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A new frontier of basic human biology has opened up, which is changing our understanding of what constitutes the human body. This new knowledge is fuelling a paradigm shift from the dominant, 20th century view that viruses, bacteria and fungi operated independently to cause disease. Now, we are beginning to view a more complex and nuanced interpretation with increased recognition of the importance of commensalism, synergy and balance of microbiota in human health.1 In this commentary we hope to briefly summarise studies into the bacterial and viral microbiome and how this shifting paradigm affects epidemiology.
The distribution of human diseases is directly linked to how different people form groups and interact with each other and their environment box 1. This interaction defines a community structure. Community structure has been long recognised as a major determinant of the spread of traditional infectious diseases. Examples range from tuberculosis in crowded slums to the recent spread of Ebola in Africa, where the human behaviours that create community structure often dictate infectious disease spread. These diseases are very sensitive to the social network configuration of the population in which they occur.2 Moreover, social networks within these populations are also important determinants of chronic and traditionally non-infectious diseases. For example, obese individuals are more likely to have other obese individuals as contacts.3 However, even in these ‘non-infectious’ diseases, microorganisms may play a greater role than previously thought.
METAGENOMIC EPIDEMIOLOGY- The study of the distribution and determinants of the microbiome structures and their relationship to disease. MICROBIOTA- A community of microorganisms (viruses, bacteria, fungi, archea) living in a defined niche
MICROBIOME- The community of commensal, symbiotic, and pathogenic microorganisms (microbiota) or their genomes sharing the human body.
METAGENOME- The totality of non-human nucleic acids belonging to all the microbiotas …
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