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Updated: May 30, 2026

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
Published on: June 3, 2012
Lysosome-associated membrane glycoprotein 3 is involved in influenza A virus replication in human lung epithelial
Zhuo Zhou1, Qinghua Xue, Yuli Wan
1State Key Laboratory of Molecular Virology and Genetic Engineering, Institute of Pathogen Biology, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100730, China.
Background:
Influenza A virus mutates rapidly, rendering antiviral therapies and vaccines directed against virus-encoded targets ineffective. Knowledge of the host factors and molecular pathways exploited by influenza virus will provide further targets for novel antiviral strategies. However, the critical host factors involved in influenza virus infection have not been fully defined.
Results:
We demonstrated that LAMP3, a member of lysosome-associated membrane glycoprotein (LAMP) family, was significantly induced in human lung epithelial (A549) cells upon influenza A virus infection. Knockdown of LAMP3 expression by RNA interference attenuated production of viral nucleoprotein (NP) as well as virus titers. Confocal microscopy results demonstrated that viral NP is colocalized within LAMP3 positive vesicles at early stages of virus infection. Furthermore, knockdown of LAMP3 expression led to a reduction in nuclear accumulation of viral NP and impeded virus replication.
Conclusions:
LAMP3 is an influenza A virus inducible gene, and plays an important role in viral post-entry steps. Our observations may provide insights into the mechanism of influenza virus replication and potential targets for novel anti-influenza therapeutics.
Insights
Lysosome-associated membrane glycoprotein 3 (LAMP3) is induced by influenza A virus. Its knockdown impairs viral replication by affecting nucleoprotein transport, suggesting LAMP3 as a novel antiviral target.
Area of Science:
- Virology
- Cell Biology
- Molecular Medicine
Background:
- Influenza A virus rapidly mutates, necessitating new antiviral strategies.
- Identifying host factors exploited by the virus is crucial for novel therapeutics.
- Critical host factors in influenza virus infection remain largely undefined.
Purpose of the Study:
- To investigate the role of host factors in influenza A virus infection.
- To identify potential new targets for antiviral therapies.
Main Methods:
- Studied influenza A virus infection in human lung epithelial (A549) cells.
- Utilized RNA interference to knockdown LAMP3 expression.
- Employed confocal microscopy to visualize viral nucleoprotein (NP) localization.
- Quantified viral NP production and virus titers.
Main Results:
- LAMP3 expression was significantly induced upon influenza A virus infection.
- Knockdown of LAMP3 attenuated viral nucleoprotein production and virus titers.
- Viral NP colocalized with LAMP3-positive vesicles during early infection.
- Reduced LAMP3 expression impeded nuclear accumulation of viral NP and virus replication.
Conclusions:
- LAMP3 is an influenza A virus-inducible gene crucial for viral post-entry.
- LAMP3 plays a significant role in influenza virus replication.
- LAMP3 represents a potential therapeutic target for novel anti-influenza drugs.
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