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Human papillomavirus and blastocyst apoptosis
Joan H Calinisan1, Steven R Chan, Alan King
1Department of Gynecology and Obstetrics, Loma Linda University School of Medicine, California 92350, USA.
Journal of Assisted Reproduction and Genetics
|May 15, 2002
Summary
Human papillomavirus (HPV) type 16 DNA caused significant DNA fragmentation in mouse blastocysts within 24 hours, suggesting apoptosis initiation. Other HPV types did not show this rapid effect.
Area of Science:
- Reproductive biology
- Molecular virology
- Developmental toxicology
Background:
- Human papillomavirus (HPV) is a common sexually transmitted infection.
- Certain HPV types are oncogenic and can integrate into host DNA.
- The impact of HPV DNA on early embryonic development is not fully understood.
Purpose of the Study:
- To investigate the effect of HPV DNA on DNA integrity in blastocyst-stage embryonic cells.
- To determine if HPV DNA disrupts blastocyst DNA.
- To assess if DNA damage intensity correlates with HPV type.
Main Methods:
- Superovulated female mice were used to obtain embryos cultured to the blastocyst stage.
- Blastocysts were exposed to PCR-synthesized DNA fragments from HPV types 16, 18, 31, or 33.
- DNA damage was quantified using comet assay and fluorescent pixel intensity measurement after 24-hour incubation.
Main Results:
- HPV type 16 DNA significantly increased DNA fragmentation in blastocysts compared to other tested HPV types.
- No correlation was found between the size of HPV DNA fragments and the extent of DNA fragmentation.
- The observed DNA damage occurred rapidly, within 24 hours of exposure.
Conclusions:
- HPV type 16 DNA appears to induce apoptosis in embryonic cells via DNA fragmentation.
- The rapid onset of DNA damage suggests a direct mechanism of action.
- While HPV 16 showed a significant effect, other HPV types may impact embryos under different experimental conditions.