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

1993

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The subgroup F adenoviruses were tested for their ability to induce interferon in semi-permissive human cells (Chang conjunctiva) and non-permissive cells (HEF, human embryo lung fibroblasts). These cells did not produce interferon spontaneously or in response to infection by either of these adenoviruses. It was concluded that interferon induction in response to subgroup F adenovirus infection is not a likely explanation of limited virus growth in culture. Adenovirus 40 and Ad41, unlike Ad2, were found to be sensitive to human lymphoblastoid interferon in Chang conjunctival cells. The addition of Ad2 to cells before pretreatment with interferon resulted in the partial and complete abrogation of Ad40 and Ad41 interferon sensitivity, respectively. The suppressive effect of Ad2 on the inhibitory action of interferon and the modulatory function of Ad2 in mixed infection with either Ad40 or Ad41 suggests the inadequate functioning of a subgroup F adenovirus gene product or products involved in suppression of the interferon-induced antiviral state.

Section: Interferon Sensitivitymentioning

confidence: 99%

Section: Indirect Immunofluorescencementioning

confidence: 99%

Sensitivity of subgroup F adenoviruses to interferon

1993

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“…We have shown recently, using a fluorescent focus assay with a subgroup F specific monoclonal antibody, that Ad 2 can provide a helper function for Ad 41 in cells otherwise non-permissive or semi-permissive for Ad 41 growth [26]. The same assay was employed in this study to monitor Ad41 counts in relation to virus dilution.…”

mentioning

confidence: 93%

Adenovirus 41 growth in semi-permissive cells shows multiple-hit kinetics

1990

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Adenovirus type 41 infection of semi-permissive Chang conjunctival cells, monitored by fluorescent focus assay, followed multiple-hit kinetics. In non-permissive human cells, type 41 showed infectivity with two-hit kinetics in the presence of type 2. Type 41 infectivity was seen to be directly proportional to input concentration (one-hit) only in 293 cells, a continuous human line expressing Ad 5 E1 products.

“…We have previously suggested coinfection with other adenoviruses as a potential promoter of subgroup F adenovirus infection in vivo by showing that Ad2 provides a helper function for Ad41 growth in vitro [19]. If this mechanism were entirely responsible for their potentiation, however, then other adenoviruses would be isolated more frequently from stools together with the subgroup F adenoviruses.…”

mentioning

confidence: 97%

“…They are characteristically defective for growth in cell lines which support the growth of other human adenoviruses [4]. Since large numbers of particles are shed during Ad 40 and Ad 41 infection in vivo [-6, 17] it has been suggested by us and others that some cellular product(s) may be involved in the potentiation of subgroup F adenovirus replication [13,19].…”

mentioning

confidence: 99%

Subgroup F adenovirus growth in foetal intestinal organ cultures

Ujfalusi

1993

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An in vitro foetal intestinal organ culture system was employed to determine the permissiveness of human intestinal cells for subgroup F adenovirus infection. Ad40 and Ad41 growth, monitored through group-specific hexon antigen production, was poor in comparison to that of Ad2 in these cultures, further demonstrating their fastidious nature in most human cells. The low growth capability of these viruses in culture, in relation to their association with gastrointestinal disease is discussed.