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Related Experiment Video

Updated: Jun 3, 2026

Analysis of Group IV Viral SSHHPS Using In Vitro and In Silico Methods

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Published on: December 21, 2019

IFI16 restricts SARS-CoV-2 replication by disrupting nucleocapsid-driven phase separation.

Ilaria Cislaghi¹, Sarah Turati¹, Dalila Vicario¹

¹Virology Unit, Department of Translational Medicine, University of Piemonte Orientale, Novara, Italy.

Communications Biology

|June 1, 2026

Summary

Interferon-inducible protein 16 (IFI16) restricts SARS-CoV-2 replication by binding viral RNA and nucleocapsid proteins. Its absence in cells promotes viral replication, offering new insights into host-virus interactions.

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Visualization of SARS-CoV-2 using Immuno RNA-Fluorescence In Situ Hybridization

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Published on: December 23, 2020

Area of Science:

Virology
Immunology
Cell Biology

Background:

Interferon-inducible protein 16 (IFI16) is known to sense viral DNA and restrict RNA virus replication.
The role of IFI16 in SARS-CoV-2 pathogenesis remains largely unexplored.

Purpose of the Study:

To investigate the function of IFI16 as a host restriction factor against SARS-CoV-2.
To elucidate the molecular mechanisms by which IFI16 impacts SARS-CoV-2 replication.

Main Methods:

Utilized IFI16 knockout cellular models.
Observed IFI16 relocalization and binding to viral components upon SARS-CoV-2 infection.
Assessed the impact of IFI16 on viral RNA-induced condensate formation.
Extended analysis to other human coronaviruses (OC43 and NL63).

Main Results:

IFI16 acts as a host restriction factor limiting SARS-CoV-2 replication.
IFI16 translocates from the nucleus to the cytoplasm during infection, interacting with the viral nucleocapsid protein and genome.
This interaction inhibits SARS-CoV-2 replication by preventing nucleocapsid protein condensate formation.
IFI16 exhibits differential effects on other human coronaviruses, enhancing OC43 replication while reducing NL63 replication.

Conclusions:

IFI16 plays a significant role in restricting SARS-CoV-2 replication through a mechanism involving viral RNA and nucleocapsid protein interactions.
The absence of IFI16 creates a cellular environment permissive to SARS-CoV-2 replication.
IFI16's effect on coronavirus replication is virus-specific, indicating complex host-pathogen interactions.