الفهرس 
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Abstract
SUMARRY
Cervical cancer is recognized as the third most common type of cancer in women worldwide and the second most prevalent cancer type and cause of cancer-related mortality in women in developing countries (Jemal et al., 2011). High-risk human papillomavirus (HPV) infection has been established as the main cause of cervical cancer (Zur Hausen, 1996).
Humanpapilloma virus is a nonenveloped DNA virus with a protein capsid. More than 120 different human papillomavirus (HPV) types have been catalogued so far, of which more than 40 infect the epithelial lining of the anogenital tract and other mucosal areas of the body (De Villiers et al., 2004).
Clinically, HPV types are classified as high-risk (HR) or low-risk (LR) based upon their cervical cancer oncogenicity, Low-risk HPV types 6 and 11 cause nearly all genital warts and a minority of subclinical HPV infections (Bosch, 2002). In contrast, the high-risk HPV types include 16, 18, 31, 33, 35, 45, and 58 and account for approximately 95 percent of cervical cancer cases worldwide. Other high-risk HPV types less often associated with neoplasia include 39, 51, 52, 56, 59, 68, 73, and 82 (Munoz, 2003).
The well-known risk factors of HPV infection in cervical lesions consist of high-risk sexual behaviors, immunosuppressant, age, contraceptive methods, other concurrent infection of sexually transmitted diseases (Deacon et al., 2000).
The relationship between HPV genital infection and CIN and cervical lesions was first proposed by German virologist Zur Hausen in the early 1980s (Shuang et al., 2010; Zur Hausen, 2000). And has attracted more and more attention. It was reported that the detection rate of HPV infection in normal women, patients with CIN I, CIN II, CIN III, and cervical cancer was 4%, 30%, 55%, 65%, and 99.8%, respectively (Kulasingam et al., 2002).
Infection with HPV is suspected by the appearance of clinical lesions and through the results of cytology, histology, and colposcopy, all of which are subjective and often inaccurate. In addition, serology is unreliable and unable to distinguish past from current infection (Carter, 2000).
This study aimed to evaluate the different methods of diagnosis of cervical HPV infection in Egyptian females by cytology, histopathology, colposcopy and HPV genotyping.
This study included 30 patient with either abnormal pap smears prior to colposcopic examination (10 cases) and abnormal T Z zone on colposcopic examination (20 cases).
We considered Pap smear result suggestive of the presence of HPV infection when we found (ASUS, LSIL, HSIL, koliocytic atypia).
We considered histopathological examination suggestive of the presence of HPV infection when we found (koliocytosis, CINI, CINII, CINIII, and SCC).
In this study the golden standard test for detection of HPV was considered PCR-ISH tissue. We found PCR-ISH tissue was positive in 16 cases (53.33%) and 14 cases (46.6%) were negative.
The age of studied group ranged from (20-50) years with mean and standard deviation (SD) 32.77+7.99 while the duration of marriage in 29 cases (0.5-30) years, as one was divorced, with mean and SD 12.95+8.26.
Comparing the result of pap smear, histopathology, colposcopy and PCR swap in diagnosis of HPV with the golden standard test ISH PCR tissue, the sensitivity were 87.5%, 100%, 62.5% and 56,2% respectively but the specificity were 78.6%, 42.9%, 28.6% and 100% respectively.
We can conclude that the conventional cytology and histopathological examination were sensitive tests for detection of HPV, cervix colposcopy showed lower sensitivity and specificity to detect HPV but this can be improved by taking multiple biopsies. PCR swap showed the highest specificity and the lowest sensitivity as blood contamination and insufficient amount of cells adversely affect It is result.