Abstract
Sub-Saharan Africa has continued leading in the prevalence and incidence of tuberculosis (TB). The epidemiological triad of infectious diseases includes a susceptible host, pathogen/agent, and environment. Sub- Saharan Africa has the highest prevalence and incidence of TB. It is imperative that all aspects of vertices of the infectious disease triad are analysed to better understand why this is so. Many studies have been done to address this intriguing reality though these have mainly addressed pathogen and environmental components of the triad regarding TB infection. The host factors have not been exhaustively studied in this high TB burden region probably due to lack of the necessary expertise and technologies among African scholars yet three components of the triad interact to determine the disease outcome. Amongst host factors, genetic structure of the host greatly affects progression of disease following exposure. Studies have revealed that Africa is the most genetically diverse region of the world in addition to being the origin of modern humans therefore it would be important to study genetics of sub-Saharan African population in relation to TB. This review seeks to analyze contribution of host genetics to the observed variation in susceptibility to TB infection in this region.
Highlights
Tuberculosis (TB) continues to devastate sub-Saharan Africa populations, a region with a total of 27 countries
We have little understanding of the genetic structure of sub-Saharan populations and the genetic basis of complex disease in African populations because very few genetic studies have been conducted in African ethnic groups [2]
human leukocyte antigen (HLA) alleles are found to be associated with susceptibility and resistance to infectious diseases including HIV/AIDS, tuberculosis, and malaria that impose huge public health burdens in sub-Saharan Africa [22]
Summary
Tuberculosis (TB) continues to devastate sub-Saharan Africa populations, a region with a total of 27 countries. The indigenous pathogens in sub-Saharan Africa co-evolved with their hosts creating unique genetic profiles in these human populations. I propose that a form of Newton’s third law of motion happens during an interaction between host and pathogen; action and reaction is equal and opposite This infers that there is a selective pressure exerted by these pathogens onto selected host genes and in response specific pathogen genes received similar pressure from the host driving host/pathogen diversity observed as unique genetic profiles in both host and pathogen accounting for co-evolution. TB was introduced in Africa by probably early settlers, sailors, colonialists, missionaries and traders The environment in this region plus the TB naïve host genetic structures of the region may have account for the rapid spread of the disease. Gene Name Arachidonate 5-lipoxygenase Butyrophilin-like 2 (MHC class II associated) Cathepsin Z
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