Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Serial undiluted passages of infectious bursal disease virus in chick embryo cells were accompanied by a von Magnus type fluctuation of infectivity in viral harvests and a gradual decrease of plaque size. From the 9th undiluted passage on, the whole virus population consisted of small plaque-forming virus. The small plaque size remained constant when subsequent infections were carried out at low multiplicities. Small plaque virus interfered with the replication of large plaque standard virus. The small plaque/low yield mutation favoured the generation of defective particles which could be separated from complete particles by their lower densities in CsCl-gradients, where six fractions became visible and could be analyzed separately. Most of the defective virus particles had lost the larger of their two dsRNA segments and showed an aberrant protein composition. They had a very low residual infectivity and were also able to interfere with the replication of complete virus.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0168-1702(86)90008-0 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!