Host-cell interaction of attenuated and wild-type strains of yellow fever virus can be differentiated at early stages of hepatocyte infection

Lefeuvre, Anabelle; Contamin, Hugues; Decelle, Thierry; Fournier, C.; Lang, Jean; Denis, Vincent; Marianneau, Philippe

doi:10.1016/j.micinf.2006.01.013

Cited by 30 publications

(24 citation statements)

References 42 publications

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“…Studies that compared the growth behavior of 17D and Asibi in HepG2 cells showed a higher susceptibility of the cells for the attenuated virus strain 17D within the first 3 days after infection (38). We also observed by IFA a lower infectivity of HepG2 cells with Asibi than that with 17D within 50 h postinfection.…”

Section: Discussionsupporting

confidence: 57%

“…To investigate the growth behavior of the different YF lineages circulating in Senegal, we performed growth kinetics on cells from the mosquito vector (Ap61) and human liver cells (HepG2). HepG2 cells have been used in several studies to investigate viral infections, especially of flaviviruses, and were thus chosen as the model cell line for our examinations (38)(39)(40)(41). The aim of this experimental setup with the two cell lines was to cover the natural system of both the transmitting vector and the vertebrate host.…”

Section: Discussionmentioning

confidence: 99%

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Biological and Phylogenetic Characteristics of Yellow Fever Virus Lineages from West Africa

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Laraway

Faye

et al. 2013

J Virol

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bThe yellow fever virus (YFV), the first proven human-pathogenic virus, although isolated in 1927, is still a major public health problem, especially in West Africa where it causes outbreaks every year. Nevertheless, little is known about its genetic diversity and evolutionary dynamics, mainly due to a limited number of genomic sequences from wild virus isolates. In this study, we analyzed the phylogenetic relationships of 24 full-length genomes from YFV strains isolated between 1973 and 2005 in a sylvatic context of West Africa, including 14 isolates that had previously not been sequenced. By this, we confirmed genetic variability within one genotype by the identification of various YF lineages circulating in West Africa. Further analyses of the biological properties of these lineages revealed differential growth behavior in human liver and insect cells, correlating with the source of isolation and suggesting host adaptation. For one lineage, repeatedly isolated in a context of vertical transmission, specific characteristics in the growth behavior and unique mutations of the viral genome were observed and deserve further investigation to gain insight into mechanisms involved in YFV emergence and maintenance in nature.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Biological and Phylogenetic Characteristics of Yellow Fever Virus Lineages from West Africa

Stock

Laraway

Faye

et al. 2013

J Virol

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“…Transport of intradermally inoculated virus to the draining lymph node is thought to be mediated by Langerhans or dendritic cells (22) and would therefore not be subject to GAGdependent inhibition of spread. We also found better replication of 17D in Vero and BHK cells as well as in ex vivo mouse macrophage cells (data not shown), compared with 17D variants with Asibi E protein changes, while others have reported more efficient growth of 17D in human liver HepG2 cells than the Asibi parent, as well as efficient replication of 17D in immature and mature human dendritic cells (1,19). Collectively, this demonstrates that the overall replication efficiency of the vaccine strain in a diverse range of cell types is not lowered.…”

Section: Vol 82 2008mentioning

confidence: 62%

E Protein Domain III Determinants of Yellow Fever Virus 17D Vaccine Strain Enhance Binding to Glycosaminoglycans, Impede Virus Spread, and Attenuate Virulence

Lee

Lobigs

2008

J Virol

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The yellow fever virus (YFV) 17D strain is one of the most effective live vaccines for human use, but the in vivo mechanisms for virulence attenuation of the vaccine and the corresponding molecular determinants remain elusive. The vaccine differs phenotypically from wild-type YFV by the loss of viscerotropism, despite replicative fitness in cell culture, and genetically by 20 amino acid changes predominantly located in the envelope (E) protein. We show that three residues in E protein domain III inhibit spread of 17D in extraneural tissues and attenuate virulence in type I/II interferon-deficient mice. One of these residues (Arg380) is a dominant glycosaminoglycan-binding determinant, which mainly accounts for more rapid in vivo clearance of 17D from the bloodstream in comparison to 17D-derived variants with wild-type-like E protein. While other mutations will account for loss of neurotropism and phenotypic stability, the described impact of E protein domain III changes on virus dissemination and virulence is the first rational explanation for the safety of the 17D vaccine in humans.The live, attenuated yellow fever virus (YFV) strain 17D vaccine has been used safely and effectively in over 500 million individuals over the past 70 years. This excellent safety record also underpins its potential application as a platform for chimeric vaccines against other medically important flaviviruses (dengue, Japanese encephalitis, and West Nile viruses), which are currently in clinical trials (reviewed in reference 13). Despite knowledge of the complete genome sequences of 17D (33) and its virulent parent (10), the Asibi strain isolated in Africa in 1927, the in vivo mechanism(s) and molecular determinants for virulence attenuation of the YFV vaccine are still not completely resolved. YFV strain 17D was the first human vaccine derived from repeated passage in tissue culture (reviewed in reference 39). More than 230 passages in embryonic mouse tissue (18 passages), chicken embryo tissue (50 passages), and chicken embryo tissue from which the head and spinal chord had been removed (152 passages) separate the 17D from the Asibi strain. The adaptation of 17D to growth in mouse and chicken embryonal tissues culture has resulted in loss of viscerotropism, a property which accounts for the major disease manifestations of yellow fever in primates: high viremia, hepatitis, renal dysfunction, hemorrhagic fever, and circulatory shock (reviewed in reference 28); it also resulted in reduced neurotropism and loss of tropism for mosquitoes, the obligatory vector in the natural transmission cycle of YFV. The complex passage history of YFV strain 17D has given rise to as many as 68 nucleotide mutations and 32 amino acid changes in the viral RNA genome (10). However, when the Asibi genome is compared to the consensus sequence of different 17D vaccine strains derived from it, the number of differences potentially contributing to the attenuated virulence phenotype can be reduced to 20 amino acids and 4 nucleotides in the 3Ј untranslated region...

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“…In addition, mutagenesis around the putative cleavage site for caspases within the FS52aa Q(E) EVD[G sequence, with a cleavage after the Asp381 residue, strongly suggested that NS1 0 was a substrate of caspase. Apoptosis of flavivirus-infected cells can limit virus replication and spread, which may be one pathway of host response to viral infection [32,33]. In flavivirus infection, multiple mechanisms were reported for the initiation of flavivirus-induced apoptosis, including ROS production [34], NF-kappa B activation [35], ER stress [19].…”

Section: Discussionmentioning

confidence: 99%

Japanese encephalitis virus NS1′ protein depends on pseudoknot secondary structure and is cleaved by caspase during virus infection and cell apoptosis

Jin

Denis

2012

Microbes and Infection

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Host-cell interaction of attenuated and wild-type strains of yellow fever virus can be differentiated at early stages of hepatocyte infection

Cited by 30 publications

References 42 publications

Biological and Phylogenetic Characteristics of Yellow Fever Virus Lineages from West Africa

Biological and Phylogenetic Characteristics of Yellow Fever Virus Lineages from West Africa

E Protein Domain III Determinants of Yellow Fever Virus 17D Vaccine Strain Enhance Binding to Glycosaminoglycans, Impede Virus Spread, and Attenuate Virulence

Japanese encephalitis virus NS1′ protein depends on pseudoknot secondary structure and is cleaved by caspase during virus infection and cell apoptosis

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