Expected Duration of Adverse Pregnancy Outcomes after Zika Epidemic.

Evidence is increasing that Zika virus-related adverse outcomes can occur throughout pregnancy. Mathematical modeling analysis using reported outcome data suggests that surveillance for these outcomes should begin as soon as an outbreak is detected and should continue for 40 weeks after the outbreak ends

Influenza interaction with cocirculating pathogens, and its impact on surveillance, pathogenesis and epidemic profile: a key role for mathematical modeling

ABSTRACT Evidence is mounting that influenza virus, a major contributor to the global disease burden, interacts with other pathogens infecting the human respiratory tract. Taking into account interactions with other pathogens may be critical to determining the real influenza burden and the full impact of public health policies targeting influenza. That necessity is particularly true for mathematical modeling studies, which have become critical in public health decision-making, despite their usually focusing on lone influenza virus acquisition and infection, thereby making broad oversimplifications regarding pathogen ecology. Herein, we review evidence of influenza virus interaction with bacteria and viruses, and the modeling studies that incorporated some of these. Despite the many studies examining possible associations between influenza and Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Neisseria meningitides , respiratory syncytial virus, human rhinoviruses, human parainfluenza viruses, etc., very few mathematical models have integrated other pathogens alongside influenza. A notable exception is the recent modeling of the pneumococcus-influenza interaction, which highlighted potential influenza-related increased pneumococcal transmission and pathogenicity. That example demonstrates the power of dynamic modeling as an approach to test biological hypotheses concerning interaction mechanisms and estimate the strength of those interactions. We explore how different interference mechanisms may lead to unexpected incidence trends and misinterpretations. Using simple transmission models, we illustrate how existing interactions might impact public health surveillance systems and demonstrate that the development of multipathogen models is essential to assess the true public health burden of influenza, and help improve planning and evaluation of control measures. Finally, we identify the public health needs, surveillance, modeling and biological challenges, and propose avenues of research for the coming years. Author Summary Influenza is a major pathogen responsible for important morbidity and mortality burdens worldwide. Mathematical models of influenza virus acquisition have been critical to understanding its epidemiology and planning public health strategies of infection control. It is increasingly clear that microbes do not act in isolation but potentially interact within the host. Hence, studying influenza alone may lead to masking effects or misunderstanding information on its transmission and severity. Herein, we review the literature on bacterial and viral species that interact with the influenza virus, interaction mechanisms, and mathematical modeling studies integrating interactions. We report evidence that, beyond the classic secondary bacterial infections, many pathogenic bacteria and viruses probably interact with influenza. Public health relevance of pathogen interactions is detailed, showing how potential misreading or a narrow outlook might lead to mistaken public health decisionmaking. We describe the role of mechanistic transmission models in investigating this complex system and obtaining insight into interactions between influenza and other pathogens. Finally, we highlight benefits and challenges in modeling, and speculate on new opportunities made possible by taking a broader view: including basic science, clinical relevance and public health

Inhibition of protein kinase C (PKC) induces apoptosis in COLO 205 human colon carcinoma cells

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Spatial dynamics of the 1918 influenza pandemic in England, Wales and the United States

There is still limited understanding of key determinants of spatial spread of influenza. The 1918 pandemic provides an opportunity to elucidate spatial determinants of spread on a large scale

Spatiotemporal dynamics in the early stages of the 2009 A/H1N1 influenza pandemic.

Epidemiology and public health planning will increasingly rely on the analysis of genetic sequence data. The ongoing influenza A/H1N1 pandemic may represent a tipping point in this trend, with A/H1N1 being the first human pathogen routinely genotyped from the beginning of its spread. To take full advantage of this genetic information, we introduce a novel method to reconstruct the spatiotemporal dynamics of outbreaks from sequence data. The approach is based on a new paradigm were ancestries are inferred directly rather than through the reconstruction of most recent common ancestors (MRCAs) as in phylogenetics. Using 279 A/H1N1 hemagglutinin (HA) sequences, we confirm the emergence of the 2009 flu pandemic in Mexico. The virus initially spread to the US, and then to the rest of the world with both Mexico and the US acting as the main sources. While compatible with current epidemiological understanding of the 2009 H1N1 pandemic, our results provide a much finer picture of the spatiotemporal dynamics. The results also highlight how much additional epidemiological information can be gathered from genetic monitoring of a disease outbreak