Viral load in the natural history of human papillomavirus type 16 infection

A nested case-control study

Long Fu Xi, James P. Hughes, Philip E. Castle, Zoe R. Edelstein, Chunhui Wang, Denise A. Galloway, Laura A. Koutsky, Nancy B. Kiviat, Mark Schiffman

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background. Viral load may influence the course of human papillomavirus type 16 (HPV-16) infection. Methods. This case-control study was nested within the 2-year Atypical Squamous Cells of Undetermined Significance and Low-Grade Squamous Intraepithelial Lesion Triage Study, in which women were followed semiannually for HPV and cervical intraepithelial neoplasia (CIN). Case patients (n=62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit. HPV-16-positive controls (n=152) without CIN2 or CIN3 were matched to cases based on the follow-up visit in which viral load was measured. Real-time polymerase chain reaction was used for HPV-16 DNA quantification. Results. The risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63; 95% confidence interval, 1.33-1.99 per 1 log10 unit increase); the association was not affected by whether HPV-16 was present at enrollment. When HPV-16 was present at both enrollment and follow-up, viral load remained high among cases (P=.77) but decreased substantially among controls (P=.004). Among women with HPV-16 found initially during follow-up, viral load in the first HPV-16-positive sample was associated with shortterm persistence; load was higher in those with infection, compared with those without infection, 1 visit after the initial positivity (P=.001). Conclusions. Viral load of newly detected infections and changes in viral load predict persistence and progression of HPV-16 infections.

Original languageEnglish (US)
Pages (from-to)1425-1433
Number of pages9
JournalJournal of Infectious Diseases
Volume203
Issue number10
DOIs
StatePublished - May 15 2011
Externally publishedYes

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Papillomavirus Infections
Human papillomavirus 16
Viral Load
Case-Control Studies
Infection
Cervical Intraepithelial Neoplasia
Triage
DNA
Real-Time Polymerase Chain Reaction
Odds Ratio
Confidence Intervals

ASJC Scopus subject areas

  • Infectious Diseases
  • Immunology and Allergy

Cite this

Viral load in the natural history of human papillomavirus type 16 infection : A nested case-control study. / Xi, Long Fu; Hughes, James P.; Castle, Philip E.; Edelstein, Zoe R.; Wang, Chunhui; Galloway, Denise A.; Koutsky, Laura A.; Kiviat, Nancy B.; Schiffman, Mark.

In: Journal of Infectious Diseases, Vol. 203, No. 10, 15.05.2011, p. 1425-1433.

Research output: Contribution to journalArticle

Xi, LF, Hughes, JP, Castle, PE, Edelstein, ZR, Wang, C, Galloway, DA, Koutsky, LA, Kiviat, NB & Schiffman, M 2011, 'Viral load in the natural history of human papillomavirus type 16 infection: A nested case-control study', Journal of Infectious Diseases, vol. 203, no. 10, pp. 1425-1433. https://doi.org/10.1093/infdis/jir049
Xi, Long Fu ; Hughes, James P. ; Castle, Philip E. ; Edelstein, Zoe R. ; Wang, Chunhui ; Galloway, Denise A. ; Koutsky, Laura A. ; Kiviat, Nancy B. ; Schiffman, Mark. / Viral load in the natural history of human papillomavirus type 16 infection : A nested case-control study. In: Journal of Infectious Diseases. 2011 ; Vol. 203, No. 10. pp. 1425-1433.
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abstract = "Background. Viral load may influence the course of human papillomavirus type 16 (HPV-16) infection. Methods. This case-control study was nested within the 2-year Atypical Squamous Cells of Undetermined Significance and Low-Grade Squamous Intraepithelial Lesion Triage Study, in which women were followed semiannually for HPV and cervical intraepithelial neoplasia (CIN). Case patients (n=62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit. HPV-16-positive controls (n=152) without CIN2 or CIN3 were matched to cases based on the follow-up visit in which viral load was measured. Real-time polymerase chain reaction was used for HPV-16 DNA quantification. Results. The risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63; 95{\%} confidence interval, 1.33-1.99 per 1 log10 unit increase); the association was not affected by whether HPV-16 was present at enrollment. When HPV-16 was present at both enrollment and follow-up, viral load remained high among cases (P=.77) but decreased substantially among controls (P=.004). Among women with HPV-16 found initially during follow-up, viral load in the first HPV-16-positive sample was associated with shortterm persistence; load was higher in those with infection, compared with those without infection, 1 visit after the initial positivity (P=.001). Conclusions. Viral load of newly detected infections and changes in viral load predict persistence and progression of HPV-16 infections.",
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AU - Edelstein, Zoe R.

AU - Wang, Chunhui

AU - Galloway, Denise A.

AU - Koutsky, Laura A.

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N2 - Background. Viral load may influence the course of human papillomavirus type 16 (HPV-16) infection. Methods. This case-control study was nested within the 2-year Atypical Squamous Cells of Undetermined Significance and Low-Grade Squamous Intraepithelial Lesion Triage Study, in which women were followed semiannually for HPV and cervical intraepithelial neoplasia (CIN). Case patients (n=62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit. HPV-16-positive controls (n=152) without CIN2 or CIN3 were matched to cases based on the follow-up visit in which viral load was measured. Real-time polymerase chain reaction was used for HPV-16 DNA quantification. Results. The risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63; 95% confidence interval, 1.33-1.99 per 1 log10 unit increase); the association was not affected by whether HPV-16 was present at enrollment. When HPV-16 was present at both enrollment and follow-up, viral load remained high among cases (P=.77) but decreased substantially among controls (P=.004). Among women with HPV-16 found initially during follow-up, viral load in the first HPV-16-positive sample was associated with shortterm persistence; load was higher in those with infection, compared with those without infection, 1 visit after the initial positivity (P=.001). Conclusions. Viral load of newly detected infections and changes in viral load predict persistence and progression of HPV-16 infections.

AB - Background. Viral load may influence the course of human papillomavirus type 16 (HPV-16) infection. Methods. This case-control study was nested within the 2-year Atypical Squamous Cells of Undetermined Significance and Low-Grade Squamous Intraepithelial Lesion Triage Study, in which women were followed semiannually for HPV and cervical intraepithelial neoplasia (CIN). Case patients (n=62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit. HPV-16-positive controls (n=152) without CIN2 or CIN3 were matched to cases based on the follow-up visit in which viral load was measured. Real-time polymerase chain reaction was used for HPV-16 DNA quantification. Results. The risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63; 95% confidence interval, 1.33-1.99 per 1 log10 unit increase); the association was not affected by whether HPV-16 was present at enrollment. When HPV-16 was present at both enrollment and follow-up, viral load remained high among cases (P=.77) but decreased substantially among controls (P=.004). Among women with HPV-16 found initially during follow-up, viral load in the first HPV-16-positive sample was associated with shortterm persistence; load was higher in those with infection, compared with those without infection, 1 visit after the initial positivity (P=.001). Conclusions. Viral load of newly detected infections and changes in viral load predict persistence and progression of HPV-16 infections.

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