of actin gene transcription remained constant after infection of HeLa cells with adenovirus serotype 2, while the level of the actin precursor in the nuclei was slightly reduced. In the infected cells, newly synthesized actin mRNA enters the cytoplasm at a very reduced rate. The deficiency of transport does not affect the steady-state level of the messages in the cytoplasm. The half-life of cytoplasmic actin mRNAs was analyzed by traditional pulse-chase experiments and by a novel procedure using 5-6-diCl-1-beta-d-ribofuranosylbenzimidazole, which does not rely on labeled RNA. Both procedures gave identical results. Uninfected HeLa cells have actin mRNAs with relatively short half-lives, from less than six to 12 hours. In contrast, the half-lives of the actin-specific mRNAs, in the cytoplasm of adenovirus-infected cells, is greater than 14 to 24 hours. These observations suggest that, although the rate of transport of actin mRNAs to the cytoplasm is reduced upon infection with adenovirus, increased half-lives result in accumulation of actin mRNAs to normal levels in the cytoplasm.

Actins↗

PubMed1990

Adenovirus infection of differentiated F9 cells results in a global shut-off of differentiation-induced gene expression.

Previous experiments have demonstrated a link between transcriptional regulatory mechanisms acting during F9 cell differentiation and transcription control by the adenovirus E1A gene. We have isolated a number of differentiation-specific genes by cDNA cloning to determine if E1A exerts a coordinated control over differentiation specific gene expression. The mRNAs encoded by these cDNAs were undetectable or only barely detectable in undifferentiated cells but then rose in concentration upon differentiation. Analysis of transcription rates in isolated nuclei revealed that all but one of the genes was transcriptionally regulated during differentiation. Interestingly, alpha 2-type IV collagen expression was activated by a post-transcriptional mechanism since the gene was transcribed in both undifferentiated and differentiated cells whereas the cytoplasmic mRNA was undetectable in undifferentiated cells but rose in abundance in parallel with other regulated transcripts. Adenovirus infection of differentiated F9 cells reduced the cytoplasmic mRNA levels of each of the differentiation specific genes to near that found in the undifferentiated cell. Of those genes that were transcriptionally activated by differentiation, adenovirus infection specifically inhibited transcription. In contrast, although the alpha 2 collagen mRNA levels were reduced by adenovirus infection similar to the other mRNAs, the control was post-transcriptional since transcription of the gene was unaffected. Thus, the mechanism for loss of gene expression mediated by E1A reflects the mechanism by which the gene was activated during differentiation. Based on these results we suggest that E1A controls the expression of the F9 cell phenotype by targeting a regulatory activity acting early in the differentiation program.

Adenoviruses, Human↗

PubMed1992

Defective synthesis of early region 4 mRNAs during abortive adenovirus infections in monkey cells.

Human adenovirus 2 grows poorly in monkey cells, partly because of defects in late gene expression. Since deletions in early region 4 (E4) cause similar defects in late gene expression, we examined E4 mRNA expression in abortive infections. Processing of E4 mRNAs was defective during abortive infections, most likely at the level of splicing. At early times in productive infections in HeLa cells, the major E4 species produced is a 2-kb mRNA; at late times, a shift occurs so that smaller spliced E4 mRNAs are also produced. In CV-1 cells, a nonpermissive monkey cell line, this shift did not take place and only the 2-kb species was produced at late times, suggesting a defect in E4 mRNA splicing during abortive infections. The adenovirus DNA-binding protein (DBP) was required for normal processing of E4 mRNAs, since a host range mutant (hr602) containing an altered DBP gene showed a normal late E4 mRNA pattern in CV-1 cells; in addition, DBP was required during infections in HeLa cells for late E4 mRNA expression. DBP was not required for production of the late E4 pattern in transient expression assays in HeLa or 293 cells, suggesting that a second factor in addition to the DBP, present during infection but not transfection, modulates E4 mRNA processing.

Adenoviridae Infections↗

PubMed1995

Disseminated adenovirus infection associated with cutaneous and visceral hemorrhages in a nursing piglet.

An unusual adenovirus infection in a conventionally raised nursing pig was characterized clinically by hemorrhagic diathesis of the skin and microscopically by disseminated viral inclusions in the endothelial, interstitial, and epithelial cells of the skin, kidney, spleen, liver, heart, and small and large intestines. This disease was confirmed ultrastructurally by demonstration of typical adenoviral particles in the nuclei of endothelial cells in the myocardium and of interstitial cells in the small intestine. This is the first report of disseminated adenovirus infection in a nursing pig in North America.

Adenoviridae Infections↗