Zuyu Yang, Heather Davies, Jane Clapham, Liza Lopez, Holly B Bratcher, Audrey Tiong, Xavier Didelot, Martin C J Maiden, Philip E Carter, Xiaoyun Ren
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引用次数: 0
Abstract
Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD), a form of bacterial meningitis and septicaemia, leading to isolated cases, outbreaks, and epidemics worldwide. Between 1991 and 2008, Aotearoa/New Zealand (NZ) experienced a prolonged hyperendemic group B IMD outbreak caused by the NZMenB epidemic strain, belonging to clonal-complex 41/44 (cc41/44) and identified by the PorA variant P1.7-2,4 (B:4:P1.7-2,4:cc41/44). NZMenB continues to account for approximately one-quarter of group B meningococcal disease cases in NZ. To understand NZMenB origin and initiation we used phylodynamic tools to analyse approximately 97 % of all NZMenB isolates submitted to the NZ Meningococcal Reference Laboratory from 1990 to 2019. We found NZMenB can be divided into three major clades: clade41, clade154, and clade42, each with distinct origins and expansion patterns. Our evidence from molecular dating and clonal expansion analysis suggests that NZMenB was circulating and had expanded before the epidemic. Comparison with international data showed multiple importations and re-introductions of NZMenB into NZ, while not suggesting close relationships with international variants. The recent COVID-19 health emergency and differing governmental responses have brought societal and environmental contributions to epidemics and pandemics into focus. We propose the NZMenB epidemic may have been triggered by increasing societal inequality and household crowding resulting from government policies at the time.
期刊介绍:
(aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID)
Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance.
However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors.
Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases.
Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .