Role Of Vitamin-D Supplementation In TB/HIV Co-Infected Patients

Abstract

Objective: This review aimed to assess the role of vitamin D supplementation on the decrement of mortality and morbidity rate among tuberculosis (TB)/human immune deficiency virus (HIV) co-infected clients.Method: Pub Med, google scholar and google search were accessed to find out all document to describe this review article.

Results: Nowadays TB/HIV co-infection has become a major global concern, particularly in low and middle-income countries. Mycobacterium tuberculosis and HIV infections are co-endemic and more susceptible to the progression of TB. Immunosuppression associated with HIV is a strong risk factor for the reactivation of latent TB to the active form. Immune cells like macrophages recognized Mycobacterium tuberculosis through TLR2/1, and it increases the expression of the vitamin D receptor (VDR) and CYP27B1. The synthesis of 1,25-dihydroxy vitamin D promotes VDR-mediated transactivation of the antimicrobial peptide cathelicidin and the killing of intracellular Mycobacterium tuberculosis. Cathelicidins have a direct antimicrobial effect through membrane disruption. Besides, it has also antiviral effects via inhibition of retrovirus (HIV) replication. In fact, as some studies showed, there was a lower induction of cathelicidin in monocytes who have low vitamin D levels.Conclusion: Therefore, vitamin D supplementation can be directly involved in the reduction of TB/HIV co-infection and its progression.

Keywords: HIV; tuberculosis; vitamin D.

Figure 1

The metabolism of vitamin D.

Figure 2

Role of vitamin D for the production of cathelicidin. Mycobacterium tuberculosis-derived macrophages with TLR2/1L stimulate the expression of VDR that connects to Vit-D and inhibits Mtb through inducing innate immune responses that produce cathelicidin.

Figure 3

The role of autophagy and CAMP in 1,25D₃-mediated inhibition of Mycobacterium tuberculosis (Mtb) and HIV. HIV budding occurs into the multivesicular endosomes of macrophages. Mtb enters through phagocytosis. Cytochrome p450, family 27, subfamily B, polypeptide 1 (CYP27B1) 1α-hydroxyls the inactive 25D₃ into the active 1,25D₃. 1,25D₃ induces the expression of camp, presumably by binding to the Vit-D (1,25D₃) receptor (VDR), which heterodimerizes with the retinoid X receptor (RXR) and directly regulates transcription by binding to the vitamin D response element (VDRE) consensus sequence located upstream of the Camp gene. The expression of camp is required both for autophagosome and phagolysosome biogenesis, which leads to killing of the microbial pathogens through autophagy. Adapted from Jo EK. Innate immunity to mycobacteria: vitamin D and autophagy. Cell Microbiol. 2010;12(8):1026-1035. ^© 2010 Blackwell Publishing Ltd.