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Eur J Immunol. 2017 Mar;47(3):432-445. doi: 10.1002/eji.201646562. Epub 2017 Feb 24.

Immunological consequences of strain variation within the Mycobacterium tuberculosis complex.

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Vaccines and Immunity Theme, Medical Research Council Unit, The Gambia, Banjul, The Gambia.
Department of Biochemistry, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon.
Wellcome Centre for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine and Department of Medicine, University of Cape Town, Observatory, Republic of South Africa.
Department of Medicine, Imperial College, London, United Kingdom.
The Francis Crick Institute, London, United Kingdom.


In 2015, there were an estimated 10.4 million new cases of tuberculosis (TB) globally, making it one of the leading causes of death due to an infectious disease. TB is caused by members of the Mycobacterium tuberculosis complex (MTBC), with human disease resulting from infection by M. tuberculosis sensu stricto and M. africanum. Recent progress in genotyping techniques, in particular the increasing availability of whole genome sequence data, has revealed previously under appreciated levels of genetic diversity within the MTBC. Several studies have shown that this genetic diversity may translate into differences in TB transmission, clinical manifestations of disease, and host immune responses. This suggests the existence of MTBC genotype-dependent host-pathogen interactions which may influence the outcome of infection and progression of disease. In this review, we highlight the studies demonstrating differences in innate and adaptive immunological outcomes consequent on MTBC genetic diversity, and discuss how these differences in immune response might influence the development of TB vaccines, diagnostics and new therapies.


Adaptive and innate immunity; Genetic diversity; Host response; Mycobacterium tuberculosis complex; Translational implications

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