» Articles » PMID: 22090448

Evolutionary Ecology of Human Papillomavirus: Trade-offs, Coexistence, and Origins of High-risk and Low-risk Types

Overview
Journal J Infect Dis
Date 2011 Nov 18
PMID 22090448
Citations 26
Authors
Affiliations
Soon will be listed here.
Abstract

Background: We address the ecological and evolutionary dynamics of human papillomavirus (HPV) that lead to the dichotomy between high-risk (HR) and low-risk (LR) types. We hypothesize that HPV faces an evolutionary tradeoff between persistence and per-contact transmission probability. High virion production enhances transmissibility but also provokes an immune response leading to clearance and limited persistence. Alternatively, low virion production increases persistence at the cost of diminished transmission probability per sexual contact. We propose that LR HPV types use the former strategy and that HR types use the latter. Sexual behaviors in a host population determine the success of each strategy.

Methods: We develop an evolutionary model of HPV epidemiology, which includes host sexual behavior, and we find evolutionarily stable strategies of HPV.

Results: A slow turnover of sexual partners favors HR HPV, whereas high frequency of partner turnover selects for LR. When both sexual behaviors exist as subcultures in a population, disruptive selection can result in the coevolution and ecological coexistence of both HR and LR HPV types.

Conclusions: Our results indicate that the elimination of HR HPV through vaccines may alter the evolutionary trajectory of the remaining types and promote evolution of new HR HPV types.

Citing Articles

The effect of phosphorylation efficiency on the oncogenic properties of the protein E7 from high-risk HPV.

Malone M, Maeyama A, Ogden N, Perry K, Kramer A, Bates C Virus Res. 2024; 348:199446.

PMID: 39127239 PMC: 11375142. DOI: 10.1016/j.virusres.2024.199446.


High rate of non-vaccine targeted high-risk HPV genotypes circulate among women in Eastern Ethiopia.

Seyoum A, Seyoum B, Gure T, Alemu A, Hailu Alemayehu D, Alemu A Sci Rep. 2024; 14(1):958.

PMID: 38200092 PMC: 10781741. DOI: 10.1038/s41598-024-51594-7.


Prevalence of Multiple High Risk Human Papilloma Virus (HR-HPV) Infections in Cervical Cancer Screening in Lazio Region, Italy.

Pisani T, Cenci M Cancer Diagn Progn. 2024; 4(1):42-45.

PMID: 38173657 PMC: 10758846. DOI: 10.21873/cdp.10283.


The cervical microbiota of Hispanics living in Puerto Rico is nonoptimal regardless of HPV status.

Vargas-Robles D, Romaguera J, Alvarado-Velez I, Tosado-Rodriguez E, Dominicci-Maura A, Sanchez M mSystems. 2023; 8(4):e0035723.

PMID: 37534938 PMC: 10469956. DOI: 10.1128/msystems.00357-23.


Retrospective Phylodynamic and Phylogeographic Analysis of the Human Papillomavirus 16 E6 Gene in the Mediterranean Region.

Souiai O, Sallemi A Bioinform Biol Insights. 2023; 17:11779322231178598.

PMID: 37313033 PMC: 10259103. DOI: 10.1177/11779322231178598.


References
1.
Koshiol J, Schroeder J, Jamieson D, Marshall S, Duerr A, Heilig C . Time to clearance of human papillomavirus infection by type and human immunodeficiency virus serostatus. Int J Cancer. 2006; 119(7):1623-9. DOI: 10.1002/ijc.22015. View

2.
Roden R, Hubbert N, Kirnbauer R, Christensen N, Lowy D, Schiller J . Assessment of the serological relatedness of genital human papillomaviruses by hemagglutination inhibition. J Virol. 1996; 70(5):3298-301. PMC: 190197. DOI: 10.1128/JVI.70.5.3298-3301.1996. View

3.
Doorbar J . Molecular biology of human papillomavirus infection and cervical cancer. Clin Sci (Lond). 2006; 110(5):525-41. DOI: 10.1042/CS20050369. View

4.
zur Hausen H . Papillomavirus infections--a major cause of human cancers. Biochim Biophys Acta. 1996; 1288(2):F55-78. DOI: 10.1016/0304-419x(96)00020-0. View

5.
de Villiers E, Fauquet C, Broker T, Bernard H, Zur Hausen H . Classification of papillomaviruses. Virology. 2004; 324(1):17-27. DOI: 10.1016/j.virol.2004.03.033. View