Site-specific inversion sequence of the herpes simplex virus genome: domain and structural features
Summary
Herpes simplex virus-1 genome rearrangements are driven by recombination within the
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Herpes simplex virus-1 (HSV-1) genome features two invertible components, L and S, flanked by inverted repeats.
- The 'a' sequences, located at termini and junctions, exhibit variable copy numbers and are crucial for genome structure.
- Previous studies indicate these repeats facilitate genome inversions, but the precise mechanisms and sequence domains remain unclear.
Purpose of the Study:
- To elucidate the structural organization and functional role of the 'a' sequences in HSV-1 genome inversions.
- To define the nucleotide sequence and repeat elements within the 'a' sequence domain.
- To investigate how variations in 'a' sequence copy number and internal structure influence genome rearrangements.
Main Methods:
- Comparative nucleotide sequence analysis of HSV-1 DNA fragments with varying 'a' sequence copy numbers.
- Identification and characterization of direct repeat elements (DR1, DR2, DR4) within the 'a' sequence.
- Experimental manipulation by inserting DNA fragments containing specific repeat sequences into the HSV-1 genome.
Main Results:
- The 'a' sequence comprises two 20-bp direct repeats (DR1) flanking a region with tandem 12-bp repeats (DR2) and 37-bp repeats (DR4).
- Amplification of 'a' sequences occurs via recombination through DR1, and variations in DR2 and DR4 copy numbers arise from unequal crossing over or slippage.
- Insertion of a DNA fragment containing 'b', 'a', and 'c' sequences induced new inversion sites, confirming the role of these elements in genome dynamics.
Conclusions:
- Recombination through DR1 is the primary mechanism for amplification of terminal and internal 'a' sequences.
- The internal structure of the 'a' sequence, particularly the number of DR2 and DR4 copies, is plastic and subject to variation.
- Genome inversions in HSV-1 are a result of intramolecular recombination between terminal and inverted 'a' sequences.
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