Related Experiment Video

Updated: Aug 21, 2026

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
07:22

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion

Published on: August 14, 2018

6.5K

Spike-mediated viral membrane fusion is inhibited by a specific anti-IFITM2 monoclonal antibody

Anna Basile1, Carla Zannella2, Margot De Marco3

  • 1Department of Medicine, Surgery and Dentistry "Schola Medica Salernitana", University of Salerno, Baronissi, SA, 84081, Italy.

Antiviral Research
|January 20, 2023
PubMed

Insights

A new antibody targeting Interferon-induced transmembrane protein 2 (IFITM2) effectively blocks SARS-CoV-2 entry into host cells. This antibody also reduces viral infection effects, suggesting IFITM2 as a target for broad antiviral therapies.

Area of Science:

  • Virology and Immunology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Viral entry relies on complex protein-host interactions and lipid rearrangements.
  • Interferon-induced transmembrane (IFITM) proteins are known inhibitors of viral entry.
  • SARS-CoV-2 utilizes IFITM2 for efficient host cell invasion.

Purpose of the Study:

  • To characterize a novel monoclonal antibody (mAb) targeting IFITM2.
  • To evaluate the antibody's efficacy in blocking SARS-CoV-2 internalization.
  • To explore IFITM2's role in the entry mechanisms of other viruses.

Main Methods:

  • Generation and characterization of a specific anti-IFITM2 mAb.
  • Assessment of the mAb's ability to inhibit Spike-mediated SARS-CoV-2 internalization.
  • Evaluation of the mAb's impact on viral cytopathic effects and syncytia formation for SARS-CoV-2, HSV, and RSV.

Main Results:

  • The anti-IFITM2 mAb significantly impairs Spike-mediated SARS-CoV-2 internalization.
  • The antibody reduces SARS-CoV-2-induced cytopathic effects and syncytia formation.
  • The anti-IFITM2 mAb also diminishes cytopathic effects caused by Herpes Simplex Virus (HSV) and Respiratory Syncytial Virus (RSV).

Conclusions:

  • IFITM2 plays a crucial role in mediating the entry of multiple viruses, including SARS-CoV-2, HSV, and RSV, into host cells.
  • The developed anti-IFITM2 mAb is a potent inhibitor of viral entry.
  • IFITM2 represents a promising cellular target for developing broad-spectrum antiviral therapeutic strategies.
Keywords:
IFITM2Monoclonal antibodySARS-CoV-2SyncytiaVirus entry

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.3K
Engineering Antiviral Agents via Surface Plasmon Resonance13:00

Engineering Antiviral Agents via Surface Plasmon Resonance

Published on: June 14, 2022

2.4K

Related Concept Videos

Fusion of Secretory Vesicles with the Plasma Membrane01:26

Fusion of Secretory Vesicles with the Plasma Membrane

Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
SNAREs and Membrane Fusion01:43

SNAREs and Membrane Fusion

Once a transport vesicle has recognized its target organelle, the vesicular membrane needs to fuse with the target membrane to unload the cargo. Transmembrane proteins called SNAREs present on organelle membranes and their vesicles, mediate vesicle fusion.
SNAREs exist in pairs that symmetrically interact and catalyze the fusion of the lipid bilayers in vesicle and target organelle. v-SNARE in the vesicle membrane are single polypeptide chains that bind to a complementary t-SNARE, composed of 2...
Inhibitors of Viral Protein Synthesis01:30

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...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...