Influenza Viral Hemagglutinin Peptide Inhibits Influenza Viral Entry by Shielding the Host Receptor

Influenza viral infection of the host begins by the attachment of viral hemagglutinin to a cell surface receptor. In the current study, a hemagglutinin fragment peptide library was screened using an H5N1 recombinant pseudotyped viral system. One peptide, designated HA-pep25, showed effective antiviral activity against both human and avian influenza viral strains (IC₅₀ = 12.0–51.0 μM). A mechanistic study demonstrated direct binding between HA-pep25 and sialyllactose, which mimics the host receptor for the influenza virus. This binding was independent of the presence of sialic acid on the cell membrane. By generating alanine substitutions in HA-pep25, eight residues were identified as essential for the peptide’s anti-influenza activity. HA-pep25 derived from hemagglutinin blocked influenza viral entry by shielding the host receptor on the cell membrane. This peptide might be a candidate drug for influenza virus entry inhibition and may be combined with other antivirals targeting different steps of the influenza viral life cycle

The detection rates of rotavirus, astrovirus, calicivirus and adenovirus in HPeV-infected and uninfected children.

<p>The detection rates of rotavirus, astrovirus, calicivirus and adenovirus in HPeV-infected and uninfected children.</p

Nucleic acid phylogenetic tree based on the VP3/VP1 conjunction region.

<p>The phylogenetic analyses were conducted in MEGA5 by using the Neighbor-Joining method. The p-distance method was applied to compute the evolutionary distances. LV was used as outgroup. A bootstrap test was replicated 1000 times and only the bootstrap values >70 are displayed. The reference strains are shown with their individual GenBank accession number and corresponding genotype.</p

Difference between controls and meditators (CTRL-MEDT) in the estimated profile of the BOLD response related to conceptual activity.

<p>Error bars represent standard errors and a reference Gamma function model for the BOLD response to a single brief stimulus is plotted as a black line for reference.</p

Clusters of activation for the contrast <i>words-nonwords</i> on the pooled data (CTRL+MEDT), thresholded at <i>p</i><0.001 and <i>k</i>>27 voxels (α<0.05).

<p>Cluster sizes are in voxels, t-values refer to the peak voxel in the cluster, and stereotactic coordinates are in MNI space (mm). Abbreviations: L = Left, MCC = middle cingulate cortex, PCC = posterior cingulate cortex, rACC = rostral anterior cingulate cortex, g = gyrus, s = sulcus, sup = superior, inf = inferior. The indices (1) and (2) are used to distinguish different clusters in similar anatomical locations.</p

Seasonal distribution of individual HPeV genotype.

<p>February and April–June were not included because no genotypes had been successfully typed in these months. Only the genotypes detected and successfully typed are indicated in each age group.</p

Activated clusters for the contrast <i>words-nonwords</i> on the pooled data (CTRL+MEDT).

<p>The <i>t</i>-map is thresholded at <i>p</i><0.001, <i>k</i>>27 voxels (α<0.05).</p

Co-infection of HPeV-infected subjects.

<p>§ This symbol denotes the corresponding pathogen was involved in co-infection and the combination patterns of the symbol represented the modes of co-infections that had been identified in this study.</p

Comparison of clinical manifestations between children with HPeV-infection alone and HPeV-infected children with co-infection or children without pathogens detected.

†<p>A Bonferroni-adjusted significance level of 0.025 is used for the multiple comparisons, and none of the comparisons are statistically significant.</p

Tests of group differences in the cumulative measure of the BOLD signal related to semantic processing in the 6–14 s post-stimulus period within each ROI.

<p>The reported <i>p</i>-values are Bonferroni corrected. Significance codes: ^*<0.05, ^**<0.01, ^***<0.001.</p