scholarly journals VACCINATION AGAINST YELLOW FEVER WITH IMMUNE SERUM AND VIRUS FIXED FOR MICE

1932 ◽  
Vol 55 (6) ◽  
pp. 945-969 ◽  
Author(s):  
W. A. Sawyer ◽  
S. F. Kitchen ◽  
Wray Lloyd
Keyword(s):  
Yellow Fever ◽  
Room Temperature ◽  
Yellow Fever Virus ◽  
Single Injection ◽  
Immune Serum ◽  
Fever Virus ◽  
Human Immune ◽  
Yellow Fever Vaccination ◽  
Observation Period

1. After preliminary experiments in monkeys, 15 persons were actively immunized by a single injection of a dried mixture of living yellow fever virus, fixed for mice, and human immune serum, with separate injections of enough additional serum to make up the amount required for protection. 2. One person was similarly immunized by injecting immune serum and dried virus separately. 3. By titration of the sera of vaccinated persons in mice, it was shown that the immunity rose in a few weeks to a height comparable to that reached after an attack of yellow fever, and remained there throughout an observation period of 6 months. 4. Yellow fever virus could not be recovered from the blood of vaccinated persons or monkeys, except when the latter had received less than the minimal effective amount of immune serum. 5. Neutralization of yellow fever virus by immune serum took place very slowly in vitro at room temperature in our experiments, and could not have been an appreciable factor in vaccination with the serum virus mixtures. 6. A mixture of fixed virus and immune serum retained its immunizing power for 8 months when dried in the frozen state and sealed in glass. 7. It appears that the immunizing reaction after yellow fever vaccination was a part of a true infectious process, as was also the observed leucopenia.

scholarly journals Yellow Fever Virus Down-Regulates mRNA Expression of SOCS1 in the Initial Phase of Infection in Human Cell Lines

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 802
Author(s):  
Michael B. Yakass ◽  
David Franco ◽  
Osbourne Quaye
Keyword(s):  
Mrna Expression ◽  
Yellow Fever ◽  
Yellow Fever Virus ◽  
Expression Patterns ◽  
Fever Virus ◽  
Effective Vaccine ◽  
Interferon Β ◽  
Infected Cells ◽  
Insight Into

Flaviviruses are constantly evolving diverse immune evasion strategies, and the exploitation of the functions of suppressors of cytokine signalling (SOCS) and protein inhibitors of activated STATs (PIAS) to favour virus replication has been described for Dengue and Japanese encephalitis viruses but not for yellow fever virus (YFV), which is still of global importance despite the existence of an effective vaccine. Some mechanisms that YFV employs to evade host immune defence has been reported, but the expression patterns of SOCS and PIAS in infected cells is yet to be determined. Here, we show that SOCS1 is down-regulated early in YFV-infected HeLa and HEK 293T cells, while SOCS3 and SOCS5 are not significantly altered, and PIAS mRNA expression appears to follow a rise-dip pattern akin to circadian-controlled genes. We also demonstrate that YFV evades interferon-β application to produce comparable viral titres. This report provides initial insight into the in vitro expression dynamics of SOCS and PIAS upon YFV infection and a basis for further investigation into SOCS/PIAS expression and how these modulate the immune response in animal models.

scholarly journals Yellow fever virus is susceptible to sofosbuvir both in vitro and in vivo

2019 ◽  
Vol 13 (1) ◽  
pp. e0007072 ◽  
Author(s):  
Caroline S. de Freitas ◽  
Luiza M. Higa ◽  
Carolina Q. Sacramento ◽  
André C. Ferreira ◽  
Patrícia A. Reis ◽  
...  
Keyword(s):  
Yellow Fever ◽  
Yellow Fever Virus ◽  
Fever Virus

scholarly journals Ontogeny of different subsets of yellow fever virus-specific circulatory CXCR5+ CD4+ T cells after yellow fever vaccination

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Quinn DeGottardi ◽  
Theresa J. Gates ◽  
Junbao Yang ◽  
Eddie A. James ◽  
Uma Malhotra ◽  
...  
Keyword(s):  
T Cells ◽  
Yellow Fever ◽  
Germinal Center ◽  
Yellow Fever Virus ◽  
Fever Virus ◽  
Mass Cytometry ◽  
Follicular Helper ◽  
Potential Biomarker ◽  
Yellow Fever Vaccination ◽  
The Relationship

Abstract Monitoring the frequency of circulatory CXCR5+ (cCXCR5+) CD4+ T cells in periphery blood provides a potential biomarker to draw inferences about T follicular helper (TFH) activity within germinal center. However, cCXCR5+ T cells are highly heterogeneous in their expression of ICOS, PD1 and CD38 and the relationship between different cCXCR5 subsets as delineated by these markers remains unclear. We applied class II tetramer reagents and mass cytometry to investigate the ontogeny of different subsets of cCXCR5+ T cell following yellow fever immunization. Through unsupervised analyses of mass cytometry data, we show yellow fever virus-specific cCXCR5 T cells elicited by vaccination were initially CD38+ICOS+PD1+, but then transitioned to become CD38+ICOS−PD1+ and CD38−ICOS−PD1+ before coming to rest as a CD38−ICOS−PD1− subset. These results imply that most antigen-specific cCXCR5+ T cells, including the CD38−ICOS−PD1− CXCR5+ T cells are derived from the CXCR5+CD38+ICOS+PD1+ subset, the subset that most resembles preTFH/TFH in the germinal center.

CULTURE OF YELLOW-FEVER VIRUS IN VITRO

The Lancet ◽  
1940 ◽  
Vol 236 (6102) ◽  
pp. 163-164 ◽  
Author(s):  
G.M. Findlay ◽  
F.O. Maccallum
Keyword(s):  
Yellow Fever ◽  
Yellow Fever Virus ◽  
Fever Virus

scholarly journals High Fidelity of Yellow Fever Virus RNA Polymerase

2004 ◽  
Vol 78 (2) ◽  
pp. 1032-1038 ◽  
Author(s):  
Konstantin V. Pugachev ◽  
Farshad Guirakhoo ◽  
Simeon W. Ocran ◽  
Fred Mitchell ◽  
Megan Parsons ◽  
...  
Keyword(s):  
Dengue Virus ◽  
Rna Polymerase ◽  
Yellow Fever ◽  
Error Rate ◽  
Yellow Fever Virus ◽  
Protein A ◽  
Fever Virus ◽  
Genome Replication ◽  
Virus Rna

ABSTRACT Three consecutive plaque purifications of four chimeric yellow fever virus-dengue virus (ChimeriVax-DEN) vaccine candidates against dengue virus types 1 to 4 were performed. The genome of each candidate was sequenced by the consensus approach after plaque purification and additional passages in cell culture. Our data suggest that the nucleotide sequence error rate for SP6 RNA polymerase used in the in vitro transcription step to initiate virus replication was as high as 1.34 × 10−4 per copied nucleotide and that the error rate of the yellow fever virus RNA polymerase employed by the chimeras for genome replication in infected cells was as low as 1.9 × 10−7 to 2.3 × 10−7. Clustering of beneficial mutations that accumulated after multiple virus passages suggests that the N-terminal part of the prM protein, a specific site in the middle of the E protein, and the NS4B protein may be essential for nucleocapsid-envelope interaction during flavivirus assembly.

scholarly journals THE ADAPTATION OF UNMODIFIED STRAINS OF YELLOW FEVER VIRUS TO CULTIVATION IN VITRO

1937 ◽  
Vol 65 (6) ◽  
pp. 801-808 ◽  
Author(s):  
Hugh H. Smith ◽  
Max Theiler
Keyword(s):  
Brain Tissue ◽  
Yellow Fever ◽  
Mouse Embryo ◽  
Yellow Fever Virus ◽  
Fever Virus ◽  
In Vitro Cultivation ◽  
Virus Content ◽  
Cultivation In Vitro ◽  
Embryo Brain

1. In a search for suitable tissues for the cultivation of yellow fever virus in vitro, mouse embryos were inoculated with this virus in utero. A titration for virus content of the various organs of the embryos indicated that the virus was present in the brain in greatest concentration. 2. Unmodified strains of yellow fever virus were readily adapted to cultivation in vitro in a medium consisting of minced mouse embryo brain tissue and Tyrode solution containing 10 per cent normal monkey serum. 3. After a continued cultivation in mouse embryo brain tissue cultures for twenty to twenty-five subcultures, these strains were readily adapted to cultivation in whole mouse embryo tissue medium. 4. There is evidence to indicate that a prolonged cultivation of the virus in mouse embryo brain medium increases its neurotropic properties. 5. Attempts to employ monkey tissues for in vitro cultivation of yellow fever virus gave entirely negative results.

scholarly journals AT-752, a double prodrug of a guanosine nucleotide analog, inhibits yellow fever virus in a hamster model

2021 ◽  
Author(s):  
Kai Lin ◽  
Steven S Good ◽  
Justin G. Julander ◽  
Abbie Weight ◽  
Adel Moussa
Keyword(s):  
Yellow Fever ◽  
Yellow Fever Virus ◽  
Limit Of Detection ◽  
Virus Titer ◽  
Fever Virus ◽  
Effective Vaccine ◽  
Hamster Model ◽  
Nucleotide Analog

Yellow fever virus (YFV) is a zoonotic pathogen re-emerging in parts of the world, causing a viral hemorrhagic fever associated with high mortality rates. While an effective vaccine is available, having an effective antiviral against YFV is critical against unexpected outbreaks, or when vaccination is not recommended. We have previously identified AT-281, the free base of AT-752, an orally available double prodrug of a guanosine nucleotide analog, as a potent inhibitor of YFV in vitro , with a 50% effective concentration (EC 50 ) of 0.31 µM. In hamsters infected with YFV (Jimenez strain), viremia rose about 4 log 10 -fold and serum alanine aminotransferase (ALT) 2-fold compared to sham-infected animals. Treatment with 1000 mg/kg AT-752 for 7 days, initiated 4 h prior to viral challenge, reduced viremia to below the limit of detection by day 4 post infection (pi) and returned ALT to normal levels by day 6 pi. When treatment with AT-752 was initiated 2 days pi, the virus titer and ALT dropped >2 log 10 and 53% by day 4 and 6 pi, respectively. In addition, at 21 days pi, 70 – 100% of the infected animals in the treatment groups survived compared to 0% of the untreated group (p<0.001). Moreover, in vivo formation of the active triphosphate metabolite AT-9010 was measured in the animal tissues, with the highest concentrations in liver and kidney, organs that are vulnerable to the virus. The demonstrated in vivo activity of AT-752 suggests that it is a promising compound for clinical development in the treatment of YFV infection.

scholarly journals Detection of Anti-Yellow Fever Virus Immunoglobulin M Antibodies at 3–4 Years Following Yellow Fever Vaccination

2012 ◽  
Vol 87 (6) ◽  
pp. 1112-1115 ◽  
Author(s):  
Katherine B. Gibney ◽  
Olga I. Kosoy ◽  
Marc Fischer ◽  
Srilatha Edupuganti ◽  
Robert S. Lanciotti ◽  
...  
Keyword(s):  
Yellow Fever ◽  
Yellow Fever Virus ◽  
Immunoglobulin M ◽  
Fever Virus ◽  
Yellow Fever Vaccination

scholarly journals An RNA Pseudoknot Is Required for Production of Yellow Fever Virus Subgenomic RNA by the Host Nuclease XRN1

2010 ◽  
Vol 84 (21) ◽  
pp. 11395-11406 ◽  
Author(s):  
Patrícia A. G. C. Silva ◽  
Carina F. Pereira ◽  
Tim J. Dalebout ◽  
Willy J. M. Spaan ◽  
Peter J. Bredenbeek
Keyword(s):  
Yellow Fever ◽  
Rna Structure ◽  
Mammalian Cells ◽  
Yellow Fever Virus ◽  
Fever Virus ◽  
Infected Mosquito ◽  
Molecular Characteristics ◽  
Subgenomic Rna ◽  
Rna Pseudoknot

ABSTRACT Cells and mice infected with arthropod-borne flaviviruses produce a small subgenomic RNA that is colinear with the distal part of the viral 3′-untranslated region (UTR). This small subgenomic flavivirus RNA (sfRNA) results from the incomplete degradation of the viral genome by the host 5′-3′ exonuclease XRN1. Production of the sfRNA is important for the pathogenicity of the virus. This study not only presents a detailed description of the yellow fever virus (YFV) sfRNA but, more importantly, describes for the first time the molecular characteristics of the stalling site for XRN1 in the flavivirus genome. Similar to the case for West Nile virus, the YFV sfRNA was produced by XRN1. However, in contrast to the case for other arthropod-borne flaviviruses, not one but two sfRNAs were detected in YFV-infected mammalian cells. The smaller of these two sfRNAs was not observed in infected mosquito cells. The larger sfRNA could also be produced in vitro by incubation with purified XRN1. These two YFV sfRNAs formed a 5′-nested set. The 5′ ends of the YFV sfRNAs were found to be just upstream of the previously predicted RNA pseudoknot PSK3. RNA structure probing and mutagenesis studies provided strong evidence that this pseudoknot structure was formed and served as the molecular signal to stall XRN1. The sequence involved in PSK3 formation was cloned into the Sinrep5 expression vector and shown to direct the production of an sfRNA-like RNA. These results underscore the importance of the RNA pseudoknot in stalling XRN1 and also demonstrate that it is the sole viral requirement for sfRNA production.

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