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Variants of human papillomaviruses 16 and 18 and their natural history in human immunodeficiency virus-positive women

¹ Albert Einstein College of Medicine, Department of Epidemiology and Population Health, 1300 Morris Park Avenue, Bronx, NY 10461, USA
² University of California, San Francisco, San Francisco, CA, USA
³ Maimonides Medical Center, Brooklyn, NY, USA
⁴ Southern Illinois University School of Medicine, Springfield, IL, USA
⁵ The Henry M. Jackson Foundation, Rockville, MD, USA
⁶ University of Southern California, Los Angeles, CA, USA
⁷ Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
⁸ National Institute of Child Health and Human Development, Bethesda, MD, USA

Correspondence
Nicolas F. Schlecht
nschlech{at}aecom.yu.edu

Highly oncogenic human papillomavirus (HPV) 16 and 18 variants might be expected to be particularly aggressive in HIV-positive women. The association of HPV16 and 18 variant lineages with race, human immunodeficiency virus (HIV) coinfection, CD4⁺ T-cell count, HIV-RNA level, time-to-clearance of HPV infection and presence of squamous intraepithelial lesions (SIL) among women in the Women's Interagency HIV Study was studied. Subjects were followed semi-annually with Pap smear and cervicovaginal lavage (CVL). HPV DNA was detected in CVLs using MY09/11 L1 PCR assay. Specimens positive for HPV16/18 underwent E6 PCR and sequencing to determine the variant present. Specimens from 195 HPV16- and 162 HPV18-positive women were classified into variant lineages based on sequencing results. African variants of HPV16 and HPV18 were significantly more prevalent among African-Americans than among Caucasians [42 versus 14 % (P=0·001) and 60 versus 13 % (P<0·001), respectively]. However, it was not possible to detect associations between the HPV16 or 18 variant lineages and other factors studied. African variants of HPV16/18 were more common in women of African descent living outside Africa, which could reflect mixing behaviours and/or immunogenetic factors. However, in a large population of HIV-infected women, the variant of HPV16 or 18 was unrelated to persistence of infection or presence of SIL. If non-European variants are more oncogenic, the effect may involve a late stage in cervical tumorigenesis.

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