EM study of fastidious adenovirus type 40 replicationin vitro

Ujfalusi, Mária J.; Kidd, Alistair H.; Bd, Schoub

doi:10.1007/bf01310820

Cited by 3 publications

(3 citation statements)

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“…Thus, the RGD loop appears to be important but dispensable for viral entry, possibly due to a surrogate YGD integrin binding motif on the virus. It is intriguing that HAdV-F40 and -F41, which are relatively fastidious enteric viruses (28, 31), also lack the penton base protein RGD motif and express the penton base YGD motif (28, 29). It is unknown at present whether the YGD on the adenovirus penton base protein is exposed sufficiently to interact with cellular integrins during virus attachment and entry.…”

Section: Discussionmentioning

confidence: 99%

Predicting the Next Eye Pathogen: Analysis of a Novel Adenovirus

Robinson

Zhou

Rajaiya

et al. 2013

mBio

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For DNA viruses, genetic recombination, addition, and deletion represent important evolutionary mechanisms. Since these genetic alterations can lead to new, possibly severe pathogens, we applied a systems biology approach to study the pathogenicity of a novel human adenovirus with a naturally occurring deletion of the canonical penton base Arg-Gly-Asp (RGD) loop, thought to be critical to cellular entry by adenoviruses. Bioinformatic analysis revealed a new highly recombinant species D human adenovirus (HAdV-D60). A synthesis of in silico and laboratory approaches revealed a potential ocular tropism for the new virus. In vivo, inflammation induced by the virus was dramatically greater than that by adenovirus type 37, a major eye pathogen, possibly due to a novel alternate ligand, Tyr-Gly-Asp (YGD), on the penton base protein. The combination of bioinformatics and laboratory simulation may have important applications in the prediction of tissue tropism for newly discovered and emerging viruses.

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Section: Discussionmentioning

confidence: 99%

Predicting the Next Eye Pathogen: Analysis of a Novel Adenovirus

Robinson

Zhou

Rajaiya

et al. 2013

mBio

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“…Cells were chosen which were known to support the growth of subgroup F adenoviruses to a limited degree (Chang conjuctival cultures) [12,27,31], or not at all (HEF cultures) [6]. Ad41 late antigen synthesis in the presence or absence of Ad 2 was monitored exclusively using a subgroup F specific monoclonal antibody and the fluorescence test was rendered as sen- There have been several other reports of members of different adenovirus subgroups complementing each other for some necessary functions [17-19, 21, 32, 33].…”

Section: Discussionmentioning

confidence: 99%

Helper function of adenovirus 2 for adenovirus 41 antigen synthesis in semi-permissive and non-permissive cells

Tiemessen

Kidd

1988

Archives of Virology

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Using a fluorescent focus assay, complementation and interference effects of Ad2 and Ad41 on each other in mixed infection were investigated. Ad2 provided a helper function for Ad41 late antigen synthesis in cells normally non-permissive for Ad41 growth (HEF cells), and enhanced Ad41 late antigen synthesis in semi-permissive Chang conjunctival cells. The degree of complementation by Ad2 was dependent on its input concentration. In addition, interference by Ad41 on Ad2 replication was seen in HEF cells. The degree of interference by Ad41 was dependent on the relative time of infection by each serotype. The complementation results in HEF cells suggest an absolute dependency of Ad41 on an adenovirus helper function in these cells. The results presented are consistent with the postulated helper function provided in trans by 293 cells, which are transformed by Ad5 early region 1.

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“…They were initially recognized by electron microscopy as adenoviruses which were present in high concentration in stools from children with gastroenteritis, but they could not be isolated in cells normally used for the isolation and propagation of human adenoviruses (12,29). The subsequent finding that the fastidious enteric adenoviruses (FEAds) could be grown in 293 cells (34), a continuous line of human embryonic kidney cells transformed with Ad5 DNA (14), has facilitated the laboratory identification and epidemiological analysis of these viruses (6,7,21,36,37).…”

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confidence: 99%

A block in release of progeny virus and a high particle-to-infectious unit ratio contribute to poor growth of enteric adenovirus types 40 and 41 in cell culture

Brown

Wilson-Friesen

Doane

1992

J Virol

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The fastidious enteric adenovirus (FEAd) types 40 (Ad4O) and 41 (Ad4l) are found in stool specimens of infants and young children in association with gastroenteritis. Although they can be isolated routinely from clinical specimens by using 293 cells, they are propagated with variable success in cell lines which support the replication of other adenovirus serotypes. HeLa cells are generally considered to be nonpermissive for the replication of FEAds, but in this study, Ad4O and Ad4l grew to comparable titers in individual 293 and HeLa cells. However, virus was not efficiently released from infected HeLa cells and thus did not undergo multiple cycles of infection in HeLa cell cultures. The block in virus release was not overcome in KB18 cells which, like 293 cells, constitutively express proteins encoded by the E1B region of a subgroup C adenovirus (in this case Ad2). Moreover, it was apparent from these studies that Ad4O and Ad41 have particle-to-infectious unit ratios several orders of magnitude greater than that for AdS, even in 293 cells which express the ElA and E1B proteins of Ad5 and are considered to be permissive for replication of the FEAds. Neither the block in release of progeny virus nor the high particle-to-infectious unit ratio is explained solely by the defect in expression of the E1B 55K protein identified by Mautner et al. (V.

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EM study of fastidious adenovirus type 40 replicationin vitro

Cited by 3 publications

References 4 publications

Predicting the Next Eye Pathogen: Analysis of a Novel Adenovirus

Predicting the Next Eye Pathogen: Analysis of a Novel Adenovirus

Helper function of adenovirus 2 for adenovirus 41 antigen synthesis in semi-permissive and non-permissive cells

A block in release of progeny virus and a high particle-to-infectious unit ratio contribute to poor growth of enteric adenovirus types 40 and 41 in cell culture

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