Related Experiment Video

Updated: Oct 2, 2026

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
09:39

Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein

Published on: April 21, 2015

The Matrix Protein of Human Parainfluenza Virus Type 3 Induces Mitophagy that Suppresses Interferon Responses

Binbin Ding1, Linliang Zhang1, Zhifei Li1

  • 1State Key Laboratory of Virology and Modern Virology Research Center, College of Life Sciences, Wuhan University, LuoJia Hill, Wuhan 430072, China.

Cell Host & Microbe
|April 14, 2017
PubMed

Insights

Human parainfluenza virus type 3 (HPIV3) matrix protein (M) induces mitophagy, a process removing damaged mitochondria. This viral M protein hijacks cellular machinery, bypassing the Parkin-PINK1 pathway to promote mitophagy and suppress immune responses.

Area of Science:

  • Cell Biology
  • Virology
  • Immunology

Background:

  • Mitophagy is a crucial cellular process for removing damaged mitochondria.
  • The Parkin-PINK1 pathway is a well-established mechanism for mitophagy induction.
  • Human parainfluenza virus type 3 (HPIV3) infection is known to induce autophagy, but the specific mechanisms are unclear.

Purpose of the Study:

  • To elucidate the mechanisms by which HPIV3 induces autophagy and mitophagy.
  • To identify the viral components responsible for mitophagy induction.
  • To investigate the impact of HPIV3-induced mitophagy on cellular immune responses.

Main Methods:

  • Investigated the subcellular localization of HPIV3 matrix protein (M).
  • Examined interactions between HPIV3 M protein, mitochondrial proteins (TUFM), and autophagy-related proteins (LC3).
  • Assessed the role of the Parkin-PINK1 pathway in HPIV3-induced mitophagy.
  • Analyzed the effect of HPIV3-induced mitophagy on the type I interferon response.

Main Results:

  • HPIV3 matrix protein (M) translocates to mitochondria and interacts with Tu translation elongation factor mitochondrial (TUFM).
  • HPIV3 M-mediated mitophagy occurs independently of the Parkin-PINK1 pathway, relying on M's interaction with LC3.
  • These interactions are essential for mitophagy induction and lead to the inhibition of the type I interferon response.

Conclusions:

  • A viral protein (HPIV3 M) is sufficient to induce mitophagy.
  • HPIV3 M acts as a bridge between autophagosomes and mitochondria, independent of the canonical Parkin-PINK1 pathway.
  • HPIV3-induced mitophagy contributes to the suppression of the host innate immune response.
Keywords:
HPIV3innate immunitymatrix proteinmitophagytype I IFN

More Related Videos

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF311:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection08:16

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

Published on: July 21, 2022

Related Concept Videos

Leaky Scanning02:28

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Influenza01:27

Influenza

Influenza is an acute, highly communicable viral disease that affects the respiratory tract and is responsible for seasonal epidemics worldwide. Influenza A is the most prevalent type associated with widespread outbreaks and is subtyped based on two surface glycoproteins: hemagglutinin (H) and neuraminidase (N), as in H1N1. These glycoproteins are essential for viral infectivity, transmission, and immune recognition. Transmission occurs primarily through respiratory droplets and contaminated...
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...