Could The Human Papillomavirus Vaccines Drive Virulence Evolution?

Definitive version as published available at: Full Cite, http://dx.doi.org/10.1098/rspb.2014.1069The 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.CIH

Revising Ecological Assumptions About Human Papillomavirus Interactions And Type Replacement

The final publication is available at Elsevier via http://dx.doi.org/10.1016/j.jtbi.2013.12.028 © 2014. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/The controversy over whether vaccine-targeted HPV types will be replaced by other oncogenic, non-vaccine-targeted types remains unresolved. This is in part because little is known about the ecology of HPV types. Patient data has been interpreted to suggest independence or facilitative interactions between types and therefore replacement is believed to be unlikely. With a novel mathematical model, we investigated which HPV type interactions and their immune responses gave qualitatively similar patterns frequently observed in patients. To assess the possibility of type replacement, vaccination was added to see if non-vaccine-targeted types increased their 'niche'. Our model predicts that independence and facilitation are not necessary for the coexistence of types inside hosts, especially given the patchy nature of HPV infection. In fact, independence and facilitation inadequately represented co-infected patients. We found that some form of competition is likely in natural co-infections. Hence, non-vaccine-targeted types that are not cross-reactive with the vaccine could spread to more patches and can increase their viral load in vaccinated hosts. The degree to which this happens will depend on replication and patch colonization rates. Our results suggest that independence between types could be a fallacy, and so without conclusively untangling HPV within-host ecology, type replacement remains theoretically viable. More ecological thinking is needed in future studies.Canadian Institutes of Health Researc

Guía de seguimiento farmacoterapéutico sobre niño enfermo

Coordinadores de esta edición: Emilio García Jiménez y Martha Milena Silva CastroEsta guía tiene por objetivo facilitar la fase de estudio necesaria para realizar seguimiento farmacoterapéutico en el niño enfermo. En primer lugar se han tratado las características farmacocinéticas y farmacodinámicas especiales de los niños. Para, a continuación presentar las características de los problemas de salud más importantes en la población infantil, así como los tratamientos de tipo farmacológico o no, indicados para tratar estos problemas de salud

Genomic epidemiology of SARS-CoV-2 in Quebec

Non UBCUnreviewedAuthor affiliation: UdeMPostdoctora

Modelling the evolution of viral oncogenesis

International audienceMost human oncogenic viruses share several characteristics, such as being DNA viruses, having long (co)evolutionary histories with their hosts and causing either latent or chronic infections. They can reach high prevalences while causing relatively low case mortality, which makes them quite fit according to virulence evolution theory. After analysing the life-histories of DNA oncoviruses, we use a mathematical modelling approach to investigate how the virus life cycle may generate selective pressures favouring or acting against oncogenesis at the within-host or at the between-host level. In particular, we focus on two oncoprotein activities, namely extending cell life expectancy and increasing cell proliferation rate. These have immediate benefits (increasing viral population size) but can be associated with fitness costs at the epidemiological level (increasing recovery rate or risk of cancer) thus creating evolutionary trade-offs. We interpret the results of our nested model in light of biological features and identify future perspectives for modelling oncovirus dynamics and evolution. Cite as Murall CL, Alizon S (2019) Modelling the evolution of viral oncogenesis

Why Human Papillomavirus Acute Infections Matter

International audienceMost infections by human papillomaviruses (HPVs) are `acute’, that is non-persistent. Yet, for HPVs, as for many other oncoviruses, there is a striking gap between our detailed understanding of chronic infections and our limited data on the early stages of infection. Here we argue that studying HPV acute infections is necessary and timely. Focusing on early interactions will help explain why certain infections are cleared while others become chronic or latent. From a molecular perspective, descriptions of immune effectors and pro-inflammatory pathways during the initial stages of infections have the potential to lead to novel treatments or to improved handling algorithms. From a dynamical perspective, adopting concepts from spatial ecology, such as meta-populations or meta-communities, can help explain why HPV acute infections sometimes last for years. Furthermore, cervical cancer screening and vaccines impose novel iatrogenic pressures on HPVs, implying that anticipating any viral evolutionary response remains essential. Finally, hints at the associations between HPV acute infections and fertility deserve further investigation given their high, worldwide prevalence. Overall, understanding asymptomatic and benign infections may be instrumental in reducing HPV virulence

Detecting within-host interactions from genotype combination prevalence data

International audienceParasite genetic diversity can provide information on disease transmission dynamics but most mathematical and statistical frameworks ignore the exact combinations of genotypes in infections. We introduce and validate a new method that combines explicit epidemiological modelling of coinfections and regression-Approximate Bayesian Computing (ABC) to detect within-host interactions. Using a susceptible-infected-susceptible (SIS) model, we show that, if sufficiently strong, within-host parasite interactions can be detected from epidemiological data. We also show that, in this simple setting, this detection is robust even in the face of some level of host heterogeneity in behaviour. These simulations results offer promising applications to analyse large datasets of multiple infection prevalence data, such as those collected for genital infections by Human Papillomaviruses (HPVs)

Quantifying the epidemic spread of Ebola virus (EBOV) in Sierra Leone using phylodynamics

International audienceMeasuring epidemic parameters early in an outbreak is essential to inform control efforts. Using the viral genome sequence and collection date from 74 infections in the 2014 Ebola virus outbreak in Sierra Leone, we estimate key epidemiological parameters such as infectious period duration (approximately 71 hours) and date of the first case in Sierra Leone (approximately April 25(th)). We also estimate the effective reproduction number, Re, (approximately 1.26), which is the number of secondary infections effectively caused by an infected individual and accounts for public health control measures. This study illustrates that phylodynamics methods, applied during the initial phase of an outbreak on fewer and more easily attainable data, can yield similar estimates to count-based epidemiological studies