The impact of vaccination and coinfection
 on HPV and cervical cancer

Crawford, Britnee A.; Kribs-Zaleta, Christopher M.

doi:10.3934/dcdsb.2009.12.279

Cited by 24 publications

(16 citation statements)

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“…After calibrating the free parameter a to be 6 Â 10 26 such that the short partnership group had an R 0 of 2 [47], we then estimated the R 0 of the other sexual behaviour groups. The R 0 was 2.9 for the casual group, less than 1 for the long partnership group and 9.3 for superspreaders (figure 3b), which is realistic though a bit low considering the high partnership turnover rates of superspreaders.…”

Section: Results (A) Unvaccinated Host Resultsmentioning

confidence: 99%

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Could the human papillomavirus vaccines drive virulence evolution?

2015

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The human papillomavirus (HPV) vaccines hold great promise for preventing several cancers caused by HPV infections. Yet little attention has been given to whether HPV could respond evolutionarily to the new selection pressures imposed on it by the novel immunity response created by the vaccine. Here, we present and theoretically validate a mechanism by which the vaccine alters the transmission-recovery trade-off that constrains HPV's virulence such that higher oncogene expression is favoured. With a high oncogene expression strategy, the virus is able to increase its viral load and infected cell population before clearance by the vaccine, thus improving its chances of transmission. This new rapid cell-proliferation strategy is able to circulate between hosts with medium to high turnover rates of sexual partners. We also discuss the importance of better quantifying the duration of challenge infections and the degree to which a vaccinated host can shed virus. The generality of the models presented here suggests a wider applicability of this mechanism, and thus highlights the need to investigate viral oncogenicity from an evolutionary perspective.

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Section: Results (A) Unvaccinated Host Resultsmentioning

confidence: 99%

“…Also note that the per-partnership transmission probability is 0.6 for HPV [46], and its R 0 is 2, though higher for core-group individuals (e.g. superspreaders) [47].…”

Section: (C) Transmission and Between-host Fitnessmentioning

confidence: 99%

Could the human papillomavirus vaccines drive virulence evolution?

2015

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“…Invasion reproductive numbers (Crawford and Kribs 2009;Martcheva 2009;Porco and Blower 1998) for autonomous systems can be derived by extending the next-generation matrix method (van den Driessche and Watmough 2002) to consider any resident (non-invading) infections as non-infectious classes (Mitchell and Kribs 2019). This method establishes conditions for the local asymptotic stability (LAS) of the boundary equilibria: the dengue-endemic equilibrium is LAS when dengue can spread alone but Zika cannot invade it (R d > 1,R z < 1), and the Zika-endemic equilibrium is LAS when ZIKV can spread alone but dengue cannot invade it (R z > 1,R d < 1).…”

Section: Irnsmentioning

confidence: 99%

Coinfection, Altered Vector Infectivity, and Antibody-Dependent Enhancement: The Dengue–Zika Interplay

Olawoyin

Kribs

2020

Bull Math Biol

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Although dengue and Zika cocirculation has increased within the past 5 years, very little is known about its epidemiological consequences. To investigate the effect of dengue and Zika cocirculation on the spread of both pathogens, we create a deterministic dengue and Zika coinfection model, the first to incorporate altered infectivity of mosquitoes (due to coinfection). The model also addresses increased infectivity due to antibody-dependent enhancement (ADE) within the human population. Central to our analysis is the derivation and interpretation of the basic reproductive number and invasion reproductive number of both pathogens. In addition, we investigate how model parameters impact the persistence of each disease. Our results identify threshold conditions under which one disease facilitates the spread of the other and show that ADE has a greater impact on disease persistence than altered vector infectivity. This work highlights the importance of ADE and illustrates that while the endemic presence of dengue facilitates the spread of Zika, it is possible for high Zika prevalence to prevent the establishment of dengue. Keywords Invasion reproductive number • Copersistence • Zika • Dengue 1 Introduction With approximately 50-100 million cases annually, dengue is one of the most prevalent mosquito-borne diseases in the world (World Health Organization 2012). Over 40% of the world's population live in areas with high risk of dengue transmission and over B Omomayowa Olawoyin

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“…R0 has been studied in numerous continuous and discrete-time epidemic models (e.g. (Allen, 1994; Allen & van den Driessche, 2008; Crawford & Kribs-Zaleta, 2009; Hernandez-Ceron, Feng, & van den Driessche, 2013; Lewis, Rencławowicz, van Den Driessche, & Wonham, 2006; Qiu, Kong, Li, & Martcheva, 2013)) and has proved useful for informing disease control strategies. Although the basic reproductive number (BRN) is invaluable, it has its restrictions.…”

Section: Introductionmentioning

confidence: 99%

Invasion reproductive numbers for discrete-time models

Olawoyin

Kribs

2019

Infectious Disease Modelling

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Although invasion reproductive numbers (IRNs) are utilized frequently in continuous-time models with multiple interacting pathogens, they are yet to be explored in discrete-time systems. Here, we extend the concept of IRNs to discrete-time models by showing how to calculate them for a set of two-pathogen SIS models with coinfection. In our exploration, we address how sequencing events impacts the basic reproductive number (BRN) and IRN. As an illustrative example, our models are applied to rhinovirus and respiratory syncytial virus co-circulation. Results show that while the BRN is unaffected by variations in the order of events, the IRN differs. Furthermore, our models predict copersistence of multiple pathogen strains under cross-immunity, which is atypical of analogous continuous-time models. This investigation shows that sequencing events has important consequences for the IRN and can drastically alter competition dynamics.

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The impact of vaccination and coinfection on HPV and cervical cancer

Cited by 24 publications

References 0 publications

Could the human papillomavirus vaccines drive virulence evolution?

Could the human papillomavirus vaccines drive virulence evolution?

Coinfection, Altered Vector Infectivity, and Antibody-Dependent Enhancement: The Dengue–Zika Interplay

Invasion reproductive numbers for discrete-time models

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