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The association between HIV genital shedding and cervical neoplasia The
concentration of the HIV-1 at the mucosal site is a determinant key for
heterosexual and perinatal transmission of the infection. In the last few
years, many efforts have been made to evaluate the regulatory factors of
HIV genital shedding both in seminal fluid and cervicovaginal secretions.
Many factors as plasma HIV-1 RNA, severity of immunocompromise, genital
ulceration and inflammation, modulate the shedding of HIV in
cervicovaginal secretions. Several
studies found that HIV-seropositive women are at higher
risk of incidence and persistence of cervical intraepithelial neoplasia
(CIN) and Human Papillomavirus (HPV) infection. Although Human
Immunodeficiency Virus (HIV) infection is a well known risk factor for
cervical intraepithelial neoplasia (CIN), the influence of CIN on
cervicovaginal shedding of HIV is poorly studied. The purpose of this
study was to evaluate the association between CIN and the shedding of HIV
in cervicovaginal secretions. Our
data suggests that the association between HIV genital shedding and
cervical neoplasia is biologically plausible and likely to be mediated by
the immune upregulation at the site of the cervical lesion. This could
lead to both increased number of intraepithelial lymphocytes and
macrophages in the squamous epithelium of the cervix and increased
intralesional concentration of proinflammatory cytokines that modulate HIV
replication. It
might be that the association between CIN and HIV genital shedding could
be mediated by Human Papillomavirus (HPV) infection . The presence of CIN lesions should be considered as a significant risk factor for genital HIV shedding. Given the high prevalence of cervical disease among HIV-positive women this finding could have important epidemiological implications both in heterosexual and perinatal transmission of HIV.
Bibliuographic reference:
Barbara Gardella Department of Obstetrics and Gynecology, IRCCS Policlinico S. Matteo, University of Pavia, Italy
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