Autophagy-Associated Proteins Control Ebola Virus Internalization Into Host Cells
Olena Shtanko1, Ann N Reyes1, William T Jackson2
1Department of Virology and Immunology, Texas Biomedical Research Institute, San Antonio.
The Journal of Infectious Diseases
|June 28, 2018
Summary
Autophagy proteins are crucial for Ebola virus (EBOV) entry into host cells. Microtubule-associated protein 1A/B light chain 3B (LC3B)-II specifically mediates EBOV-containing vesicle internalization.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Ebola virus (EBOV) entry into host cells occurs via macropinocytosis, a cellular process not fully understood.
- Autophagy, a cellular degradation pathway, shares components with macropinocytosis, suggesting a potential role in viral entry.
Purpose of the Study:
- To investigate the role of autophagy-associated proteins in EBOV macropinocytosis.
- To determine the specific contribution of microtubule-associated protein 1A/B light chain 3B (LC3B) in EBOV uptake.
Main Methods:
- Depletion of autophagy-associated proteins (beclin 1, ATG7, LC3B) in host cells.
- Assessment of EBOV uptake and macropinocytic vesicle formation.
- Analysis of LC3B-I and LC3B-II interaction with macropinocytic structures.
Main Results:
- Depletion of beclin 1, ATG7, or LC3B significantly inhibited EBOV uptake.
- Autophagy protein depletion blocked macropinocytic vesicle formation at the cell surface.
- LC3B-II was identified as critical for the internalization of macropinocytic vesicles containing EBOV.
Conclusions:
- Autophagy-associated proteins are essential for EBOV trafficking and cellular entry.
- LC3B-II plays a critical role in the internalization of macropinosomes, facilitating EBOV infection.
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