Sequence signatures in envelope protein may determine whether flaviviruses produce hemorrhagic or encephalitic syndromes

Barker, Winona C.; Mazumder, Raja; Vasudevan, Sona; Sagripanti, José-Luis; Wu, Cathy H.

doi:10.1007/s11262-009-0343-4

Cited by 17 publications

(17 citation statements)

References 39 publications

(48 reference statements)

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“…We also note that residues 132 and 272 map near one another in domain 1 (Figure 6b), and both are close to previously described neutralizing epitopes (as determined from the position of escape mutants45). We also included position 67, a reported marker of hemorrhagic disease, in our analysis46, but found Asn at this position, in all DENV strains, regardless of reported disease severity. We found Asn at position 390 in all DENV except DENV4, where His predominates.…”

Section: Resultsmentioning

confidence: 99%

PCP Consensus Sequences of Flaviviruses: Correlating Variance with Vector Competence and Disease Phenotype

Danecek

Schein

2010

Journal of Molecular Biology

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Section: Resultsmentioning

confidence: 99%

PCP Consensus Sequences of Flaviviruses: Correlating Variance with Vector Competence and Disease Phenotype

Danecek

Schein

2010

Journal of Molecular Biology

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“…With view to WNV-associated haemolysis in other species, a few cases of WNV-associated haemorrhagic fever in humans have been described [31]. A recent study has associated sequence signatures in the envelope protein of human pathogenic flaviviruses with the primary syndrome that they produce (encephalitis or haemorrhagic disease) [32]. These authors speculated that the electrostatic charge differences caused by the presence of either glycosilated asparagine (Asn, haemorrhagic viruses) or Aspartic acid (Asp, encephalitic viruses) at position 67 of the domain II of the envelope protein could be responsible for the phenotype and related disease syndrome.…”

Section: Discussionmentioning

confidence: 99%

Natural Bagaza virus infection in game birds in southern Spain

Gamino

Gutiérrez-Guzmán

Fernández-de-Mera

et al. 2012

Vet Res

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In late summer 2010 a mosquito born flavivirus not previously reported in Europe called Bagaza virus (BAGV) caused high mortality in red-legged partridges (Alectoris rufa) and ring-necked pheasants (Phasianus colchicus). We studied clinical findings, lesions and viral antigen distribution in naturally BAGV infected game birds in order to understand the apparently higher impact on red-legged partridges. The disease induced neurologic signs in the two galliform species and, to a lesser extent, in common wood pigeons (Columba palumbus). In red-legged partridges infection by BAGV caused severe haemosiderosis in the liver and spleen that was absent in pheasants and less evident in common wood pigeons. Also, BAGV antigen was present in vascular endothelium in multiple organs in red-legged partridges, and in the spleen in common wood pigeons, while in ring-necked pheasants it was only detected in neurons and glial cells in the brain. These findings indicate tropism of BAGV for endothelial cells and a severe haemolytic process in red-legged partridges in addition to the central nervous lesions that were found in all three species.

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“…Barker et al . [25] noticed that flaviviruses that cause hemorrhagic disease have asparagine (Asn) at position 67 of the E protein, corresponding to the glycosylation site, whereas neurotropic viruses contain Asp at this position. Experiments should be designed to study these associations.…”

Section: Introductionmentioning

confidence: 99%

West Nile Virus: Immunity and Pathogenesis

Lim

Koraka

Osterhaus

et al. 2011

Viruses

105

106

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West Nile virus (WNV) is a neurotropic, arthropod-borne flavivirus that is maintained in an enzootic cycle between mosquitoes and birds, but can also infect and cause disease in horses and humans. WNV is endemic in parts of Africa, Europe, the Middle East, and Asia, and since 1999 has spread to North America, Mexico, South America, and the Caribbean. WNV infects the central nervous system (CNS) and can cause severe disease in a small minority of infected humans, mostly immunocompromised or the elderly. This review discusses some of the mechanisms by which the immune system can limit dissemination of WNV infection and elaborates on the mechanisms involved in pathogenesis. Reasons for susceptibility to WNV-associated neuroinvasive disease in less than 1% of cases remain unexplained, but one favored hypothesis is that the involvement of the CNS is associated with a weak immune response allowing robust WNV replication in the periphery and spread of the virus to the CNS.

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Sequence signatures in envelope protein may determine whether flaviviruses produce hemorrhagic or encephalitic syndromes

Abstract: We analyzed the envelope proteins in patho-

Cited by 17 publications

References 39 publications

PCP Consensus Sequences of Flaviviruses: Correlating Variance with Vector Competence and Disease Phenotype

PCP Consensus Sequences of Flaviviruses: Correlating Variance with Vector Competence and Disease Phenotype

Natural Bagaza virus infection in game birds in southern Spain

West Nile Virus: Immunity and Pathogenesis

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