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Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
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Cyclophilin B enhances HIV-1 infection
Jason DeBoer1, Christian J Madson1, Michael Belshan2
1Department of Medical Microbiology and Immunology, Creighton University, Omaha, NE, USA.
Virology
|January 18, 2016
Summary
Cyclophilin B (CypB) enhances human immunodeficiency virus type 1 (HIV-1) infection by aiding viral DNA
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Cyclophilin B (CypB) is an intracellular chaperone with diverse cellular roles.
- CypB interacts with HIV-1 Gag protein and is implicated in HIV replication.
- CypB is found in the ER, nucleus, and can be secreted from cells.
Purpose of the Study:
- To investigate the role of Cyclophilin B (CypB) in human immunodeficiency virus type 1 (HIV-1) infection.
- To determine how CypB influences viral DNA nuclear import during HIV replication.
Main Methods:
- Over-expression of CypB in cells.
- Analysis of HIV infection enhancement with CypB.
- Assessment of cyclosporine treatment effects.
- N-terminal deletion mutants of CypB were created and analyzed.
- Experiments involving passive transfer of secreted CypB.
Main Results:
- Over-expression of CypB significantly enhances HIV infection.
- CypB enhances infection by increasing the nuclear import of viral DNA.
- The N-terminus of CypB is crucial for this enhancement and proper localization.
- Deletion of the N-terminus leads to mislocalization and suppressed HIV infection.
- Secreted CypB does not affect HIV infection levels.
Conclusions:
- Intracellular Cyclophilin B (CypB) plays a critical role in modulating HIV nuclear import.
- The N-terminus of CypB is essential for its function in enhancing HIV infection.
- CypB's effect on HIV is dependent on its intracellular localization, not its secreted form.
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