PMID- 31031349
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220408
IS  - 0970-2113 (Print)
IS  - 0974-598X (Electronic)
IS  - 0970-2113 (Linking)
VI  - 36
IP  - 3
DP  - 2019 May-Jun
TI  - Host genetics and tuberculosis: Theory of genetic polymorphism and tuberculosis.
PG  - 244-252
LID - 10.4103/lungindia.lungindia_146_15 [doi]
AB  - BACKGROUND AND OBJECTIVE: Tuberculosis (TB), the leading cause of morbidity and 
      mortality by a single infectious agent, Mycobacterium tuberculosis, is still a 
      major health problem in the world. To date, many studies have shown evidence of 
      association between host genetic polymorphisms and TB susceptibility, including 
      chemokine (C-C motif) ligand 2 (CCL-2)/monocyte chemoattractant protein1 (MCP-1), 
      natural resistance-associated macrophage protein 1 (NRAMP-1)/solute carrier 
      protein 11A1 (SLC11A1), Immunity-related GTPase family M protein (IRGMI), 
      interleukin (IL)-8, toll-like receptor (TLR), and nucleotide-binding 
      oligomerization domain containing protein-2 (NOD-2) genes. Most of these genes 
      participate in immune response, and their polymorphism can alter immunity and 
      lead to genetic susceptibility to TB. MATERIALS AND METHODS: This is a special 
      article compiled with reference to various case-control studies, meta-analysis, 
      and other research work on different genes and TB. The genes selected and a 
      number of studies from different countries and ethnic groups for this article are 
      shown below. The genes selected for the study are: NRAMP-1 (SLC11 A1), Vitamin D 
      receptor, low molecular weight polypeptide/transporter with antigen processing, 
      CCL-2/MCP-1, IRGM-1, IL-1, IL-8, IL-10, IL-12, TLR, NOD-2, human leukocyte 
      antigen, mannose-binding lectin, major histocompatibility complex, tumor necrosis 
      factor, P2X 7, epiregulin, SP110, and interferon gamma (IFN-gamma). RESULTS: 
      Genetic polymorphisms in different genes showed variable levels of significance 
      in relation to TB. All these were proved by the researchers using appropriate 
      statistical methods and tools. CONCLUSIONS: Based on different research works 
      across the world, there is sufficient evidence to prove that TB is a genetically 
      primed and determined infectious disease caused by M. tuberculosis and the 
      genetic polymorphism is the mechanism that leads to progression from infection to 
      TB disease. Why only 10-15% of the people infected with M. tuberculosis progress 
      toward TB disease has continued to be an unresolved debate. Hence, for provoking 
      thoughts and encouraging more research in the field of genetics and TB I 
      formulated hypothesis and algorithms, and theory. Genetic susceptibility to TB 
      has been substantiated based on the extensive literature review and the research 
      findings that are well narrated.
FAU - Aravindan, P P
AU  - Aravindan PP
AD  - Former Addl. DHS, Kerala Health Services, Palakkad, Kerala, India.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Lung India
JT  - Lung India : official organ of Indian Chest Society
JID - 8405380
PMC - PMC6503728
OTO - NOTNLM
OT  - Algorithm
OT  - genes
OT  - genetic polymorphism
OT  - theory
OT  - tuberculosis
COIS- None
EDAT- 2019/04/30 06:00
MHDA- 2019/04/30 06:01
PMCR- 2019/05/01
CRDT- 2019/04/30 06:00
PHST- 2019/04/30 06:00 [entrez]
PHST- 2019/04/30 06:00 [pubmed]
PHST- 2019/04/30 06:01 [medline]
PHST- 2019/05/01 00:00 [pmc-release]
AID - LungIndia_2019_36_3_244_256914 [pii]
AID - LI-36-244 [pii]
AID - 10.4103/lungindia.lungindia_146_15 [doi]
PST - ppublish
SO  - Lung India. 2019 May-Jun;36(3):244-252. doi: 10.4103/lungindia.lungindia_146_15.