A matched prospective study of human immunodeficiency virus serostatus, human papillomavirus DNA, and cervical lesions detected by cytology and colposcopy

Abstract

Objective: To compare the prevalence and type of human papillomavirus (HPV) infections in the genital tract of human-immunodeficiency-virus- (HIV) seropositive and -seronegative women matched for cytology and to examine prospectively the relationship of HPV DNA, colposcopic findings and cervical squamous intraepithelial lesions (SIL) in these matched seropositive and seronegative cohorts.Methods: A matched prospective study of HIV-seropositive and -seronegative women undergoing cytologic screening, colposcopy, and testing for HPV DNA and other infections at each visit.Results: Twenty-three HIV-seropositive women were matched with 23 seronegative women by cervical cytology reading, lifetime number of sexual partners, age, and follow-up length. Fourteen pairs of these women had follow-up visits every 4 months, for 56 and 53 total visits in seropositive and seronegative women, respectively. After matching, the groups had a similar overall prevalence of HPV DNA and of HPV oncogenic (high risk) types at baseline. On follow up, HIV-seropositive women were more likely than seronegative women to develop SIL (38% vs. 10%), less likely to have negative cytology (34% vs. 60%, overall P 0.03), more visits with HPV DNA detected (68% vs. 40% P 0.04), and more visits with multiple HPV DNA types detected (18% vs. 0%, P 0.02).Colposcopic lesions in the seropositive women were more likely to have sharp borders or mosaicism or to be thick white (P 0.009).Conclusions: After matching for baseline Papanicolaou smear readings, these data suggest that over time seropositive women have more visits that yield abnormal cytology, more persistent HPV DNA detection, and more colposcopic abnormalities than seronegative women.

Polymorphisms in 9q32 and TSCOT are linked to cervical cancer in affected sib-pairs with high mean age at diagnosis

“…TSCOT represents a possible risk factor in 9q32 and the encoded protein might inXuence the ability of T-lymphocytes to recognize and eradicate HPV infections. HPV persistence has been associated with malignant cervical epithelial neoplasia (Ho et al 1995;Schlecht et al 2001) and in order to establish long term infection, HPV needs to escape recognition and eradication by T-cells (Critchlow et al 1998;Eckert et al 1999;Hillemanns et al 1996;MinkoV et al 1998;Palefsky et al 1997;Palefsky et al 1998;Sun et al 1997). Women with low MAAD may have been inXuenced by tumour suppressor genes and oncogenes that together with HPV infection caused a faster progression and an earlier onset of disease.…”

Cell-Mediated Immune Response to Human Papillomavirus Infection

“…Such individuals show increased prevalence of anogenital HPV infection (31,32,60,(105)(106)(107) as well as longer periods of HPV persistence (31,40,46,90,136). In addition, infection with multiple HPV types and with oncogenic types are more common (9,31,46,78,90,107,136). Associations between markers of HIV disease status (e.g., viral load and CD4 lymphocyte count) and HPV infection have been inconsistent.…”

“…Such individuals show increased prevalence of anogenital HPV infection (31, 32, 60, 105-107) as well as longer periods of HPV persistence (31,40,46,90,136). In addition, infection with multiple HPV types and with oncogenic types are more common (9,31,46,78,90,107,136).…”

“…These differences may have been due to specific population characteristics, such as young age, or early stages of HIV infection (93). The risk of abnormal cervical or anal cytology as well as of HPVrelated anogenital disease (cervical SIL or anal intraepithelial neoplasia) is also increased in HIV-infected individuals (9,33,46,60,73,78,93,105,106,117,147). While, as mentioned above, most studies have suggested that the association between HIV infection and increased prevalence of HPV infection and disease is related to the immunosuppression seen in HIV infection, there is also some evidence that mechanisms other than immunosuppression, such as direct molecular interactions between HIV and HPV viral genes, may influence the natural history of HPV (8,43,93,146).…”

Immune Response Profiling of Patients with Anogenital Warts

“…22 In the 1990s, as the diagnosis of HPV infection by molecular diagnosis was developed, there were many reports confirming the rise in the incidence of infection with HPV 23 and other comorbidities, which included warts 24 and cervical squamous intraepithelial lesions 25 in patients who were immunosuppressed. The association of reduced cell-mediated immunity and consequent increase in HPV infection and associated disease in HIV-infected individuals has been demonstrated in various studies wherein these patients have shown increased prevalence [26][27][28][29][30][31] and longer period of persistence of HPV infection, 26,[32][33][34][35] which also provides a strong evidence to support the role of cell-mediated immunity. One of the major limitations in studies of cellmediated immune responses to HPV infection due to its highly localized nature of tissue tropism is squamous epithelial sites.…”