Human immunodeficiency virus (HIV) is a retrovirus belonging to the lentivirus family and is the causative agent of AIDS. Numerous studies have documented a high prevalence of HPV coinfection (19), with an increase in both latent and symptomatic HPV infection. HIV alters the natural history of HPV infection with decreased regression rates and more rapid progression to high-grade and invasive lesions, resulting in a more aggressive phenotype. High-grade lesions have been associated with both high- and low-risk HPV types, leading to speculation that HIV may increase the oncogenicity of the HR types, and possibly the activity of low-risk types also (20). However, whereas the development of AIDS-related malignancies, such as Kaposi's sarcomas and non-Hodgkin's lymphoma are attributable to immune deficiency, the relation between HIV and cervical cancer remains to be elucidated.
There are two major pathways involved in cervical cancer tumorigenesis. The first is the loss of heterozygosis (LOH) (see 8); the other involves genetic instability at the microsatellite loci (MSI). This instability originates as a result of defects in the mismatch repair genes, making them unable to repair errors occurring during replication. Loss of cell-cycle checkpoints could also cause this instability. MSI occurs at low rate in cervical cancer (8-10%) (21); however, a significantly higher frequency of MSI has been observed in HIV-related CIN lesions, and these changes were independent from the HIV-induced immune suppression (22). Thus, it is possible that HIV-associated cervical cancers may progress through the microsatellite instability pathway, whereas HIV negative ones progress through LOH.
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