A host-cell-selected variant of influenza B virus with a single nucleotide substitution in HA affecting a potential glycosylation site was attentuated in virulence for volunteers

1990 ◽  
Vol 110 (1-2) ◽  
pp. 37-46 ◽  
Author(s):  
J. S. Oxford ◽  
G. C. Schild ◽  
T. Corcoran ◽  
R. Newman ◽  
D. Major ◽  
...  
2004 ◽  
Vol 74 (2) ◽  
pp. 336-343 ◽  
Author(s):  
Takehiko Saito ◽  
Yoko Nakaya ◽  
Takashi Suzuki ◽  
Reiko Ito ◽  
Toshinori Saito ◽  
...  

1967 ◽  
Vol 126 (1) ◽  
pp. 93-108 ◽  
Author(s):  
Jean Lindenmann ◽  
Paul A. Klein

A2G mice could be solidly immunized against the Ehrlich ascites tumor by single intraperitoneal injections of homogenized and lyophilized tumor cells which had been infected with oncolytic strains of influenza A virus. Similar homogenates from noninfected tumor cells were not immunogenic, even when mixed with egg-grown virus. The immunizing principle in viral oncolysates could not be separated from the oncolytic virus by differential centrifugation or adsorption to and elution from red cells. It could be inhibited by antibody raised in rabbits against the egg-grown oncolytic virus. This reaction showed serologic specificity. Thus, the immunogenicity of an oncolysate produced with the WSA strain of neurotropic influenza virus could be inhibited by rabbit anti-WSA, but not by rabbit antibody to the TUR strain of fowl plague virus. Conversely, the immunogenicity of an oncolysate prepared with the TUR strain could be inhibited by rabbit anti-TUR, but not by anti-WSA. When mice were preimmunized (primed) with egg-grown WSA virus, their antitumor response to a later injection of WSA oncolysate was of the anamnestic type. Priming with egg-grown influenza B virus had no such effect. It was concluded that the immunogenicity of certain host cell components was greatly increased by incorporation into the makeup of the oncolytic virus.


1955 ◽  
Vol 101 (4) ◽  
pp. 437-450 ◽  
Author(s):  
Edwin D. Kilbourne ◽  

The administration of cortisone to chick embryos inoculated with large quantities of inactive influenza B virus results in a rate of viral increase greater than is concommittantly observed with inocula of comparable infectivity which are devoid of inactive particles. Thus, more than a mere negation of autointerference is effected. It is concluded that in the presence of cortisone reactivation has occurred of non-infective virus to a state in which it can participate in viral synthesis. Cortisone-induced viral reactivation is dependent upon a high partide/cell ratio and is thus analogous to the previously described phenomenon of "multiplicity reactivation." Cortisone does not influence either homologous or heterologous viral interference unless reactivation of the inactive interfering virus occurs. Virus reactivable with cortisone possesses both interfering and enzymatic properties. Reactivation of virus with cortisone cannot be effected in vitro but is mediated by the host cell. Two hypotheses concerning the action of cortisone are presented.


2013 ◽  
Vol 19 (3) ◽  
pp. 511-512 ◽  
Author(s):  
Rogier Bodewes ◽  
Danny Morick ◽  
Gerrie de Mutsert ◽  
Nynke Osinga ◽  
Theo Bestebroer ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (1) ◽  
pp. e0116302 ◽  
Author(s):  
Nipaporn Tewawong ◽  
Kamol Suwannakarn ◽  
Slinporn Prachayangprecha ◽  
Sumeth Korkong ◽  
Preeyaporn Vichiwattana ◽  
...  

Vaccines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 800
Author(s):  
Jongsuk Mo ◽  
Stivalis Cardenas-Garcia ◽  
Jefferson J. S. Santos ◽  
Lucas M. Ferreri ◽  
C. Joaquín Cáceres ◽  
...  

Influenza B virus (IBV) is a major respiratory pathogen of humans, particularly in the elderly and children, and vaccines are the most effective way to control it. In previous work, incorporation of two mutations (E580G, S660A) along with the addition of an HA epitope tag in the PB1 segment of B/Brisbane/60/2008 (B/Bris) resulted in an attenuated strain that was safe and effective as a live attenuated vaccine. A third attempted mutation (K391E) in PB1 was not always stable. Interestingly, viruses that maintained the K391E mutation were associated with the mutation E48K. To explore the contribution of the E48K mutation to stability of the K391E mutation, a vaccine candidate was generated by inserting both mutations, along with attenuating mutations E580G and S660A, in PB1 of B/Bris (B/Bris PB1att 4M). Serial passages of the B/Bris PB1att 4M vaccine candidate in eggs and MDCK indicated high stability. In silico structural analysis revealed a potential interaction between amino acids at positions 48 and 391. In mice, B/Bris PB1att 4M was safe and provided complete protection against homologous challenge. These results confirm the compensatory effect of mutation E48K to stabilize the K391E mutation, resulting in a safer, yet still protective, IBV LAIV vaccine.


Author(s):  
Hiroshi Yamagishi ◽  
Megumi Jikuya ◽  
Kanako Okushiro ◽  
Ayako Hashimoto ◽  
Asumi Fukunaga ◽  
...  

AbstractCytoplasmic male sterility (CMS) observed in many plants leads defect in the production of functional pollen, while the expression of CMS is suppressed by a fertility restorer gene in the nuclear genome. Ogura CMS of radish is induced by a mitochondrial orf138, and a fertility restorer gene, Rfo, encodes a P-type PPR protein, ORF687, acting at the translational level. But, the exact function of ORF687 is still unclear. We found a Japanese variety showing male sterility even in the presence of Rfo. We examined the pollen fertility, Rfo expression, and orf138 mRNA in progenies of this variety. The progeny with Type H orf138 and Rfo showed male sterility when their orf138 mRNA was unprocessed within the coding region. By contrast, all progeny with Type A orf138 were fertile though orf138 mRNA remained unprocessed in the coding region, demonstrating that ORF687 functions on Type A but not on Type H. In silico analysis suggested a specific binding site of ORF687 in the coding region, not the 5′ untranslated region estimated previously, of Type A. A single nucleotide substitution in the putative binding site diminishes affinity of ORF687 in Type H and is most likely the cause of the ineffectiveness of ORF687. Furthermore, fertility restoration by RNA processing at a novel site in some progeny plants indicated a new and the third fertility restorer gene, Rfs, for orf138. This study clarified that direct ORF687 binding to the coding region of orf138 is essential for fertility restoration by Rfo.


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