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CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites
Published on: November 14, 2018
Archetype JC virus efficiently propagates in kidney-derived cells stably expressing HIV-1 Tat
Souichi Nukuzuma1, Masanori Kameoka, Shigeki Sugiura
1Department of Microbiology, Kobe Institute of Health, 4-6, Minatojima-Nakamachi, Chuo-ku, Kobe, Hyogo 650-0046, Japan. s-nuku@gj8.so-net.ne.jp
Microbiology and Immunology
|November 12, 2009
Summary
HIV-1 Tat protein significantly increases archetype John Cunningham virus (JCV) replication in kidney cells. This finding suggests Tat
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Progressive multifocal leukoencephalopathy (PML) is caused by pathogenic JCV with rearranged regulatory regions.
- Archetype JCV, typically found in the kidneys, may convert to the PML-type under immunosuppression.
- HIV-1 Tat protein is known to enhance JCV late promoter activity.
Purpose of the Study:
- To investigate the influence of HIV-1 Tat on archetype JCV propagation.
- To establish a cell culture system for studying Tat's role in JCV replication.
Main Methods:
- Utilized kidney-derived COS-7 cells permitting archetype JCV replication.
- Established COS-tat cells stably expressing HIV-1 Tat.
- Compared archetype JCV propagation in COS-7 and COS-tat cells.
Main Results:
- Archetype JCV propagation was significantly greater in COS-tat cells compared to COS-7 cells.
- HIV-1 Tat expression directly correlated with increased archetype JCV production.
- SV40 T antigen expression, though slightly enhanced by Tat, was not the primary driver of increased JCV replication.
Conclusions:
- COS-tat cells provide a novel system for studying Tat's role in archetype JCV replication.
- This research offers insights into the development of PML in HIV-1-infected individuals.
- The efficiency of JCV propagation is dependent on functional Tat expression.
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