pubmed-article:669819 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0029347 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0597363 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0042960 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C1549078 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C1997894 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0220825 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C1551074 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C1553024 | lld:lifeskim |
pubmed-article:669819 | lifeskim:mentions | umls-concept:C0042645 | lld:lifeskim |
pubmed-article:669819 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:669819 | pubmed:dateCreated | 1978-9-30 | lld:pubmed |
pubmed-article:669819 | pubmed:abstractText | The Hong Kong/68-ts-1[E] virus and its Udorn/72 and Georgia/74 recombinants, which have a 38 degrees C shutoff temperature and a ts lesion(s) on the genes coding for the P3 and NP proteins, were adequately attenuated and immunogenic in adult volunteers who lacked serum hemagglutination-inhibiting antibody (titer, </=1:8), but who possessed serum neuraminidase-inhibiting antibody. Two Victoria/75-ts-1[E] clones that also had a 38 degrees C shutoff temperature and a ts lesion(s) on the same two genes were administered to adult volunteers who lacked both serum hemagglutination-inhibiting antibody (titer, </=1:8) and neuraminidase-inhibiting antibody (titer, </=1:4). In contrast to the behavior of the earlier ts-1[E] recombinants, the Vic/75-ts-1[E] recombinants retained the capacity to cause febrile, systemic illness. However, the recombinants were attenuated compared with wild-type virus. The Vic/75-ts-1[E] virus vaccinees shed a larger amount of virus for a longer time than the previous ts-1[E] vaccinees, but they shed less virus than volunteers infected with wild-type virus. The ts-1[E] virus shed retained its ts phenotype in most instances and failed to spread to susceptible contacts. Vaccinees were partially protected against homologous wild-type virus challenge. The failure of HK/68, Udorn/72, and Georgia/74 ts-1[E] vaccinees to develop systemic reactions may reflect the presence of neuraminidase immunity before infection. In this situation, attenuation probably resulted from the degree of defectiveness of the ts-1[E] recombinant virus and the existence of neuraminidase immunity in the recipients. The 50% human infectious dose of the Vic/75 ts-1[E] virus was less than 10(5.2) 50% tissue culture infective doses. This suggests that at the time of a pandemic shift involving both the hemagglutinin and neuraminidase glycoproteins, a small amount of live virus vaccine might be effective in initiating infection. | lld:pubmed |
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pubmed-article:669819 | pubmed:language | eng | lld:pubmed |
pubmed-article:669819 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:669819 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:669819 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:669819 | pubmed:month | Jun | lld:pubmed |
pubmed-article:669819 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:LevineM MMM | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:ChanockR MRM | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:DouglasR GRG | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:KendalA PAP | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:CouchR BRB | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:WatermanD HDH | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:MurphyB RBR | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:BettsR FRF | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:CateT RTRJr | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:HolleyH PHPJr | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:MarkoffL JLJ | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:HosierN TNT | lld:pubmed |
pubmed-article:669819 | pubmed:author | pubmed-author:RusselI III | lld:pubmed |
pubmed-article:669819 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:669819 | pubmed:volume | 20 | lld:pubmed |
pubmed-article:669819 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:669819 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:669819 | pubmed:pagination | 671-7 | lld:pubmed |
pubmed-article:669819 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:669819 | pubmed:year | 1978 | lld:pubmed |
pubmed-article:669819 | pubmed:articleTitle | Temperature-sensitive mutants of influenza A virus: evaluation of A/Victoria/3/75-ts-1[E] recombinant viruses in volunteers. | lld:pubmed |
pubmed-article:669819 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:669819 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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