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Updated: May 27, 2026
08:26
Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
Genotypic characterization of herpes simplex virus DNA polymerase UL42 processivity factor
Sonia Burrel1, Zaïna Aït-Arkoub, Henri Agut
1UPMC Univ Paris 06, ER1 DETIV, F-75013, Paris, France. sonia.burrel@psl.aphp.fr
Antiviral Research
|November 9, 2011
Summary
Genetic variations in the herpes simplex virus (HSV) UL42 processivity factor were analyzed for antiviral resistance. The UL42 protein appears highly conserved and unlikely to be a primary cause of drug resistance in HSV.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Herpes simplex virus (HSV) DNA polymerase comprises UL30 and UL42 subunits.
- UL42 enhances DNA polymerase processivity during viral replication.
- HSV drug resistance often involves mutations in thymidine kinase or DNA polymerase.
Purpose of the Study:
- To characterize genetic variations in the HSV UL42 processivity factor.
- To assess the role of UL42 variations in antiviral resistance.
Main Methods:
- Sequencing of the full-length UL42 gene from laboratory strains and clinical isolates (drug-sensitive and ACV-resistant).
- Analysis of natural polymorphism and identification of mutations in UL42.
Main Results:
- The UL42 protein is highly conserved across HSV strains, with lower variability in HSV-2.
- Previously known and novel polymorphisms were found in ACV-resistant isolates.
- A frameshift mutation in UL42 was identified in three clinical isolates.
Conclusions:
- The UL42 processivity factor exhibits limited variability and is unlikely to be a major contributor to HSV antiviral resistance.
- Further research may be needed to fully elucidate resistance mechanisms.
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