Immune response in cervical dysplasia induced by human papillomavirus: the influence of human immunodeficiency virus-1 co-infection - review

Abstract

Human immunodeficiency virus (HIV-1) has become an important risk factor for human papillomavirus (HPV) infection and the development of HPV associated lesions inKey words: human papillomavirus -human immunodeficiency virus-1 -cervical intraepithelial neoplasiacervical immunity response -womenAll papillomaviruses have a nonenveloped icosahedral capsid that is 55 nm in diameter and that contains a double-stranded circular DNA genome of about 7900 nucleotide pairs (Howley 1995, Shah & Howley 1995 that codes for at least eight early and two late (capsid) proteins. The expression of viral genes is modulated by an 800-base pair long-control region (LCR) that is epithelial tissue specific and regulated by physiological signals. The products of the early genes E6 and E7 are oncoproteins that destabilize the cellular tumor supressors p53 and pRB (Dyson et al. 1989, Hawley-Nelson et al. 1989.Human papillomavirus (HPV) is currently detected in a large number of mammals and have been shown highly species-specific. HPV subtypes are defined by DNA sequence analysis and represent genotypes. There are over 100 different types of virus; approximately 130 additional isolates represent only partially characterized putative novel genotypes (de Villiers 1997, zur Hausen 1999. Among them, more than 20 types can infect the genital epithelia. In order to be considered a new HPV type, the E6, E7 and L1 gene sequence in the HPV genome has to differ by more than 10% from those of any previously described HPV types. The viral E6 and E7 oncoproteins are essential components in malignant conversion, although, in spite of being necessary, they are not sufficient for the development of the malignant phenotype (revised by zur Hausen 1999).+ Corresponding

Frequency and types of human papillomavirus among pregnant and non-pregnant women with human immunodeficiency virus infection in Recife determined by genotyping

“…The viral types 16,31,33,38,52,58 and 67 are all grouped in the same branch of the phylogenetic tree, thus indicating their similarity regarding oncogenic potential (IARC 2007). In the present study, the high prevalence of HPV 58 is in agreement with other studies that revealed the importance of this type in some regions of Brazil (North, Northeast and Centre-West) and in the Orient (Mota 2002, Câmara et al 2003, Yokoyama et al 2003, Clifford et al 2005, Nicol et al 2005, Pereira et al 2007). The results obtained here corroborate the idea that there are regional variations of certain HPV types in Brazil (Câmara et al 2003, Queiroz et al 2004, Pereira et al 2007.…”

“…The cervical environment probably favoured the establishment of oncogenic types of HPV due to the set of local immunological factors, such as immunoglobulin secretions, local levels of CD4, Langerhans cells and concomitant infections (Mota 2002, Nicol et al 2005, Santegoets et al 2008. Pregnancy can hasten and intensify infection by high-risk HPV (in particular, by HPV 16) and presents highly sensitive conditions for HPV activation, persistence and transformation (Armbruster-Moraes et al 2000).…”

Concentration levels of IL-10 and TNFαcytokines in patients with human papilloma virus (HPV) DNA+and DNA−cervical lesions

“…In contrast, Song et al (2007) reported that TNFα and IL-10 levels did not correlate with pre-cancerous lesions of the cervix after HPV infection. Still, other investigators (i.e., see Nicol et al, 2005) documented the fact that malignant transformed cervical epithelial cells had a decreased ability to express TNFα and suggested that this loss of expression by cervical cancer cells may have modulated the tumor microenvironment and thereby supported continuing tumor growth.…”

The first ten years: achievements and challenges of the Brazilian program of universal access to HIV/AIDS comprehensive management and care, 1996-2006

“…HPV infection is relatively prevalent in the Brazilian general population 60 , and especially prevalent and aggressive among women living with HIV/AIDS 61,62,63,64,65 . HIV infection may increase the oncogenicity of high-risk HPV types and the activation of low risk types, with higher rates of squamous intraepithelial lesions (SIL), and uterine cancer, over time 63,66 .…”