Recombinant Yellow Fever Virus produced in E. coli migrates at 12kDa.
Recombinant Yellow Fever Virus is fused to a 6xHis tag at its C-terminus and purified by proprietary chromatographic technique.
Escherichia Coli.
The following FAQs address key research considerations for Yellow Fever Virus (YFV), structured to reflect academic rigor and methodological depth. Questions are categorized into basic and advanced tiers, with evidence-based answers drawing from virology, immunology, and epidemiology studies.
YFV exhibits three transmission cycles:
Sylvatic (jungle): Non-human primates → forest canopy mosquitoes (Haemagogus spp. in Americas, Aedes spp. in Africa)
Intermediate (savannah): Mixed human/non-human primate → Aedes spp. at forest edges
Methodological considerations:
Vector competence experiments require species-specific colonization under biosafety level 3 (BSL-3) conditions.
Field studies must account for seasonal mosquito population dynamics and zoonotic reservoirs.
Phase IV trials track seroconversion rates using PRNT90 (90% plaque reduction threshold) .
Longitudinal cohorts monitor neutralizing antibody titers over decades (e.g., 99% efficacy at 10 years, declining to 80% by 30 years) .
Challenge studies in non-human primates show sterilizing immunity correlates with titers ≥1:10 .
Contradiction: Human studies report case fatality rates of 30-60% , yet murine models often show attenuated virulence.
Resolution strategies:
Humanized mouse models (e.g., FRG KO mice with hepatocyte engraftment) recapitulate viscerotropic disease .
Comparative omics of primate vs. rodent host responses identify IFN-γ and IL-6 as critical mediators of hepatic necrosis .
Key findings from recent studies:
Methodological note: Longitudinal sampling (days 7, 30, 90 post-vaccination) captures dynamic immune trajectories.
Bayesian coalescent models estimate mutation rates at 4.8 × 10<sup>−4</sup> substitutions/site/year (95% HPD: 3.6–6.1 × 10<sup>−4</sup>) .
Structural predictions of E protein glycosylation sites (e.g., Asn<sup>153</sup>) explain altered vector specificity in emergent strains.
Issue: Discrepancies in vaccine durability studies (lifelong vs. decadal immunity ).
Resolution framework:
Yellow fever is a viral disease caused by the yellow fever virus, a member of the Flavivirus genus within the Flaviviridae family. It is transmitted to humans through the bites of infected mosquitoes, primarily Aedes and Haemagogus species . The disease can cause severe symptoms, including fever, jaundice, and hemorrhage, and can be fatal in some cases .
The yellow fever virus is an enveloped, positive-stranded RNA virus with a genome approximately 11 kilobases in length . The genome encodes a single polypeptide that is proteolytically processed into functional proteins necessary for viral replication . The virus has been a significant public health concern, particularly in tropical regions of Africa and South America, where it is endemic .
The live-attenuated yellow fever 17D vaccine is one of the most effective viral vaccines available today . Developed in the 1930s, it has been used for over 70 years to prevent yellow fever. The vaccine is prepared from infected chicken embryos and induces long-lasting immunity in over 95% of vaccinees within 10 days . The safety record of the 17D vaccine is outstanding, with serious adverse reactions being extremely rare .
Recombinant yellow fever viruses have been genetically engineered to carry and express foreign antigenic sequences. These recombinant viruses are being explored as potential therapeutic vaccines for various diseases, including cancer . For example, recombinant yellow fever viruses expressing a cytotoxic T-lymphocyte epitope derived from chicken ovalbumin have been shown to induce protective immunity against malignant melanoma in mice .
The construction of recombinant yellow fever viruses involves inserting foreign genes into the viral genome. One approach described involves the insertion of a green fluorescent protein variant (EGFP) into the yellow fever 17D virus . This methodology takes into account the presence of functional motifs and amino acid sequence conservation flanking the E and NS1 intergenic region to ensure the correct processing of the viral polyprotein precursor . The recombinant virus is then grown in cell cultures, such as Vero cells, and its stability and immunogenicity are assessed .
Recombinant yellow fever viruses have several potential applications: