Racial differences in susceptibility to infection by Mycobacterium tuberculosis


Background: The prevalence of tuberculosis among blacks is known to be higher than among whites. The basis for these differences remains unclear. The purpose of this paper is to review the literature and evaluate the data which bears on the question of racial differences in susceptibility to tuberculosis. Materials and Methods: Systematic review of peer reviewed studies identified through Medline. The search was restricted to articles published in English. The references of the identified papers for further relevant publications were also reviewed. Results: For the review, 31 papers were eligible from 417 identified in the search. The prevalence of TB among black skin people was 81.5% and 18.5% in white skin people. The black subjects demonstrated higher frequency of the Fok1 E2-C4T F allele, Bsm1 E8-G-+ 284A- B allele, APa1 e9-T-48G- a allele, and Taq1 E9-T-32C- t allele and marked differences in IL-6, IL-10, TNF-α, TGF-β, and IFN-γ than white subject. There were no significant differences in MCP-1 2518 A, G allele between black and white subjects. White subjects tended to have borderline significantly higher mean serum of vitamin D (58.4 nmol/l) than black subjects (37.7 nmol/l). The capacities of skin to synthesize vitamin D Post-UVB were significantly higher in whites than in black subjects. Conclusions: Black skin people had consistently higher susceptibility to infection by M. tuberculosis than are whites skin peoples. The mechanism of a racial difference in infectibility by M. tuberculosis is the result of a complex interaction between the environmental, immunologic, and genetic factors.

Keywords: African, caucasian, ethnicity, race, tuberculosis

How to cite this article:
Fares A. Racial differences in susceptibility to infection by Mycobacterium tuberculosis. Ann Trop Med Public Health 2012;5:307-12
How to cite this URL:
Fares A. Racial differences in susceptibility to infection by Mycobacterium tuberculosis. Ann Trop Med Public Health [serial online] 2012 [cited 2020 Nov 24];5:307-12. Available from: https://www.atmph.org/text.asp?2012/5/4/307/102032

Despite reductions in the global burden of tuberculosis (TB), the great majority of TB incidence remains higher among certain racial/ethnic minorities. The basis for the different rates of TB among various ethnocultural populations remains unclear. TB is a multifactorial disorder in which the environment interacts with host-related factors, contributing to the overall clinical spectrum. [1] Improved understanding of the individual balance between degree of exposure and inherited genetic susceptibility to infection, as well as the respective effects of environmental and host-related factors on the development of disease, will have strong implications for TB control and prevention. [2] The present study designs combining different research methods, but it offers the advantage of assessing together the roles of environmental, immunologic, and genetic factors in susceptibility to infection by Mycobacterium tuberculosis and disease development.

Materials and Methods

Search strategy

Electronic databases, MEDLINE, EMBASE, and Cochran Library, were used in this review to identified peer-reviewed relevant studies up to June 1, 2011 with keywords TB, Race, Ethnicity, African, Caucasian OR Vitamin, Race, Ethnicity, African, and Caucasian. The electronic search was tailored to each database in order to locate articles that met the eligibility criteria as described below. Relevant publications and epidemiological data were also downloaded from websites of international agencies such as World Health Organisation (WHO) or online peer-review journal such as American Journal of Clinical Nutrition and Journal of Metabolism and Endocrinology. In addition, the bibliographies of the relevant articles identified through the searches for any additional articles that met the inclusion criteria were reviewed. No contact was made with authors of the papers.

Eligibility criteria

Sources were screened for relevance to the topic, originality, a well-described methodology, rigor of statistical analysis, and an adequate sample size, where relevant. Sources were excluded where sample size was inadequate (except in qualitative studies), methodology was not well described, statistical analysis was unclear, and where the full article was unavailable. In addition, only papers published in English language were considered and dealt with human subjects. Studies dealing with brown skin color like Hispanic, Asian, or Chinese subjects were excluded. Studies deals with health subjects were included; subject with conditions known to be associated with vitamin D deficiency (e.g., rickets and osteoporosis) were excluded. In some cases, control groups of healthy subjects exist in studies of home nursing residents or subjects with condition known to be associated with vitamin D deficiency; in these cases, control groups were included in the study. Some of the studies reported random selection of population-based participants in all age, gender, and ethnic groups, and another studies reported random selection participants in selected age and gender strata, in these cases black and white skin groups were included in the study. In these studies we used a nmol/dl unit to express serum level of 25(OH)D; therefore, in the studies using ng/dl unit as outcome measurements of 25(OH)D was converted to nmol /dl unit.

Data abstraction

Data were abstracted from each eligible study: (1) study characteristics including the sample size and the mean follow-up time; (2) patient characteristics including mean age, age range, female and male number, and type of skin color; and (3) serum level of chemokines, cytokines, and vitamin D.


A total of 417 studies were identified from the initial Pubmed search. Of these articles, 31 studies met the inclusion criteria. Five of these studies investigated the prevalence of TB among black and white people. Among these, 81.5% of black skin people were TB positive, while 18.5% of white skin people were TB positive [Table 1].

Table 1: Prevelance of TB among black and white

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Four controlled BCG trials provided information on annual TB cases. The average annual TB case rates per 100,000 in these four studies were 413 among black’s and 213 among white’s reactors [Table 2].

Table 2: Annual TB case rates among intial Tuberclin reactor[8]

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Three studies investigated vitamin D receptor polymorphisms and susceptibility to TB among healthy subject, at a total of 101 white and 643 black subjects. The black subjects demonstrated higher frequency of the Fok1 E2-C4T F allele, Bsm1 E8-G-+ 284A- B allele, APa1 e9-T-48G- a allele, and Taq1 E9-T-32C- t allele than white subject. While white subjects had a significant higher frequency of the Fok1 E2-C4T -f allele, Bsm1 E8-G-+ 284A- b allele, APa1E9-T-48G- A allele, and Taq1 E9-T-32C- T [Table 3].

Table 3: Vitamin D receptor

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A total of 11 studies with 22,858 subjects from two racial groups (white and black) were conducted in USA and UK. White subjects tended to have borderline significantly higher mean serum of vitamin D (58.4 nmol/l) than black subjects (37.7 nmol/l) [Table 4].

Table 4: Serum Vitamin D level

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For the MCP-1 – 2518 SNP, a total of 162 white and 36 black subjects were enrolled in two studies. There were no significant differences in MCP-1 2518 A, G allele between black and white subjects [16],[30] [Table 5].

Table 5: Chemokines difference bewteen black and white subjects

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Two studies investigated the differences in serum cytokines level between black and white subjects; in one study black subjects demonstrated marked differences in the inheritance patterns for polymorphisms in several cytokine genes such as IL-6, IL-10, TNF-α, TGF-β, and IFN-γ. In another study, the proinflammatory cytokine interleukin-6 IL6-174 G/G genotype was 36.5 times more common among African Americans. IL10-1082 A/A genotype was 2.8 times more common in African-American than in the white. TNF-a did not differ significantly between African-American and white [Table 6].

Table 6: Cytokines difference bewteen black and white subjects

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Four small studies have evaluated the differing capacities of skin to absorb ultraviolet radiation (UVR) and synthesize vitamin D among black and in comparison to white subjects. One of the study conducted in USA showed the effect of increased skin pigment on the cutaneous production of vitamin D3, circulating vitamin D concentrations were determined in two Caucasian and three black volunteers after exposure to a single standard dose of UVR. Exposure of Caucasian subjects to one minimal erythemal dose (MED) of UVR greatly increased serum vitamin D concentrations by up to 60-fold 24-48 h after exposure, whereas this dose did not significantly change serum vitamin D concentrations in black subjects. Re-exposure of one black subject to a dose of UVR six times larger than the standard dose increased circulating vitamin D to concentrations similar to those recorded in Caucasian subjects after exposure to the lower dose. [33] In another study, the serum vitamin D concentrations of six dark skin Asians in response to 1.5 times their MED of whole-body UVR was studied. The mean serum vitamin D concentrations rose from a baseline of 4.98 ± 4.98 nmol/L to a peak of 94.6 ± 29.8 nmol/L at 24 h. This concentration was gradually declining back to baseline by day 9. The UVR needed to produce an MED in Asians, with their darker skin, was greater (49-133 mJ/cm 2 ) than that required in Caucasians (31-48 mJ/cm 2 ). Asians may need longer exposure to sunlight than Caucasians do to give a similar response. [34] In another study conducted among healthy young subjects from three racial groups (white, Indian, and black), following whole-body exposure to 27 mJ/cm 2 of UVB (wavelengths, 290-320 nm), there was a significant racial group effect on serum vitamin D3 levels. Post-UVB levels were significantly higher in whites (31.4 ± 4.4 nmol/L) than in Indians or blacks (12.8 ± 2.9 and 9.1 ± 2.1 nmol/L, respectively). [35] In one more study, 13 white and 7 black adults ranging from 22 to 35 years of age were submitted to sequential total body suberythemal doses of UVB (280-315 nm) biweekly for 6 weeks. Initial UVB dose was 5% below the MED for the most sensitive skin, followed by 10% increase per exposure for 4 weeks. Blood samples were drawn weekly. Baseline vitamin D concentrations were significantly lower in blacks compared to whites, but the increases in serum vitamin D concentrations were similar in both groups. [36]


The result of this review confirms the well-known fact that the prevalence of TB infection is higher among blacks than that among whites. The mechanism of a racial difference in infectibility by M. tuberculosis is the result of a complex interaction between the host and environmental factors. Several studies from different regions, ethnic groups, and cultures show positive association between the serum level of vitamin D and susceptibility to TB infection or reactivation. [37] Serum vitamin D concentrations are significantly lower in TB patients compared with those in control groups. Several mechanisms have been proposed to explain this relation, most of them concerned with the possibility of the role of active metabolite vitamin D (25-(OH) D) in the hosts defence against human TB, thus suggesting that metabolites (25-(OH) D) can act to suppress the growth of M. tuberculosis through the induction of nitric oxide (NO) production by macrophages. [38]

Despite large variation probably originating in differences in culture (clothing, time spent outdoors), vitamin D intake, genetic factors, and study-related factors such as selection of participants, and method used to determine 25(OH)D. The overall level of vitamin D in this study was significantly higher in Caucasian than African populations. Since UVB radiation from direct sunlight stimulates the production of vitamin D in humans through natural chemical reactions, people with increased levels of melanin in their skin produce much lower levels of the vitamin than those with lower levels of melanin, as those whose skin contains higher levels of melanin filtrate the sun’s UVR, thereby limiting the amount of the vitamin produced through this particular mechanism. Furthermore, the most evident study about the role of melanin in immune system showed that the melanin was equally effective in inhibiting production of TNF by monocytes stimulated with the purified protein derivative of M. tuberculosis also inhibit production of IL-6 by IL-1-stimulated human fibroblasts and endothelial cells. [39] This result suggests that the people with dark or semi-dark skin are at more risk to disease development than white skin as a consequence of melanin on vitamin D production and immune system function inhibition. Therefore, vitamin D supplementation or dietary could make for a remarkably effective method for reducing the infection rate of TB in peoples of African descent. Clinical trials for TB endemic regions in Africa have been proposed to test if these laboratory results can be replicated on a larger scale and to verify if lower rates of the incidence of TB would result.

A number of polymorphisms in the human VDR gene (located on chromosome 12q12-14) have previously been associated with TB susceptibility, of which most commonly, FokI, BsmI, ApaI, and TaqI. The active metabolite of vitamin D, 1,25 dihydroxyvitamin D3, is an important immunoregulatory hormone. Its effects are exerted via the VDR, which is present on human monocytes and activated T- and B-lymphocytes. Considering the role of the VDR and it specific immunological functions, including activation of monocytes, stimulation of cell-mediated immunity, and suppression of lymphocyte proliferation, immunoglobulin production and cytokine synthesis, variation in the VDR genes may contribute to disease susceptibility. However, several studies in different ethnic populations investigate the possible association of VDR gene in TB susceptibility but the result was inconsistent with specific populations. In this review, one can find similarity in the frequency of SNP Fok1 allele between Venda population (South Africa) and Gambian and that could be profound effect on susceptibility to TB in black people.

MCP-1 is suggested to play an initial role in attracting immune cells to combat TB. Several studies conducted in on different ethnic groups strongly suggest an influence of MCP-1 variation on TB susceptibility. Positive linkage of an association of MCP-1 -2581G with TB susceptibility in Mexican and Korean TB patients [40] has been observed. In contrast, no association of MCP-1 -2581 was found in Brazilian multicase families [41] and in a Chinese patient group from Hong Kong. [42] In the present study, it was found that the white subjects had no significant differences in frequency of the G and A alleles compared with black subjects. One can believe that, at present, the overall data do not sufficiently support any major involvement of that variant in TB susceptibility or protection.

TNF- α has been implicated as a key protective cytokines involved in macrophage activation and granuloma formation. [43] M. tuberculosis induces TNF-α secretion by macrophages, dentric cells, and T cells. [44] In humans, when anti-TNF-α was used to treat patients with crohn and rheumatoid arthritis, it was associated with occurrence or reactivation of M. tuberculosis leading to clinical TB. [43] The most widely studied SNP in the TNF-α gene is the G to A substitution at position-308. The high frequency of the functional SNP associated with low TNF-α production may limit effective immunity to M. tuberculosis infection in the black subjects.

IFN-γ, a classical macrophage activator, has been implicated multiple immunological function, produced by both CD4+ and CD8+ T cells, as well as by NK cells. [44] Humans defective in genes for IFN-γ or the IFN-y receptor are prone to serious mycobacterial infection. [44] The lack of IFN-γ expression was associated with deficient production of nitric oxide, nitric oxide synthase, and reactive oxygen intermediates by infected macrophage, which are thought to be key in facilitating the killing of bacilli. In the context of the present study, the high prevalence of the functional SNP associated with low IFN-γ production may develop a less efficient cytokines response, which is required to contain M tuberculosis in black subjects. [16]

The evidence data from experimental study indicate that the secretion of IL-6 by infected macrophage may contribute to the inability of immune system to eradicate M. tuberculosis by inhibiting the responses of uninfected macrophages to IFN-y. [45] Therefore, the high frequency of the functional SNP associated with high IL-6 production may limit effective immunity to M. tuberculosis in black people.

Interleukin-10 is a potent immunomodulatory cytokine that has been shown in vitro to directly or indirectly affect multiple cell types, including macrophages, monocytes, dendritic cells, CD4 T cells, and CD8 T cells. [46] The dominant function of IL-10 is to deactivate macrophages, resulting in diminished Th1 cytokine production, [46],[30] decreased production of reactive nitrogen or oxygen species, [40] and limited Ag presentation. [39] It has been also identified as a correlate of susceptibility for TB [30] in both mice and humans. [45] The high frequency of the functional SNP associated with low IL-6 production may limit effective immunity to M. tuberculosis in black people.


Black skin people had consistently higher susceptibility to infection by M. tuberculosis than are whites skin peoples. The data also suggest that the racial differences in chemokine’s and cytokines production, as well as serum vitamin D level and cutaneous vitamin D synthesis may play a vital role in protection the body from the infection by M. tuberculosis.

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.102032


[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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