| Literature DB >> 2143875 |
D Pieniazek1, N J Pieniazek, D Macejak, R B Luftig.
Abstract
It had been postulated that due to lack of growth of enteric adenovirus 41 (Ad41) on human primary cells and its growth on Graham-293 cells there was a defect in the Ad41 E1A region. However, we found as a result of careful evaluation of Ad41 growth on several primary cell lines (HEK, WI-38, or Detroit 551) that efficient viral multiplication is possible if the serum concentration in the medium used postinfection (p.i.) is kept between 0.2 and 1%. In contrast, only slight growth of Ad41 occurs in infected cells maintained in 5% serum and virtually no viral replication is found in infected cells cultivated in medium with 10% serum. The serum inhibitory effect appears limited to primary cells because no difference in Ad41 replication, as assayed by accumulation of Ad41 DNA, was found in infected continuous cell lines (HEp-2, 293) cultivated p.i. in either 1 or 10% FBS. Also, this effect appears specific for enteric adenoviruses, such as Ad41, since conventional adenoviruses, such as Ad5, grow well in both 1 and 10% FBS. The above results show that Ad41 can grow in a variety of primary cell lines, under specific culture conditions. In addition, we found that Ad41-infected primary cells grown in medium containing 0.2% serum had an increase in synthesis of the 70-kDa heat shock protein (HSP70) at about 6 hr p.i. and also Ad41 was able to complement the Ad5 E1A deletion mutant dl312. These results show that the E1A function of Ad41 is not impaired in infected cells.Entities:
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Year: 1990 PMID: 2143875 DOI: 10.1016/0042-6822(90)90380-a
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616