The role of conventional antibodies targeting the CD4 binding site and CD4-induced epitopes in the control of HIV-1 CRF01_AE viruses

HIV-1 CRF01_AE viruses are highly prevalent in Southeast Asia. However, vulnerability sites in Env of CRF01_AE viruses have not been investigated sufficiently. We examined the sensitivity of CRF01_AE viruses from Japan and Vietnam, together with subtype B viruses from Japan, to neutralization and Fc...

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Published inBiochemical and biophysical research communications Vol. 508; no. 1; pp. 46 - 51
Main Authors Thida, Win, Kuwata, Takeo, Maeda, Yosuke, Yamashiro, Tetsu, Tran, Giang Van, Nguyen, Kinh Van, Takiguchi, Masafumi, Gatanaga, Hiroyuki, Tanaka, Kazuki, Matsushita, Shuzo
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.01.2019
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Summary:HIV-1 CRF01_AE viruses are highly prevalent in Southeast Asia. However, vulnerability sites in Env of CRF01_AE viruses have not been investigated sufficiently. We examined the sensitivity of CRF01_AE viruses from Japan and Vietnam, together with subtype B viruses from Japan, to neutralization and Fc-mediated signaling. Neutralization coverage of broadly neutralizing antibodies (bnAbs), 2G12 and b12, was significantly low against CRF01_AE viruses, compared with subtype B viruses. In contrast, the conventional antibody targeting the CD4 binding site (CD4bs), 49G2, showed better neutralization and Fc-mediated signaling activities against CRF01_AE viruses than subtype B viruses. Fc-mediated signaling activity of anti-CD4 induced (CD4i) antibody, 4E9C, was also detected against CRF01_AE viruses more than subtype B viruses. These results suggest that conventional antibodies against CD4bs and CD4i may play an important role in the control of CRF01_AE viruses. •Compared with subtype B, CRF01_AE viruses were resistant to bnAbs, 2G12 and b12.•Abs to CD4bs and CD4i are relatively effective against CRF01_AE viruses.•Conventional Abs may play an important role in the control of CRF01_AE viruses.
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ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.11.063