Human papillomavirus (HPV) genotypes and HPV16 variants in human immunodeficiency virus-positive Italian women

Abstract

Human immunodeficiency virus (HIV)-positive women have high rates of cervical squamous intraepithelial lesions (SIL) and concurrent human papillomavirus (HPV) infections with a variety of genotypes whose oncogenic risk is poorly documented. The prevalence and persistence of HPV genotypes and HPV16 variants were analysed in 112 HIV-positive and 115 HIV-negative Italian women. HIV-positive women were more likely than HIV-negative women to be infected by HPV at the initial examination (39.3 vs 13.9 %, P,0.001) and to have a higher period prevalence of HPV infection over a 3-year follow-up (43.8 % vs 17.4 %, P,0.001), regardless of CD4 + cell counts and anti-retroviral therapy. 18, 31, 33, 35, 45, 52, 58 and 66), among the 20 different viral genotypes identified, were predominant in HIV-positive (33.9 %) compared with HIV-negative (13.9 %) women. Among HIV-infected women, with normal cytology as well as with SIL of any grade, the most common genotypes were HPV16 followed by HPV81, isolates from 18 HIV-positive and eight HIV-negative women were classified into variant lineages based on sequencing analysis of E6 and E7 genes and the long control region. Whilst the HPV16 G350 European variant was prevalent in both HIV-positive (10.7 %) and -negative women (3.5 %), HPV16 African 2 variant was only detected in HIV-positive women (3.6 %), suggesting different sexual mixing behaviours. The increased prevalence of uncommon viral genotypes and HPV16 variants in HIV-positive Italian women underscores the need to target a wide range of HPV types in cervical screening of high-risk women. INTRODUCTIONInfection with genital human papillomaviruses (HPVs) has been established as the primary cause of cervical squamous intraepithelial lesion (SIL) and invasive cervical cancer (zur Hausen, 1987;Bosch et al., 1995; IARC, 1995;Walboomers et al., 1999). To date, more than 40 HPV genotypes have been identified in the female genital tract and have been grouped as (i) 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59), associated with a high relative risk of cervical cancer; (ii) 11, 40, 42, 43, 44, 54, 61, 70, 72, 81 and 89), associated with benign epithelial proliferations; (iii) 'probable carcinogenic' viruses (HPV types 26, 53, 66, 68, 73 and 82), associated with cervical cancer in a few casecontrol studies; and (iv) 'undetermined risk' viruses (HPV types 2a, 3, 7, 10, 27, 28, 29, 30, 32, 34, 55, 57, 62, 67, 69, 71, 74, 77, 83, 84, 85, 86, 87, 90 and 91), whose oncogenicity has not yet been determined (Muñoz et al., 2003(Muñoz et al., , 2006Smith et al., 2007).Epidemiological studies, performed mainly on human immunodeficiency virus (HIV)-negative women, have shown that, despite the high prevalence and strong association with cervical neoplasia, the majority of HPV infections with high-and low-risk types are transient and only a fraction of persistent infections progress on to highgrade SIL and invasive cancer, underscoring the interplay of a number of environmental, viral and host factors in HPV-related tumour progression (Massa...

HPV infection-associated anogenital cyto-colpo-histological findings and molecular typing in HIV-positive women

“…The incidence of SCCA is particularly high in HIV+ men and women (Poggio, 2011). HIV+ women more frequently present persistent infection with multiple HPV genotypes (Corrêa et al, 2011;Pantanowitz and Michelow, 2011), probably owing to the inability of an HIV-compromised system to control the expression and replication of HPV (Tornesello et al, 2008).…”

Differences and changes in human papillomavirus type 16 variant status in human immunodeficiency virus-positive adults are not uncommon

“…The ability to sample both anatomical sites at multiple visits may have increased our ability to detect variant differences. Other studies that tested for variants longitudinally did not report changes in either cervical (Emeny et al, 1999;Tornesello et al, 2008) or anal (Xi et al, 1998) samples.…”

“…The ability to sample both anatomical sites at multiple visits may have increased our ability to detect variant differences. Other studies that tested for variants longitudinally did not report changes in either cervical (Emeny et al, 1999;Tornesello et al, 2008) or anal (Xi et al, 1998) samples.Our results illustrate the limitations in HPV typing and HPV variant detection to distinguish between persistent and recurrent infection. Failure to detect a type or specific variant at one time point or in one sample cannot be taken as evidence of clearance, as a negative HPV result is an imperfect indicator for the absence of infection.…”

Human papillomavirus DNA and mRNA prevalence and association with cervical cytological abnormalities in the Irish HIV population

“…Similar HPV DNA prevalence has been found in other HIV-positive population studies. [13][14][15][16][17] The prevalence of HPV DNA was increased in HIV-positive women in comparison to the HIV-negative population of Ireland, 19.8%. 17 Correspondingly, as expected, the rate of cervical cytology abnormalities was higher in this study population compared to the general Irish population, 28.7% versus 11.1%.…”