Abstract
The yellow fever virus vaccine, 17D, was derived through the serial passage of the wild-type (WT) strain Asibi virus in mouse and chicken tissue. Since its derivation, the mechanism of attenuation of 17D virus has been investigated using three 17D substrains and WT Asibi virus. Although all three substrains of 17D have been sequenced, only one isolate of Asibi has been examined genetically and all interpretation of attenuation is based on this one isolate. Here, we sequenced the genome of Asibi virus from three different laboratories and show that the WT strain is genetically homogenous at the amino acids that distinguish Asibi from 17D vaccine virus.
Highlights
Parent to Live-Attenuated 17DYellow fever virus (YFV) is the causative agent of yellow fever (YF), a hemorrhagic disease involving the liver, kidney and heart
The genomes of Asibi-Yale, Asibi-LSHTM and Asibi-FC were identical in length, 10,862 nucleotides (Genbank accession numbers MT956628, MT956629 and MT956630, respectively)
Asibi-LSHTM differs from Asibi-Yale by one additional nucleotide and Asibi-FC by two nucleotides (Table 1)
Summary
Parent to Live-Attenuated 17DYellow fever virus (YFV) is the causative agent of yellow fever (YF), a hemorrhagic disease involving the liver, kidney and heart. As there are no antivirals approved for use against YFV, vaccination with the live-attenuated vaccine, termed 17D, is the primary disease control strategy [2]. The wild-type (WT) YFV strain Asibi was isolated from the blood of a Ghanaian man with a mild case of YF. The 17D vaccine is produced as three substrains, 17D-204, 17D-213 and 17DD, which represent different passages of the original 17D vaccine (i.e., passage 204, 239 and 287–288, respectively, of wild-type strain Asibi). These substrains are considered safe and effective as a vaccine
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