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Inhibitors of Viral Protein Synthesis

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

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Related Experiment Video

Updated: Mar 19, 2026

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

The IFITMs Inhibit Zika Virus Replication.

George Savidis¹, Jill M Perreira¹, Jocelyn M Portmann¹

¹Department of Microbiology and Physiological Systems (MaPS), University of Massachusetts Medical School, Worcester, MA 01655, USA.

|June 9, 2016

Summary

Interferon-induced proteins with tetratricp_e_repeat motifs 1 and 3 (IFITM1 and IFITM3) restrict Zika virus replication early in infection. IFITM3 also protects cells from Zika virus-induced death, suggesting IFITM boosting as a therapeutic strategy.

Keywords:

IFITM IFITM1 IFITM3 Zika virus flavivirus host factors interferon intrinsic immunity

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High-throughput Antiviral Assays to Screen for Inhibitors of Zika Virus Replication

High-throughput Antiviral Assays to Screen for Inhibitors of Zika Virus Replication

Published on: October 30, 2021

Area of Science:

Virology
Immunology
Cell Biology

Background:

Zika virus (ZIKV) poses a significant global health risk.
The Interferon-induced proteins with tetratricp_e_repeat motifs (IFITMs) are known to inhibit various viruses, including flaviviruses like West Nile virus and dengue virus.

Purpose of the Study:

To investigate the role of IFITM1 and IFITM3 in restricting Zika virus infection.
To determine if IFITM3 can protect against ZIKV-induced cellular damage.

Main Methods:

Cell-based assays to assess ZIKV replication in the presence of IFITM1 and IFITM3.
Analysis of cell viability following ZIKV infection and IFITM expression.

Main Results:

IFITM1 and IFITM3 were found to inhibit ZIKV infection at an early stage of the viral life cycle.
IFITM3 demonstrated the ability to prevent cell death induced by ZIKV.

Conclusions:

IFITM1 and IFITM3 are effective restriction factors against Zika virus.
Enhancing IFITM activity or levels could be a potential therapeutic approach for emerging flavivirus infections.