Citation

BibTex format

@article{Li:2014:10.1007/s12250-014-3525-8,
author = {Li, C and Jin, W and Du, T and Wu, B and Liu, Y and Shattock, RJ and Hu, Q},
doi = {10.1007/s12250-014-3525-8},
journal = {Virol Sin},
pages = {381--392},
title = {Binding of HIV-1 virions to α4β 7 expressing cells and impact of antagonizing α4β 7 on HIV-1 infection of primary CD4+ T cells.},
url = {http://dx.doi.org/10.1007/s12250-014-3525-8},
volume = {29},
year = {2014}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - HIV-1 envelope glycoprotein is reported to interact with α4β7, an integrin mediating the homing of lymphocytes to gut-associated lymphoid tissue, but the significance of α4β7 in HIV-1 infection remains controversial. Here, using HIV-1 strain BaL, the gp120 of which was previously shown to be capable of interacting with α4β7, we demonstrated that α4β7 can mediate the binding of whole HIV-1 virions to α4β7-expressing transfectants. We further constructed a cell line stably expressing α4β7 and confirmed the α4β7-mediated HIV-1 binding. In primary lymphocytes with activated α4β7 expression, we also observed significant virus binding which can be inhibited by an anti-α4β7 antibody. Moreover, we investigated the impact of antagonizing α4β7 on HIV-1 infection of primary CD4(+) T cells. In α4β7-activated CD4(+) T cells, both anti-α4β7 antibodies and introduction of short-hairpin RNAs specifically targeting α4β7 resulted in a decreased HIV-1 infection. Our findings indicate that α4β7 may serve as an attachment factor at least for some HIV-1 strains. The established approach provides a promising means for the investigation of other viral strains to understand the potential roles of α4β7 in HIV-1 infection.
AU - Li,C
AU - Jin,W
AU - Du,T
AU - Wu,B
AU - Liu,Y
AU - Shattock,RJ
AU - Hu,Q
DO - 10.1007/s12250-014-3525-8
EP - 392
PY - 2014///
SP - 381
TI - Binding of HIV-1 virions to α4β 7 expressing cells and impact of antagonizing α4β 7 on HIV-1 infection of primary CD4+ T cells.
T2 - Virol Sin
UR - http://dx.doi.org/10.1007/s12250-014-3525-8
UR - https://www.ncbi.nlm.nih.gov/pubmed/25527342
VL - 29
ER -