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PubMed2002

Adenovirus infection of primary malignant lymphoid cells.

Adenovirus infection represents a cellular stress that induces host cell pro-apoptotic responses. To overcome this barrier to productive infection, viral polypeptides modulate a variety of host cell pathways. The interface of these early viral gene products with key cellular regulatory proteins has provided considerable information concerning basic cellular mechanisms operative in cell cycle regulation, transcriptional control and apoptosis. The overlap of these mechanisms with those impacted during oncogenesis provides the opportunity to use adenoviruses and adenovirus mutants to characterize the state of key regulatory pathways in specific malignant cells. For example, adenoviruses mediate cytotoxicity after infection of chronic lymphocytic leukemia (CLL) cells, mantle cell lymphoma (MCL) cells and multiple myeloma cell lines. Specific adenovirus mutants demonstrate enhanced cytotoxicity and, in many cases, apoptosis is not the primary mechanism of cell death. Analysis of these infections with respect to both the features of the primary malignant cell and the mechanisms of adenovirus-mediated cytotoxicity holds the prospect of providing novel insights into the status of key regulatory pathways in individual patient malignant cells. These studies also hold the prospect of supporting the development of specific attenuated adenoviruses as therapeutic agents with selective cytotoxicity for specific primary lymphoid malignancies.

Adenoviridae↗
PubMed1986

Interaction of immunosuppressive agents and human adenovirus infection in mice.

It was examined whether sensitivity of mice to human adenovirus infections is affected by immunosuppressive agents. Mice treated with the lymphotropic cytostatic dianhydrodulcitol (DAD) or antilymphocytic serum (ALS) did not become susceptible to human adenovirus type 12 infection, as the virus did not replicate--not even in its component forms--in the animals. On the other hand, the effect of both DAD and ALS on the lymphoid organs of mice was intensified by human adenovirus infection. In tissue cultures the reproduction of adenovirus was facilitated by DAD.

Adenoviridae Infections↗
PubMed2004

Identification of pretreatment agents to enhance adenovirus infection of bladder epithelium.

Adenovirus has been used widely as a gene transfer vector in the laboratory and clinic for the purpose of gene therapy. Conditionally replication-competent oncolytic adenoviruses are capable of multiplying up to a thousand old in target cells, a property that might prove to be of tremendous potential in the area of cancer therapy. Intravesicular therapy of refractory superficial bladder cancer employing an oncolytic adenovirus would allow for local administration and efficient delivery of virus to bladder tumor. The glycosaminoglycan layer on the surface of the bladder urothelium acts as a nonspecific antiadherence barrier and may be a significant roadblock to efficient infection of the urothelium by adenoviruses. Several laboratories have investigated the potential utility of bladder pretreatment with chemical agents to enhance the adenovirus infection of bladder urothelium but with limited success. A class of compounds has been identified that is effective for pretreatment of urothelium, permitting efficient adenoviral infection. In a murine model, pretreatment of the bladder with 0.1% dodecyl-beta-D-maltoside (DDM) or sodium dodecyl sulfate (SDS) for 5 min resulted in >90% transduction of the urothelial layer within 15 min after exposure to a replication-defective adenovirus compared to </=5% transduction in untreated bladders. DDM could be coformulated with adenovirus, and complete transduction of the urothelium was achieved following retention of the admixture in the bladder for 45 min. A similar enhancement of adenoviral infection following pretreatment of bladder with DDM and SDS was observed in a rat model. The use of these compounds may facilitate the development of adenovirus-based therapy for bladder cancer.

Adenoviridae↗
PubMed2005

A surveillance study of adenovirus infection in adult solid organ transplant recipients.

Little is known about adenovirus infections in adult organ transplant recipients. We prospectively assessed adenovirus infection in 263 transplant recipients using polymerase chain reaction (PCR) on plasma samples at regular intervals post-transplant. Adenovirus DNA was detected in 19 of 263 patients (7.2%). Viremia by transplant type was: liver (n = 10 of 121 [8.3%]), kidney (n = 6 of 92 [6.5%]) and heart (n = 3 of 45 [6.7%]). Time to viremia onset was within 10 days post-transplant (n = 4), on day 28 (n = 1), on day 100 (n = 7) and between months 6 and 12 (n = 7). At the time of viremia, 11 of 19 (58%) patients had no symptoms, 2 of 19 (10.5%) had gastrointestinal (GI) symptoms, 2 of 19 (10.5%) had respiratory symptoms and 4 patients (21%) had vague/non-specific symptoms. All patients recovered spontaneously. Only 1 of 19 (5%) patients had subsequent acute rejection. Adenovirus viremia is relatively common in adult liver, kidney and heart transplant recipients and most infections are asymptomatic, transient and self-limited. No serious clinical sequelae or effects on subsequent acute rejection were observed.

Adenoviridae↗
PubMed2003

Modulation of adenovirus infection in vitro by antisense oligodeoxynucleotides.

OBJECTIVE: Antisense oligodeoxynucleotides (ODNs) may represent a novel, airway directed approach to the treatment of adenovirus infection of the lung, for which no specific therapy exists. This study assessed the efficacy of antisense ODNs in modulating adenovirus infection in vitro. METHODOLOGY: A biological assay, which quantified viral plaque formation by wild type adenovirus 5 in a lung epithelial cell line (A549), was used to evaluate the inhibitory effect of a number of antisense ODNs targeted to the early (E) 1 A and protein IX genes of adenovirus 5. Antisense ODNs (20-21mers, phosphorothioate end-protected) were designed to straddle the initiation of translation (AUG) codon of the mRNA of the targeted gene. RESULTS: There was a consistent and significant (P < 0.005) reduction in viral plaque formation in those cells treated with an E1A antisense ODN, compared with the nonsense control ODN. Neither the addition of a cationic lipid (Lipofectamine), nor increasing the concentration of ODN from 1 micro mol to 15 micro mol enhanced the original inhibitory effect observed with the E1A antisense ODN. CONCLUSIONS: An antisense ODN targeted to the E1A gene can specifically inhibit adenovirus 5 infection in vitro, suggesting a potential therapeutic role for antisense ODNs in adenovirus infection of the lung.

Adenoviridae↗
PubMed2001

Adenovirus infections in adult recipients of blood and marrow transplants.

Adenoviruses are increasingly recognized pathogens that affect blood and marrow transplant (BMT) recipients. Experiences with 2889 adult BMT recipients were reviewed to study the incidence, clinical spectrum, risk factors for dissemination, response to therapy, and outcome of adenovirus infections. Eight-five patients (3%) were diagnosed by means of culture (n=85) or culture and histopathological examination (n=6). Nine patients had asymptomatic viruria, and 76 had symptomatic infections, which included upper respiratory tract infection (n=20), enteritis (n=18), hemorrhagic cystitis (n=10), pneumonia (n=15), and disseminated disease (n=13). The overall mortality rate was 26%. A higher mortality rate was observed among patients with pneumonia (73%) and disseminated disease (61%). Risk factors for dissemination included receipt of an allogeneic transplant, presence of graft-versus-host disease (GVHD), and receipt of concurrent immunosuppressive therapy. Intravenous ribavirin was not associated with an appreciable benefit among 12 patients who received this treatment. In conclusion, adenovirus infections are an important cause of morbidity and mortality in adult BMT recipients, particularly allogeneic transplant recipients with GVHD who are receiving immunosuppressive therapy. The need for an effective, nontoxic antiviral therapy is apparent.

Adenoviridae Infections↗
PubMed1983

Synthesis and processing of simian virus 40-specific RNA in adenovirus-infected, simian virus 40-transformed human cells.

Human simian virus 80 (SV80) cells transformed by simian virus 40 (SV40) synthesize substantial quantities of the SV40 large T-antigen (Henderson & Livingston, 1974; Tjian, 1978) and cytoplasmic, poly(A)-containing RNA species that exhibit spliced structures characteristic of the SV40, early messenger RNA species that encode both large and small T-antigens (Flint & Beltz, 1979). When SV80 cells were infected with type C adenovirus, both the synthesis of SV40 large T-antigen and the appearance in the cytoplasm of newly synthesized, SV40-specific RNA sequences were inhibited during the late phase of infection. The results of hybridization to SV40 DNA of SV80 nuclear RNA, prepared from mock- or adenovirus-infected cells after labeling for short periods in vivo or in vitro, indicated that transcription of integrated SV40 was, by contrast, not disrupted during the late phase of adenovirus infection. Poly(A)-containing, nuclear RNA species that hybridized to SV40 DNA sequences and exhibited the sizes of spliced, large and small T-antigen mRNA species were also synthesized in infected cells at a time when the corresponding mRNA sequences did not leave the nucleus. These results suggest that the failure of non-adenoviral mRNA sequences to enter the cytoplasm of adenovirus-infected cells does not reflect inhibition of either their transcription or the normal enzymatic processing reactions to which pre-mRNA species are subject. Several lines of evidence do, however, establish that nuclear, SV40-specific RNA sequences are less stable in adenovirus-infected compared to mock-infected SV80 cells.

Adenoviruses, Human↗
PubMed1994

Hemorrhagic cystitis due to adenovirus infection following bone marrow transplantation.

Immunocompromised patients are at significant risk for infection with adenovirus. We report 3 cases of hemorrhagic cystitis in patients following bone marrow transplantation. Of the patients 2 had positive viral urine cultures and 1 had positive stool culture but negative urine culture and biopsy proved viral cystitis. Diagnosis of adenovirus should be considered when gross hematuria follows bone marrow transplantation even when urine culture is negative for adenovirus.

Adenoviridae Infections↗
PubMed1999

Coxsackievirus and adenovirus receptor cytoplasmic and transmembrane domains are not essential for coxsackievirus and adenovirus infection.

Coxsackievirus and adenovirus receptor (CAR) from which the cytoplasmic domain had been deleted and glycosylphosphatidylinositol (GPI)-anchored CAR lacking both transmembrane and cytoplasmic domains were both capable of facilitating adenovirus 5-mediated gene delivery and infection by coxsackievirus B3. These results indicate that the CAR extracellular domain is sufficient to permit virus attachment and entry and that the presence of a GPI anchor does not prevent infection.

Adenoviridae↗
PubMed1985

Adenovirus infections in young children.

The importance of adenovirus in initiating respiratory disease in young children is stressed in this report. The incidence, clinical illness, asymptomatic carriage, and serologic response of acute adenovirus-associated infection are described in a carefully followed cohort of normal children cultured with each episode of febrile respiratory illness. During a 6-year period, 8.2% of 1,416 nasal washings obtained from sick infants and children less than 7 years of age yielded adenovirus. Adenoviruses were isolated from only 1/174 (0.6%) cultures taken from well children. Typing of 98 isolates showed 81% to be types 1 or 2. A greater than or equal to fourfold rise in neutralizing titer was seen in 45/59 (76%) sampled. In a subset of the cohort observed for 2-week periods in a day care setting, 14 of 21 well children (67%) exposed to symptomatic children with adenovirus infection developed febrile respiratory symptoms and shedding of the same serotype within 2 weeks of exposure. This study confirms that adenovirus has a high attack rate and causes significant respiratory disease in young children.

Adenoviridae Infections↗
PubMed1987

Adenovirus infections and respiratory illnesses in children in group day care.

Adenovirus infections and respiratory illnesses among 123 children attending a research day care center were analyzed from data collected prospectively from 1967 through 1981. During the 15-year study period, 298 adenovirus isolates were recovered from respiratory secretions of the study children, and five different serotypes were identified, with types 1, 2, and 5 accounting for 92% of the typed isolates. Annual incidence of each serotype varied greatly, with types 2 and 5 predominating before 1975 and type 1 thereafter. Exposure to adenovirus in the day care center correlated with acquisition of infection. Through two years of age, children were exposed to 3.4 +/- 0.9 (mean +/- SD) different serotypes and became infected by 2.1 +/- 0.8 different types. Most infections occurred before the child's second birthday, and incidence was highest from six to 12 months of age (1.4 primary infections/child-year). Mild and febrile illness accompanied 75% of primary isolations. Otitis media occurred in 37% of illnesses over all ages and in greater than 50% of illnesses among infants.

Adenoviridae Infections↗
PubMed1984

Effect of adenovirus infection on expression of human histone genes.

The influence of adenovirus type 2 infection of HeLa cells upon expression of human histone genes was examined as a function of the period of infection. Histone RNA synthesis was assayed after run-off transcription in nuclei isolated from mock-infected cells and after various periods of adenovirus infection. Histone protein synthesis was measured by [3H]leucine labeling of intact cells and fluorography of electrophoretically fractionated nuclear and cytoplasmic proteins. The cellular representation of RNA species complementary to more than 13 different human histone genes was determined by RNA blot analysis of total cellular, nuclear or cytoplasmic RNA by using a series of 32P-labeled cloned human histone genes as hybridization probes and also by analysis of 3H-labeled histone mRNA species synthesized in intact cells. By 18 h after infection, HeLa cell DNA synthesis and all parameters of histone gene expression, including transcription and the nuclear and cytoplasmic concentrations of core and H1 mRNA species, were reduced to less than 5 to 10% of the control values. By contrast, transcription and processing of other cellular mRNA sequences have been shown to continue throughout this period of infection. The early period of adenovirus infection was marked by an inhibition of transcription of histone genes that accompanied the reduction in rate of HeLa cell DNA synthesis. These results suggest that the adenovirus-induced inhibition of histone gene expression is mediated in part at the transcriptional level. However, the persistence of histone mRNA species at concentrations comparable to those of mock-infected control cells during the early phase of the infection, despite a reduction in histone gene transcription and histone protein synthesis, implies that histone gene expression is also regulated post-transcriptionally in adenovirus-infected cells. These results suggest that the tight coupling between histone mRNA concentrations and the rate of cellular DNA synthesis, observed when DNA replication is inhibited by a variety of drugs, is not maintained after adenovirus infection.

Adenoviruses, Human↗
PubMed1983

Control of cellular gene expression during adenovirus infection: induction and shut-off of dihydrofolate reductase gene expression by adenovirus type 2.

Infection of human cells by adenovirus results in multiple alterations of host gene expression. To examine the effects of viral infection on the expression of a single gene, a line of human cells was developed which is resistant to growth in methotrexate and which contains amplified RNA and protein specific for dihydrofolate reductase (DHFR). Cytogenetic evidence indicated the presence of amplified DNA. Adenovirus infection of these cells caused an induction and subsequent decline in the synthesis of DHFR protein. The maximum DHFR induction occurred 16 to 19 h after infection and reached a level 2.5-fold greater than that observed in uninfected cells. Induction of DHFR protein synthesis was accompanied by concomitant increases in the level of steady-state DHFR-specific cytoplasmic RNA. The relative rate of DHFR mRNA production (i.e., the appearance of DHFR-specific mRNA sequences in the cytoplasm) also increased 2.5-fold during induction. Later in infection, the relative rate of DHFR protein synthesis declined, reaching a level below that observed in uninfected cells. This decline was accompanied by a similar decline in the steady-state levels of DHFR RNA and in the relative rate of synthesis of DHFR mRNA. These data suggest that adenovirus infection controls DHFR gene expression by increasing and subsequently decreasing the relative rate at which DHFR-specific mRNA sequences appear in the cytoplasm and enter the pool of mRNA available for translation.

Adenovirus Infections, Human↗
PubMed1984

Nuclear-cytoplasmic transport and VAI RNA-independent translation of influenza viral messenger RNAs in late adenovirus-infected cells.

Influenza virus-specific proteins are synthesized at essentially the same levels in late adenovirus-infected HeLa cells as in cells not infected with adenovirus, indicating that influenza viral mRNA escapes the blocks exerted by adenovirus against host-cell mRNA expression-transport from the nucleus and translation. A significant proportion of the influenza viral mRNAs synthesized in these cells possesses the 5' ends of the major late adenovirus transcripts, resulting from capped RNA-primed initiation of influenza viral mRNA synthesis. We determined whether the ability of influenza viral mRNA to escape from the adenovirus-imposed blocks is due to utilization of the adenovirus-specific transport and translational systems because of the adenovirus 5' ends on the influenza viral mRNAs, or to establishment of influenza virus-specific transport and translational systems. Our results indicate that the second mechanism is operating, as the transport of influenza viral mRNAs from the nucleus and their translation is independent of the presence of adenovirus 5' ends. Furthermore, efficient translation of influenza viral mRNAs, but not of either adenovirus or host mRNAs, occurs in cells infected by the adenovirus deletion mutant dl331 , which does not synthesize VAI RNA ( Thimmappaya et al., 1982). Consequently, utilizing the translational machinery that had been inactivated by adenovirus, influenza virus establishes a system that selectively translates influenza viral mRNAs.

Adenoviruses, Human↗
PubMed1987

Adenovirus infection reverses the antiviral state induced by human interferon.

HeLa cells treated with human lymphoblastoid interferon do not synthesize poliovirus proteins. The antiviral state against poliovirus is reversed if cells are previously infected with adenovirus type 5. A late gene product seems to be involved in this reversion, since no effect is observed at early stages of infection or in the presence of aphidicolin.

Adenine Nucleotides↗
PubMed2001

[Studies on epidemic feature of enteric adenoviruses infection in feces of infants with diarrhea in Shenzhen].

OBJECTIVE: To estimate the enteric adenoviruses infection in feces of infants with diarrhea in Shenzhen. METHODS: All 195 fecal samples of infants were tested by PCR. Amplimers were analysed by Rsa I endonucleases and the type of enteric adenovirus identified. RESULTS: The positive rate of adenovirus DNA in fecal samples was 13.33% (26/195) while the prevalence rates of enteric adenovirus type 40, adenovirus type 41 and the other type of adenovirus were 2.56% (5/195), 8.21% (16/195) and 2.56% (5/195) respectively. Fever was the characteristic symptom of adenovirus infection. CONCLUSION: Enteric adenovirus type 40 and 41 were important pathogens which caused infant diarrhea in Shenzhen, with latter the majorty.

Adenoviridae Infections↗