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[Protein E 98-113 sequence is a fusion site of tick-borne encephalitis virus with cellular membrane]

T D Volkova1, O M Vol'pina, V T Ivanov

  • 1Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia. fmdv@ibch.siobc.ras.ru

Bioorganicheskaia Khimiia
|November 14, 1998
PubMed

Insights

A synthetic peptide from tick-borne encephalitis virus protein E inhibits viral infection of macrophages. This peptide, located at the fusion site, is crucial for viral entry into host cells.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Context:

  • Tick-borne encephalitis virus (TBEV) is a significant human pathogen.
  • Protein E is a key component of the flavivirus envelope.
  • The function of conserved protein sequences in flavivirus infection is not fully understood.

Purpose:

  • To investigate the role of the conserved 98-113 sequence of TBEV protein E in flavivirus functioning.
  • To identify potential targets for antiviral therapies.

Summary:

  • A synthetic peptide corresponding to the 98-113 sequence of TBEV protein E was synthesized and studied.
  • This peptide demonstrated inhibition of in vitro macrophage infection by TBEV.
  • An antibody targeting this peptide blocked viral entry into liposomes, suggesting its role in membrane fusion.
  • The 98-113 sequence is identified as the fusion site for viral envelope and cellular membrane interaction.

Impact:

  • Identifies a critical fusion site within TBEV protein E.
  • Provides a potential target for developing novel antiviral strategies against TBEV and other flaviviruses.
  • Enhances understanding of flavivirus-host cell interactions at the molecular level.

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