期刊
IMMUNOLOGICAL REVIEWS
卷 264, 期 1, 页码 6-24出版社
WILEY
DOI: 10.1111/imr.12264
关键词
host; pathogen; adaptation; virulence; selection
类别
资金
- NIH [R01 AI090928]
- Swiss National Science Foundation [PP00P3_150750]
- European Research Council [309540-EVODRTB]
- SystemsX.ch
- Swiss National Science Foundation (SNF) [PP00P3_150750] Funding Source: Swiss National Science Foundation (SNF)
The causative agent of human tuberculosis (TB), Mycobacterium tuberculosis, is an obligate pathogen that evolved to exclusively persist in human populations. For M.tuberculosis to transmit from person to person, it has to cause pulmonary disease. Therefore, M.tuberculosis virulence has likely been a significant determinant of the association between M.tuberculosis and humans. Indeed, the evolutionary success of some M.tuberculosis genotypes seems at least partially attributable to their increased virulence. The latter possibly evolved as a consequence of human demographic expansions. If co-evolution occurred, humans would have counteracted to minimize the deleterious effects of M.tuberculosis virulence. The fact that human resistance to infection has a strong genetic basis is a likely consequence of such a counter-response. The genetic architecture underlying human resistance to M.tuberculosis remains largely elusive. However, interactions between human genetic polymorphisms and M.tuberculosis genotypes have been reported. Such interactions are consistent with local adaptation and allow for a better understanding of protective immunity in TB. Future genome-to-genome' studies, in which locally associated human and M.tuberculosis genotypes are interrogated in conjunction, will help identify new protective antigens for the development of better TB vaccines.
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