Analysis of human tonsil and cancer DNAs and RNAs for DNA sequences of group C (serotypes 1, 2, 5, and 6) human adenoviruses

Green, Maurice; Wold, William S.M.; Mackey, Jesse K.; Rigden, Patricia

doi:10.1073/pnas.76.12.6606

Cited by 92 publications

(40 citation statements)

References 22 publications

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“…Finally, this study is distinct from studies in which human sera have been analyzed to determine the relative contribution of neutralizing antibodies against each of the major capsid proteins (12,52,55,59,60,67,68,73,75,79) since those studies examined the effects of subsets of antibodies rather than whole, unfractionated neutralizing serum on the infectivity of Ad. While this report does not test the hypothesis that Fc receptor-mediated uptake of Ad-immune complexes could be a means of propagating a wild-type infection in a host organism, it is interesting that persistent subgroup C Ad infections have been reported in lymphoid tissue of humans and mice (13,15,18,31,38,51,54,58,64,72), where a high concentration of Fc receptor-bearing cells resides. Also of interest, follicular dendritic cells, T lymphocytes, and B lymphocytes are all capable of expressing Fc receptors (40,71) and persistent Ad infections have been noted in patients with neutralizing anti-Ad antibodies (64).…”

Section: Fig 8 Fc␥r-mediated Gene Transfer By Neutralizedmentioning

confidence: 81%

Neutralized Adenovirus-Immune Complexes Can Mediate Effective Gene Transfer via an Fc Receptor-Dependent Infection Pathway

Leopold

Wendland

Vincent

et al. 2006

J Virol

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Section: Fig 8 Fc␥r-mediated Gene Transfer By Neutralizedmentioning

confidence: 81%

Neutralized Adenovirus-Immune Complexes Can Mediate Effective Gene Transfer via an Fc Receptor-Dependent Infection Pathway

Leopold

Wendland

Vincent

et al. 2006

J Virol

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“…In immunocompetent people, Ad cause persistent, but self-limited infections (1,2). Although not oncogenic in humans, Ad are capable of transforming human cells in vitro to a state where the cells are tumorigenic in immunocompromised rodents (3,4). Cells transformed by Ad are virion free and only two viral genes (E1A and E1B) are consistently expressed (5).…”

mentioning

confidence: 99%

“…H uman adenoviruses (Ad) 3 are common human pathogens. In immunocompetent people, Ad cause persistent, but self-limited infections (1,2).…”

mentioning

confidence: 99%

Adenovirus E1A Oncogene Expression in Tumor Cells Enhances Killing by TNF-Related Apoptosis-Inducing Ligand (TRAIL)

Routes

Ryan²,

Clase³

et al. 2000

The Journal of Immunology

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Expression of the adenovirus serotype 5 (Ad5) E1A oncogene sensitizes cells to apoptosis by TNF-α and Fas-ligand. Because TNF-related apoptosis-inducing ligand (TRAIL) kills cells in a similar manner as TNF-α and Fas ligand, we asked whether E1A expression might sensitize cells to lysis by TRAIL. To test this hypothesis, we examined TRAIL-induced killing of human melanoma (A2058) or fibrosarcoma (H4) cells that expressed E1A following either infection with Ad5 or stable transfection with Ad5-E1A. E1A-transfected A2058 (A2058-E1A) or H4 (H4-E1A) cells were highly sensitive to TRAIL-induced killing, but Ad5-infected cells expressing equally high levels of E1A protein remained resistant to TRAIL. Infection of A2058-E1A cells with Ad5 reduced their sensitivity to TRAIL-dependent killing. Therefore, viral gene products expressed following infection with Ad5 inhibited the sensitivity to TRAIL-induced killing conferred by transfection with E1A. E1B and E3 gene products have been shown to inhibit TNF-α- and Fas-dependent killing. The effect of these gene products on TRAIL-dependent killing was examined by using Ad5-mutants that did not express either the E3 (H5dl327) or E1B-19K (H5dl250) coding regions. A2058 cells infected with H5dl327 were susceptible to TRAIL-dependent killing. Furthermore, TRAIL-dependent killing of A2058-E1A cells was not inhibited by infection with H5dl327. Infection with H5dl250 sensitized A2058 cells to TRAIL-induced killing, but considerably less than H5dl327-infection. In summary, expression of Ad5-E1A gene products sensitizes cells to TRAIL-dependent killing, whereas E3 gene products, and to a lesser extent E1B-19K, inhibit this effect.

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“…These viruses tend to become latent in the tonsils [4], the peripheral lymphocytes [5], and the lung [6]. The E1A region of the adenovirus was used as the target DNA for amplification in this study because this region of the virus is responsible for the transformation of the cells and for sensitizing the infected cells to cytolysis by tumour necrosis factor (TNF) [7], natural killer (NK) cells, and activated macrophages [8].…”

mentioning

confidence: 99%

Detection of adenovirus E1A DNA in pulmonary fibrosis using nested polymerase chain reaction

Kuwano¹,

Nomoto²,

Kunitake³

et al. 1997

Eur Respir J

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The history of patients with idiopathic pulmonary fibrosis (IPF)shows that the disease may be preceded by a viral-like illness. Although viruses have not been demonstrated, it is possible that viruses were not detected in culture because they do not replicate during latency.We investigated the presence of adenovirus in IPF and interstitial pneumonia associated with collagen vascular disease (CVD-IP), using the nested polymerase chain reaction (PCR) and in situ hybridization (ISH) for the E1A region of the adenovirus genome. Studies were performed on lung tissues obtained by transbronchial lung biopsy from 19 patients with IPF, 10 patients with CVD-IP and, for comparison, from 20 patients with sarcoidosis.The E1A DNA was present in 3 out of 19 (16%) cases of IPF, in 5 of 10 (50%) cases of CVD-IP, and in 2 of 20 (10%) cases of sarcoidosis. The incidence of E1A DNA in CVD-IP was significantly higher than that in sarcoidosis (p<0.05). In patients with IPF and CVD-IP, E1A DNA was more prevalent in patients treated with corticosteroids (6 out of 9 cases; 67%) than in those without it (2 out of 20 cases; 10%) (p<0.01). ISH studies showed that 1 out of 8 cases of IPF and CVD-IP, in which E1A DNA was detected by PCR, was positive for E1A DNA.We conclude that adenovirus E1A is unlikely to be aetiologically involved in the pathogenesis of idiopathic pulmonary fibrosis or interstitial pneumonia associated with collagen vascular disease. However, a latent adenovirus infection may be reactivated or may newly infect the host following corticosteroid administration.

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Analysis of human tonsil and cancer DNAs and RNAs for DNA sequences of group C (serotypes 1, 2, 5, and 6) human adenoviruses

Cited by 92 publications

References 22 publications

Neutralized Adenovirus-Immune Complexes Can Mediate Effective Gene Transfer via an Fc Receptor-Dependent Infection Pathway

Neutralized Adenovirus-Immune Complexes Can Mediate Effective Gene Transfer via an Fc Receptor-Dependent Infection Pathway

Adenovirus E1A Oncogene Expression in Tumor Cells Enhances Killing by TNF-Related Apoptosis-Inducing Ligand (TRAIL)

Detection of adenovirus E1A DNA in pulmonary fibrosis using nested polymerase chain reaction

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