Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The resistance of avian infectious bronchitis virus (IBV) to several chemical and physical treatments was studied. Ten strains, including four Japanese strains, were used. 1. All strains were sensitive to heating at 56 degrees C for 15 minutes; although two of them, KH and Massachusetts-41, were resistant to heating at 45 degrees C for 90 minutes. 2. All strains were resistant to pH 3.0 and most of the strains were sensitive to pH 11.0. 3. All strains were completely inactivated by chloroform and sodium deoxycholate and all except Beaudette-42 and Connaught were relatively stable to ether. 4. All strains rapidly lost their infectivities upon ultraviolet irradiation. 5. Trypsin did not affect the infectivity of any strain. 6. From these results, the ten strains were classified into three groups based on their stabilities to exposure to heating at 45 degrees C for 90 minutes and to ether.
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PMID:Studies on avian infectious bronchitis virus (IBV). I. Resistance of IBV to chemical and physical treatments. 3 36

To investigate the adaptation of avian infectious bronchitis virus (IBV) in a human cell line may be beneficial to understanding the potential mechanisms of coronavirus interspecies infection. The current study addressed the poor replication of IBV in the HeLa human cell line demonstrated in previous reports. We showed that IBV strains M41, H52, H120 and Gray could be propagated in HeLa cells with distinct cytopathic effect. The virus titre in freshly dispersed HeLa cells was 1000-fold higher than in cell monolayers. Trypsin was not the determinant for the viral replication, suggesting that the restriction of IBV replication in HeLa cells is the result of intracellular events rather than the binding to or fusion with host cells. These IBV strains replicated to an average titre of 10(3.4+/-0.2)/0.1 ml median tissue culture infectious doses in freshly dispersed HeLa cells and maintained this titre for the first 12 passages. Then an approximately 10-fold increase (10(4.20+/-0.19)/0.1 ml) occurred in passage 13, which was maintained to passage 16, after which there was another, bigger rise to 10(6.6+/-0.3)/0.1 ml in passage 17. This titre was maintained until passage 24 when the experiment was terminated. The IBV M41 S1 gene was amplified and sequenced for passages 0, 5 and 21. There was only one amino acid replacement in the S1 protein, in passage 21. The presence of sialic acid on HeLa cells contributed to efficient virus replication, while human aminopeptidase N was not involved in the infection. Haemagglutinin activity gradually reduced with increased passages. These results indicated that the virus adaptation would probably be determined by host cell modification such as receptor glycosylation and different receptor utilization instead of viral gene mutation.
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PMID:Infection of HeLa cells by avian infectious bronchitis virus is dependent on cell status. 1762 Jan 71