Infection and cell-to-cell spread of VG9-E and VTT-E in six cell types.

<p>Confluent cells were infected at an MOI of 0.05 with VG9-E (A) and VTT-E (B), fixed at 24 and 48 h post-infection, respectively, then incubated with an anti-VV-specific polyclonal antibody and immunostained at 24 and 48 h pi.</p

Inhibition of ABT on HIV-1 entry and replication.

<p>A. Inhibition of HIV-1_NL4-3 Env-pseudotyped virus in single-cycle assay that demonstrates the virus-cell membrane fusion. B. Inhibition of wild-type HIV-1_NL4-3 replication. ABT shows significantly higher potency than T20 in inhibiting HIV-1_NL4-3 entry and replication. The data were derived from the results of three independent experiments and are expressed as means ± standard deviations.</p

Effect of human serum on the anti-HIV activity of ABT.

<p>The human sera were freshly isolated from a HIV-seronegative healthy volunteer. The peptide was mixed with various concentrations (5, 10, 20 and 50%) of human sera freshly isolated from a HIV-seronegative healthy volunteer and incubated for 2 h at 37°C. The mixture was then diluted with a DMEM-based complete medium supplemented with 10% FCS and subjected to the single-cycle infection assay. The percent inhibition by ABT was calculated as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032599#s4" target="_blank">materials and method</a>. The data were derived from the results of three independent experiments and are expressed as means ± standard deviations.</p

Inhibition of ABT on subtype A, B and C HIV-1 strains^a.

a<p>The inhibitory activity of each peptide was determined in triplicate by a single-cycle infectivity assay. The data were derived from the results of three independent experiments and are expressed as means ± standard deviations.</p>b<p>Co-R: coreceptor use.</p

Biophysical characterization of ABT by CD spectroscopy.

<p>A. CD spectra of NHR and CHR-derived peptides and their complexes. B. Thermostability of the complex formed by N36 and ABT or C34. The unfolding temperature of each complex was scanned at 222 nm by CD spectroscopy, and their <i>Tm</i> values were calculated. The final concentration of each peptide in PBS is 1 µM.</p

Inhibition of ABT on CRF07_BC, CRF01_AE and B'HIV-1 variants^a.

a<p>The inhibitory activity of each peptide was determined in triplicate by a single-cycle infectivity assay. The data were derived from the results of at least three independent experiments and are expressed as means ± standard deviations.</p>b<p>HIV-1 subtypes: B/C, CRF07_BC; A/E, CRF01_AE; B′, Tai B.</p>c<p>Co-R: coreceptor use.</p

Inhibition of ABT on 6-HB formation and cell membrane fusion.

<p>A. ABT and C34 can efficiently inhibit 6-HB formation in a dose-dependent manner, but T20 has no such effect. B. Inhibition of HIV-1_HXB2 Env-mediated cell-cell membrane fusion by ABT, C34 and T20. The data were derived from the results of three independent experiments and are expressed as means ± standard deviations.</p

A visualized map of HEV ORF3 protein-human protein interactions.

<p>Yellow nodes: HEV ORF3 protein; green nodes: host proteins identified as interacting partners of the HEV ORF3 protein using the Y2HGold system; tiny nodes: secondary interactors of the host proteins interacting with the ORF3 protein.</p

Schematic illustration of HIV-1 gp41 and peptide fusion inhibitors.

<p>A. View of the gp41 functional regions. The residue numbers of each region correspond to their positions in gp160 of HIV-1_HXB2. FP, fusion peptide; NHR, N-terminal heptad repeat; CHR, C-terminal heptad repeat; TM, transmembrane domain. B. Sequence of CHR-derived anti-HIV-1 peptides. ABT is engineered with three amino acids different from C34 (marked in bold). The 13th residue serine (S) of C34 was changed to lysine (K) which allows a single modification by 3-maleimidopropionic acid (MPA).</p

Enriched canonical pathways in the HEV ORF3 protein and human protein interaction network (p≦0.05).

<p>The canonical pathways are mapped to the x-axisand the y-axis represents the % of genes mapped to a given pathway within the network and in human genome.</p