## Abstract Specific types of human papillomavirus (HPV) are known to play a causal role in the development of cervical cancer, with human papillomavirus type 16 (HPV‐16) identified as the predominant type. Despite this, little is known about cervical immune responses to this pathogen. The aim of t
Alterations of T-cell surface markers in older women with persistent human papillomavirus infection
✍ Scribed by Ana Cecilia Rodríguez; Alfonso J. García-Piñeres; Allan Hildesheim; Rolando Herrero; Matthew Trivett; Marcus Williams; Ivannia Atmella; Margarita Ramírez; Maricela Villegas; Mark Schiffman; Robert Burk; Enrique Freer; José Bonilla; Concepción Bratti; Ligia A. Pinto
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- French
- Weight
- 176 KB
- Volume
- 128
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
We previously reported decreased lymphocyte proliferative responses among older women with persistent human papillomavirus (HPV) infection. To characterize the phenotype of peripheral lymphocytes associated with persistent HPV infection, we evaluated the expression of different cell surface markers in peripheral blood mononuclear cells (PBMCs) from a case–control study within a 10,049 woman population‐based cohort study in Guanacaste, Costa Rica. Women in the cohort aged 46–74 and with HPV results at their 5th year anniversary visit were considered, and all women (n = 87) with persistent HPV infections, all women (n = 196) with transient HPV infections and a random sample of HPV DNA‐negative women (n = 261) frequency‐matched to cases on age were selected for this study. A median of 3 years after the case–control matching visit, cervical cells were collected for liquid‐based cytology and repeat HPV DNA genotyping. Blood was obtained from which PBMCs were extracted and cryopreserved for immunological phenotyping via flow cytometry. Significant increases in risk of HPV persistence were observed for 3 marker subsets indicative of immune cell activation/differentiation. Relative risk estimates were 5.4 (95% CI = 2.2–13.3) for CD69^+^CD4^+^, 2.6 (95% CI = 1.2–5.9) for HLADR^+^CD3^+^CD4^+^ and 2.3 (95% CI = 1.1–4.7) for CD45RO^+^CD27^−^CD8^+^. A significant decrease in HPV persistence was observed for a subset marker indicative of an immature, undifferentiated memory state CD45RO^+^CD27^+^CD4^+^ (OR = 0.36; 95% CI = 0.17–0.76). Adjustment for these markers only partially explained the previously reported association between decreased lymphoproliferative responses and persistent HPV infection. Whether phenotypic alterations observed predispose to HPV persistence or result from it should be the focus of future studies.
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