OBJECTIVE: We sought to determine the relationship of human immunodeficiency virus serostatus to carriage of oncogenic human papillomavirus. MATERIAL AND METHODS: A total of 268 human immunodeficiency virus-infected and 265 human immunodeficiency virus-uninfected women were seen every 6 months, at which time they had laboratory tests performed including a CD4 count. Human papillomavirus deoxyribonucleic acid was analyzed by polymerase chain reaction. Statistical methods included Kaplan-Meier and Cox's proportional hazard models. RESULTS: The prevalence at baseline of any human papillomavirus type was 73% and 43% among human immunodeficiency virus-seropositive and seronegative women, respectively (p < 0.0001) and of oncogenic types was 32.5% and 17.0% (p < 0.001). The prevalence of oncogenic human papillomavirus was higher in women with CD4 counts <200 mm3 (p < 0.001). The rate of detection of new oncogenic human papillomavirus per 100 patient years of follow-up in human immunodeficiency virus-seropositive women was almost three times higher than among human immunodeficiency virus-seronegative women (p < 0.01). The rate of loss of an oncogenic human papillomavirus was higher in the human immunodeficiency virus-seronegative women but the difference was not significant. The relative risk of a human immunodeficiency virus-infected woman who did not initially have a specific type of oncogenic human papillomavirus having one detected during follow-up was 6.6 times greater than among human immunodeficiency virus-negative women (p < 0.001). CONCLUSIONS: Human immunodeficiency virus-seropositive women are more likely to have newly detectable oncogenic types of human papillomavirus at follow-up and to show persistent carriage of oncogenic types of human papillomavirus types. Among human immunodeficiency virus-infected women, those with higher CD4 counts were more likely to have a newly detected oncogenic human papillomavirus during follow-up.
OBJECTIVE: We sought to determine the relationship of human immunodeficiency virus serostatus to carriage of oncogenic human papillomavirus. MATERIAL AND METHODS: A total of 268 human immunodeficiency virus-infected and 265 human immunodeficiency virus-uninfected women were seen every 6 months, at which time they had laboratory tests performed including a CD4 count. Human papillomavirus deoxyribonucleic acid was analyzed by polymerase chain reaction. Statistical methods included Kaplan-Meier and Cox's proportional hazard models. RESULTS: The prevalence at baseline of any human papillomavirus type was 73% and 43% among human immunodeficiency virus-seropositive and seronegative women, respectively (p < 0.0001) and of oncogenic types was 32.5% and 17.0% (p < 0.001). The prevalence of oncogenic human papillomavirus was higher in women with CD4 counts <200 mm3 (p < 0.001). The rate of detection of new oncogenic human papillomavirus per 100 patient years of follow-up in human immunodeficiency virus-seropositivewomen was almost three times higher than among human immunodeficiency virus-seronegative women (p < 0.01). The rate of loss of an oncogenic human papillomavirus was higher in the human immunodeficiency virus-seronegative women but the difference was not significant. The relative risk of a human immunodeficiency virus-infectedwoman who did not initially have a specific type of oncogenic human papillomavirus having one detected during follow-up was 6.6 times greater than among human immunodeficiency virus-negative women (p < 0.001). CONCLUSIONS: Human immunodeficiency virus-seropositivewomen are more likely to have newly detectable oncogenic types of human papillomavirus at follow-up and to show persistent carriage of oncogenic types of human papillomavirus types. Among human immunodeficiency virus-infectedwomen, those with higher CD4 counts were more likely to have a newly detected oncogenic human papillomavirus during follow-up.
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