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Transduction of cellular sequence by a human immunodeficiency virus type 1-derived vector.
G Sun1, P K O'Neil, H Yu
1Department of Molecular Genetics & Microbiology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.
Journal of Virology
|November 2, 2001
Summary
Human Immunodeficiency Virus type 1 (HIV-1) captured a human cellular sequence during replication. This study demonstrates HIV-1
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- The rate of human immunodeficiency virus type 1 (HIV-1) mutation is crucial for viral evolution and drug resistance.
- Understanding viral replication mechanisms can reveal novel pathways for therapeutic intervention.
Purpose of the Study:
- To investigate the mechanisms of HIV-1 mutation during a single replication cycle.
- To identify and characterize any non-viral sequences acquired by HIV-1 during replication.
Main Methods:
- Analysis of proviral DNA sequences from HIV-1 replication studies.
- Database searches to identify the origin of inserted sequences.
- Chromosomal mapping of viral integration sites.
Main Results:
- An HIV-1 provirus contained a 147 bp insertion including a tRNA sequence and a 66 bp non-viral insertion.
- The 66 bp insertion showed homology to human CpG island sequences on chromosomes 6, 14, and 17.
- This represents the first documented instance of HIV-1 capturing a cellular sequence.
- The parental provirus integrated at chromosome 1p32.1, which did not contain homologous sequences to the captured CpG island.
Conclusions:
- HIV-1 is capable of transducing human cellular sequences during replication.
- The captured CpG island sequence likely originated from human chromosomes 6, 14, or 17.
- The acquisition of cellular sequences by HIV-1 is not necessarily linked to the viral integration site.