Abstract:
:For successful penetration of HIV-1, the formation of a fusion pore may be required in order to accumulate critical numbers of fusion-activated gp41 with the help of fluidization of the plasma membrane and viral envelope. An increase in temperature to 40 degrees C after viral adsorption at 25 degrees C enhanced the infectivity by 1.4-fold. The enhanced infectivity was inhibited by an anti-CXCR4 peptide, T140, and anti-V3 monoclonal antibodies (0.5beta and 694/98-D) by post-attachment neutralization, but not by non-neutralizing antibodies (670-30D and 246-D) specific for the C5 of gp120 and cluster I of gp41, respectively. Anti-HLA-II and an anti-HTLV-I gp46 antibody, LAT27, neutralized the molecule-carrying HIV-1(C-2(MT-2)). The anti-V3 antibodies suppressed the fluidity of the HIV-1(C-2) envelope, whereas the non-neutralizing antibodies did not. The anti-HLA-II antibody decreased the envelope fluidity of HIV-1(C-2(MT-2)), but not that of HIV-1(C-2). Therefore, fluidity suppression by these antibodies represents an important neutralization mechanism, in addition to inhibition of viral attachment.
journal_name
Virologyjournal_title
Virologyauthors
Harada S,Monde K,Tanaka Y,Kimura T,Maeda Y,Yusa Kdoi
10.1016/j.virol.2007.08.021subject
Has Abstractpub_date
2008-01-05 00:00:00pages
142-50issue
1eissn
0042-6822issn
1096-0341pii
S0042-6822(07)00556-9journal_volume
370pub_type
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