Selected article for: "genetic recombination and genome sequence base"

Author: Li, Xiao-Bo; Wang, Shu-Qing; Xu, Wei-Ren; Wang, Run-Ling; Chou, Kuo-Chen
Title: Novel Inhibitor Design for Hemagglutinin against H1N1 Influenza Virus by Core Hopping Method
  • Document date: 2011_11_30
  • ID: 16syz1o7_4
    Snippet: Owing to its deep active site cleft, the NA has been an attractive target for drug design. Both zanamivir and oseltamivir were designed by modifying the sialic acid (SA) structure. The two FDA-approved clinical drugs were once successfully used to inhibit the spread of influenza viral progeny [15] by binding to viral surface glycoprotein of neuraminidase (NA) [15] . However, it has also been found from several clinical cases [16, 17, 18] that ose.....
    Document: Owing to its deep active site cleft, the NA has been an attractive target for drug design. Both zanamivir and oseltamivir were designed by modifying the sialic acid (SA) structure. The two FDA-approved clinical drugs were once successfully used to inhibit the spread of influenza viral progeny [15] by binding to viral surface glycoprotein of neuraminidase (NA) [15] . However, it has also been found from several clinical cases [16, 17, 18] that oseltamivir failed to treat avian influenza virus. It is both antigenic drift (sequence base mutations) and antigenic shift (genetic recombination) of segmented RNA genome of influenza viruses that have caused the NA inhibitor being resistant [19, 20] .

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