tetano
Editor, Senior Moderator
Sci Rep. 2017 Jul 7;7(1):4875. doi: 10.1038/s41598-017-04777-4.
[h=1]Inhibition of highly pathogenic avian influenza (HPAI) virus by a peptide derived from vFLIP through its direct destabilization of viruses.[/h] Moon HJ[SUP]1,[/SUP][SUP]2[/SUP], Nikapitiya C[SUP]1[/SUP], Lee HC[SUP]1[/SUP], Park ME[SUP]1,[/SUP][SUP]3[/SUP], Kim JH[SUP]1[/SUP], Kim TH[SUP]1[/SUP], Yoon JE[SUP]1,[/SUP][SUP]3[/SUP], Cho WK[SUP]4[/SUP], Ma JY[SUP]4[/SUP], Kim CJ[SUP]1[/SUP], Jung JU[SUP]5[/SUP], Lee JS[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The antiviral activities of synthesized Kα2-helix peptide, which was derived from the viral FLICE-like inhibitor protein (vFLIP) of Kaposi's sarcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were investigated in vitro and in vivo, and mechanisms of action were suggested. In addition to the robust autophagy activity of the Kα2-helix peptide, the present study showed that treatment with the Kα2 peptide fused with the TAT peptide significantly inhibited IAV replication and transmission. Moreover, TAT-Kα2 peptide protected the mice, that were challenged with lethal doses of highly pathogenic influenza A H5N1 or H1N1 viruses. Mechanistically, we found that TAT-Kα2 peptide destabilized the viral membranes, depending on their lipid composition of the viral envelop. In addition to IAV, the Kα2 peptide inhibited infections with enveloped viruses, such as Vesicular Stomatitis Virus (VSV) and Respiratory Syncytial Virus (RSV), without cytotoxicity. These results suggest that TAT-Kα2 peptide is a potential antiviral agent for controlling emerging or re-emerging enveloped viruses, particularly diverse subtypes of IAVs.
PMID: 28687749 DOI: 10.1038/s41598-017-04777-4
Free PMC Article
[h=1]Inhibition of highly pathogenic avian influenza (HPAI) virus by a peptide derived from vFLIP through its direct destabilization of viruses.[/h] Moon HJ[SUP]1,[/SUP][SUP]2[/SUP], Nikapitiya C[SUP]1[/SUP], Lee HC[SUP]1[/SUP], Park ME[SUP]1,[/SUP][SUP]3[/SUP], Kim JH[SUP]1[/SUP], Kim TH[SUP]1[/SUP], Yoon JE[SUP]1,[/SUP][SUP]3[/SUP], Cho WK[SUP]4[/SUP], Ma JY[SUP]4[/SUP], Kim CJ[SUP]1[/SUP], Jung JU[SUP]5[/SUP], Lee JS[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The antiviral activities of synthesized Kα2-helix peptide, which was derived from the viral FLICE-like inhibitor protein (vFLIP) of Kaposi's sarcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were investigated in vitro and in vivo, and mechanisms of action were suggested. In addition to the robust autophagy activity of the Kα2-helix peptide, the present study showed that treatment with the Kα2 peptide fused with the TAT peptide significantly inhibited IAV replication and transmission. Moreover, TAT-Kα2 peptide protected the mice, that were challenged with lethal doses of highly pathogenic influenza A H5N1 or H1N1 viruses. Mechanistically, we found that TAT-Kα2 peptide destabilized the viral membranes, depending on their lipid composition of the viral envelop. In addition to IAV, the Kα2 peptide inhibited infections with enveloped viruses, such as Vesicular Stomatitis Virus (VSV) and Respiratory Syncytial Virus (RSV), without cytotoxicity. These results suggest that TAT-Kα2 peptide is a potential antiviral agent for controlling emerging or re-emerging enveloped viruses, particularly diverse subtypes of IAVs.
PMID: 28687749 DOI: 10.1038/s41598-017-04777-4
Free PMC Article