Risk Factors for Low-Grade Cervical Abnormalities Differ from Those for Human Papillomavirus Infection

Risk Factors for Low-Grade Cervical Abnormalities Differ from Those for Human Papillomavirus Infection

to demonstrate the expression of biomarkers, detected by immunohistochemical techniques in healthy tissues, as well as in preneoplastic and neoplastic lesions of the uterine cervix. In HPV-positive tissues, HSV infection and replication induced significant cytopathic effects (CPE), but the tissues were able to recover and maintain a certain degree of tissue integrity and architecture. It is estimated that some percentage of the population does suffer from HVH at one time or other. At baseline and follow-up visits, women were tested for HPV and cervical abnormalities, and were interviewed about their sexual behaviors and substance use. In a cross-sectional study, we investigated the role of herpes simplex virus type 2 as a cofactor to human papillomavirus in cervical cancer. The extent of CPE induced by HSV is dependent on the magnitude of HPV replication and gene expression at the time of HSV infection. In 4 of the others, beta- streptococci were cultured from their cervical specimens.

Risk Factors for Low-Grade Cervical Abnormalities Differ from Those for Human Papillomavirus Infection
Analyses of the factors that increase the risk of developing low-grade squamous intraepithelial lesions were based on 496 women who were HPV-infected at baseline or tested positive later in the follow-up period. Human papillomavirus tests were also performed. Between 400,000 and 500,000 new cases are reported each year with nearly 200,000 deaths Bai et al., 2000 and Mohar and Frias-Mendivil, 2000. There are two antigenic groups of herpes virus hominis i.e. In univariate analyses, the risk of acquiring HPV increased as a woman’s number of lifetime partners, number of recent partners and monthly number of new partners increased. As only a minority of low-grade dysplastic lesions of the cervix uteri will eventually progress to carcinoma, predicting the behavior of these lesions could be of high value in clinical practice. This is a multistep process and the long period of latency from the initial time of infection to the development of disease suggests that other determinants may be involved as possible cofactors in the pathogenesis of HPV-related genital cancers.

An infected cell produces 1000 virus particles, with or without envelops, but only 5 to 10 per cent are infectious. A history of herpes or vulvar warts also continued to be associated with an increased risk (3.5 and 2.7, respectively), and pill users continued to have a lower risk than women not using this method of contraception (0.5). Of the 496 women in the study of risk factors for low-grade lesions, 109–about one in four–developed lesions during the follow-up period. S. Herpes virus antibody complexes may be infectious. Again, the multivariate calculations by and large confirmed the univariate results. Women who had had HPV for intervals up to three years had sharply increased risks of lesions (relative hazards, 6.1-10.3); those who smoked cigarettes daily also had an elevated risk (1.7).

Since HSV and HPV are transmitted sexually and infect the same cell type, both viruses have the potential to interact with each other, impacting neoplastic progression. It has also been very probably associated with cervical cancer, though no definite etiologic relationship between the two has yet been established.

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