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However, HIV-1 particles interacting only weakly with fusion inhibitors would still be able to enter target cells. In macaques, protection from vaginal challenge with simian human immunodeficiency virus was achieved by vaginally delivered inhibitors of virus-cell fusion moreover, two small molecule inhibitors binding to viral gp120 and cellular CCR5, respectively, prevent receptor binding by gp120, and a 53-residue peptide containing the C-terminal heptad repeat region of gp41 inhibited the gp41-mediated virus-cell fusion. Similarly, the human monoclonal 5H/I1-BMV-D5 single-chain variable region fragment (scFv) antibody selected from phage-displayed libraries has been shown to bind to the N-terminal heptad repeat region of gp41 and thus inhibited the formation of fusion intermediates in vitro and the replication of diverse clinical isolates of HIV-1. coli) strain secreting HIV-1 gp41-hemolysin to block HIV fusion with target cells, the use of an interchain disulfide bond-stabilized trimeric 45-residue fusion peptide to inhibit the fusion of a large number of HIV isolates with target cells, and the inhibition of HIV-1 infection of CD4 + T cells by microbial HSP70. Other approaches include the construction of a highly colonizing Escherichia coli ( E. Enfuvirtide, a synthetic peptide already in clinical use corresponding to the conserved extramembranous sequence 643 to 678 of the HIV-1 envelope glycoprotein gp41, was found to prevent the conformational change of gp41 necessary for HIV-1 fusion with CD4 + cells. One approach to interfere with HIV-1 infection at an early stage is to block viral entry. Therefore, additional concepts for inhibiting HIV-1 replication, particle assembly, and escape have been developed. Nevertheless, all current therapeutic approaches have been hampered by viral resistance mutations, undesired side effects, and high treatment cost. Treatment of HIV-1 infection has made considerable progress. Rapid uptake of this intracellular stable and inhibitory peptide into the cells implies that this peptide may have the potential to attenuate HIV-1 replication in vivo. Moreover, HIV-1 replication is inhibited by this peptide in HIV-1-infected CEM-GFP cells as revealed by HIV-1 p24 ELISA and real-time RT-PCR of HIV-1 RNA. The resulting synthetic 64-residue peptide was found to bind to the two enhancers of the HIV-1 long terminal repeat, cross the plasma membrane and the nuclear envelope of human cells, and suppress the HIV-1 enhancer-controlled expression of a green fluorescent protein reporter gene. An artificial HIV-1 enhancer-binding peptide was extended by nine consecutive arginine residues at the C-terminus and by the nuclear localization signal of SV40 large T antigen at the N-terminus.