Human papillomavirus type 16 viral load in relation to HIV infection, cervical neoplasia and cancer in Senegal.
BACKGROUND
The importance of human papillomavirus (HPV) viral load in the pathogenesis of cervical cancer among HIV-infected and HIV-uninfected women has not yet been established.


METHODS
In this cross-sectional study, HPV-16 viral loads were measured using previously-collected and frozen cervical swab samples from 498 HPV-16 positive Senegalese women (368 HIV-seronegative, 126 HIV-1 and/or HIV-2 seropositive). The real-time polymerase chain reaction assay was used to quantify HPV-16 E7 copy number normalized by human cellular DNA (β-actin), and viral loads were log10 transformed. Associations between HPV-16 viral load, degree of cervical abnormality, and HIV status were assessed using multinomial and linear regression methods.


RESULTS
Compared to women with normal cytology, the likelihood of CIN1 (ORa: 1.21, 95% CI 0.93-1.57), CIN2-3 (ORa: 2.38, 95% CI 1.72-3.29) and cancer (ORa: 2.12, 95% CI 1.52-2.96) was found to increase for each 1-unit log10 increase in HPV-16 viral load. Compared to HIV-negative women, HIV-positive women had higher average HPV-16 viral load values (βa: 0.39, 95% CI 0.03-0.75), even after accounting for degree of cervical abnormality.


CONCLUSIONS
In our study of women including those with cancer, HPV-16 viral load was associated with a higher likelihood of cervical abnormalities. However, substantial overlaps across categories of disease severity existed. Higher viral load among HIV-infected individuals may indicate that HIV infection influences HPV viral replication factors.
Department of Epidemiology, School of Public Health, University of Washington, Box 357236, Seattle, WA 98195, USA; International Agency for Research on Cancer, Section of Environment and Radiation, 150 Cours Albert Thomas, Lyon Cedex 08 69372, France. Electronic address: hanischr@fellows.iarc.fr.
Rachel A
RA
Hanisch
Department of Pathology, Harborview Medical Center, Seattle, WA 98104, USA.
Stephen L
SL
Cherne
Service des Maladies Infectieuses Ibrahima DIOP MAR - CHU de Fann, Université Cheikh Anta Diop, Dakar, Senegal.
Papa Salif
PS
Sow
Department of Epidemiology, School of Public Health, University of Washington, Box 357236, Seattle, WA 98195, USA.
Rachel L
RL
Winer
Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA 98195, USA.
James P
JP
Hughes
Department of Pathology, Harborview Medical Center, Seattle, WA 98104, USA.
Qinghua
Q
Feng
Division of Allergy and Infectious Diseases and Department of Global Health, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Geoffrey S
GS
Gottlieb
Service des Maladies Infectieuses Ibrahima DIOP MAR - CHU de Fann, Université Cheikh Anta Diop, Dakar, Senegal.
Macoumba
M
Toure
Service des Maladies Infectieuses Ibrahima DIOP MAR - CHU de Fann, Université Cheikh Anta Diop, Dakar, Senegal.
Ahmadou
A
Dem
Department of Pathology, Harborview Medical Center, Seattle, WA 98104, USA.
Nancy B
NB
Kiviat
Department of Epidemiology, School of Public Health, University of Washington, Box 357236, Seattle, WA 98195, USA.
Stephen E
SE
Hawes
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000150:complications*; D052162:Human papillomavirus 16; D006801:Humans; D008875:Middle Aged; D030361:Papillomavirus Infections / Q000150:complications / Q000821:virology*; D060888:Real-Time Polymerase Chain Reaction; D012675:Senegal; D002583:Uterine Cervical Neoplasms / Q000821:virology*; D019562:Viral Load; D055815:Young Adult
Cervical neoplasia; Human papillomavirus; Senegal; Viral load; hpv