Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study
Open accessAbstract
BACKGROUND: Identifying people at higher risk of developing tuberculosis with human immunodeficiency virus (HIV) infection may improve clinical management of co-infections. Iron influences tuberculosis (TB) pathogenesis, but understanding the exact mechanisms of how and timing of when iron is involved remains challenging since biological samples are rarely available from the disease susceptibility period due to the difficulty in predicting in who and when, if ever, TB will develop. The objective of this research was to determine how host iron status measured at HIV diagnosis and genotypes related to host iron metabolism were associated with incident TB. METHODS: Archived clinical data, plasma and DNA were analyzed from 1139 adult participants in a large HIV-1, HIV-2 and dual seroprevalent cohort based at the Medical Research Council Laboratories in The Gambia. Incident pulmonary and/or extrapulmonary TB diagnoses a minimum of 28 days after HIV diagnosis were independently re-confirmed using available evidence (n=152). Multiple host iron status biomarkers, Haptoglobin and solute carrier family 11, member 1 (SLC11A1) genotypes were modeled to characterize how indicators of host iron metabolism were associated with TB susceptibility. RESULTS: Hemoglobin (incidence rate ratio, IRR=0.88, 95% CI=0.79-0.98), plasma transferrin (IRR=0.53, 0.33-0.84) and ferritin (IRR=1.26, 1.05-1.51) were significantly associated with TB after adjusting for TB susceptibility factors. While genotype associations were not statistically significant, SLC11A1 associations replicated similar directions as reported in HIV-seronegative meta-analyses. CONCLUSIONS: Evidence of host iron redistribution at HIV diagnosis was associated with incident TB, and genetic influences on iron homeostasis may be involved. Low hemoglobin was associated with subsequent diagnosis of TB, but when considered in combination with additional iron status biomarkers, the collective findings point to a mechanism whereby anemia and iron redistribution are likely due to viral and/or bacteria-driven processes and the host immune response to infection. As a result, iron supplementation may not be efficacious or safe under these circumstances. Clinical and nutritional management of HIV and Mycobacterium tuberculosis co-infected individuals, especially in regions where food insecurity and malnutrition co-exist, may be further improved when the iron-related TB risk factors identified here are better understood and managed to favor host rather than pathogen outcomes.
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Increased availability of iron promotes the growth of M. tuberculosis and exacerbates TB.
“It is well-established that increased availability of iron promotes the growth of M. tuberculosis and exacerbates TB (163–166).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [165]
Host iron overload is associated with poor clinical outcomes in infectious diseases such as AIDS, malaria, and tuberculosis.
“In support of this notion, host Fe overload is associated with poor clinical outcomes in a number of infectious diseases such as AIDS (i.e., co-infections resulting from HIV-driven immunodeficiency), malaria, and tuberculosis [19][20][21][22]”
From The Iron age of host–microbe interactions (2015) · cites this paper as [21]
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- Authors
- McDermid, J. M., Hennig, B. J., van der Sande, M., Hill, A. V., Whittle, H. C., Jaye, A., & Prentice, A. M.
- Affiliations
- Cornell University (US)
- London School of Hygiene & Tropical Medicine (GB)
- Centre for Human Genetics (GB)
- Corresponding author
- McDermid, Joann M
- Venue
- BMC Infectious Diseases
- Published
- 2013-01-29
- Volume
- 13
- Issue
- 1
- Pages
- 48-48
- ISSN
- 1471-2334 (ISSN-L)
- PMC
- PMC3568026
- OpenAlex
- W2120091037
- Cited by
- 75
- References
- 34
- Citations by year
- 2025: 4 · 2024: 4 · 2023: 6 · 2022: 5 · 2021: 7 · 2020: 4 · 2019: 6 · 2018: 9 · 2017: 6 · 2016: 2 · 2015: 10 · 2014: 8 · 2013: 4
- FWCI
- 5.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- BMC Infectious Diseases (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Greater South Information System
- Funders
- Bristol-Myers Squibb
- Mead Johnson Nutrition
- Wellcome Trust (090532)
- Canadian Institutes of Health Research
- Medical Research Council
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Surgery › Infectious Diseases and Tuberculosis
- Keywords
- tuberculosis, HIV infection, iron redistribution, anemia, hemoglobin, transferrin, ferritin, SLC11A1, haptoglobin, tuberculosis-HIV coinfection, iron supplementation, genetic risk factors, extrapulmonary tuberculosis, malnutrition, food insecurity
- MeSH terms
- Adult, Alleles, Female, Genotype, Humans, Iron, Male, Middle Aged, Retrospective Studies, Risk Factors, Tuberculosis, Biomarkers, HIV Infections, CD4 Lymphocyte Count, Genetic Predisposition to Disease, Young Adult, Coinfection
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