engleski

DETECTING HPV L1 PROTEIN CAPSID IN CERVICAL LESION

Cohort studies have shown that for developing precancerous lesions of uterine cervix HPV infection is crucial. The main event in the carcinogenesis is not a simple infection, but its persistency and viral integration. Problems with HPV detecting tests is that they can not tell the difference between persistent or transient infection of HPV. Papilloma infection is very common among adolescent and young women and the goal of investigators is to differentiate a persistant infection, since it represents a main cause of developing cervical lesion. Because of viral intergration into host genom, genetic instability occurs, and some of the cellular proteins are overexpressed. That is what happens in HSIL, and cellular proteins like P16INK4a can be detected in majority of HSIL cases or cancers. HPV capsid is composed of two structural proteins: minor L2 and L1 major protein.The last one is a main target of immune system. Because of the genetic instability in host cells with integated virus, intraepithelial maturation of cells is disturbed, problem in expression of viral proteins occurs and consequently reduction in L1 capsid antigen production results in reduction of celullar immune response. It has been shown by other authors that the absence of L1 correlates with progression and positivity means regresion of cervical lesion. Aim of the study is to investigate the prevalence of HPV L1 capsid protein in low grade and high grade squamous lesion(LSIL/HSIL) of the uteine cervix using cytoactive method and compare with finding of p16INK4a protein in HSIL smears. Since June2007-December 2007, we rull out 67 high risk HPV positive patients and analysed their cervical smears. After decolourising slides we preformed immunoassaying with cytoaktiv screening test for HPV L1 (Cytoimmun diagnostic GbmH, Pirmanses, Germany) and p16INK4a staining using DAKO monoclonal antibody. Results:Cytological diagnose od LSIL was made in fifty-three patients(53/67), and fourteen patients had HSIL. In all HSIL patients, diagnosis was confirmed by biopsy or cold knife conisation. After immunoassaying positive HPV L1 was found in 60, 4%(32/53) of LSIL and in 21, 4% (3/14) of HSIL smears.Strong p16INK4a positive stain was seen in eleven HSIL smears(78, 6%). Conclusion:Lower L1 detection rate in HSIL can be explained by possible loss of viral L genes and consequently lower production of capsid proteins. On the other hand positive p16 INK4a stain represents viral integration into the host genome and genetic instability of the host cell which can lead to its malignant transformation. Hence in L1 negative and p16 positive smears, lesions will most likely progress so patients can be advised for shorter control period or sooner histological confirmation.

HPV L1; cytology; progression of cervical lesions

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