Related Experiment Videos
The relationship of herpes simplex virus latency associated transcript expression to genome copy number: a
Xiao-Ping Chen1, Marina Mata, Mary Kelley
1Department of Neurology, University of Pittsburgh School of Medicine, Pennsylvania, USA.
Journal of Neurovirology
|June 8, 2002
Summary
Herpes simplex virus (HSV) latency involves varying genome numbers in neurons. LAT expression during HSV latency does not solely depend on genome quantity, suggesting neuron-specific regulatory factors are crucial.
Area of Science:
- Virology
- Neuroscience
- Molecular Biology
Background:
- Herpes simplex virus (HSV) establishes lifelong latency in neurons.
- Latency-associated transcripts (LATs) are key viral products during latency.
- The relationship between HSV genome copy number and LAT expression is not fully understood.
Purpose of the Study:
- To quantitatively assess the relationship between latent HSV genomes and LAT expression in individual neurons.
- To determine the number of HSV genomes in LAT-positive and LAT-negative neurons during latency.
Main Methods:
- Laser capture microdissection (LCM) to isolate individual neurons from mouse trigeminal ganglia (TG).
- In situ hybridization (ISH) to detect LAT-positive and LAT-negative neurons.
- Polymerase chain reaction (PCR) and quantitative real-time PCR to quantify HSV genomes (ICP47 and UL44).
Main Results:
- Both LAT-positive and LAT-negative neurons contained detectable HSV genomes.
- HSV genome counts per neuron followed a Poisson distribution.
- Mean genome counts were 178 per LAT-positive neuron and 68 per LAT-negative neuron, with overlapping ranges.
Conclusions:
- LAT expression detectable by ISH is not solely determined by the number of HSV genomes per neuron.
- Neuron-specific factors likely play a significant role in regulating LAT expression during HSV latency.