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

Infection and Drug Resistance Dovepress open access to scientific and medical research Infection and Drug Resistance downloaded from https://www.dovepress.com/ by 153.229.40.219 on 03-Jun-2020 For personal use only. Open Access Full Text Article Role Of Vitamin-D Supplementation In TB/HIV Co-Infected Patients This article was published in the following Dove Press journal: Infection and Drug Resistance Birhanu Ayelign 1 Meseret Workneh 1 Meseret Derbew Molla Gashaw Dessie 2 2 1 Department of Immunology and Molecular Biology, School of Biomedical And Laboratory Sciences, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia; 2 Department of Biochemistry, School of Medicine, College of Medicine And Health Sciences, University of Gondar, Gondar, Ethiopia 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 coendemic 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 1,25dihydroxy 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: vitamin D, tuberculosis, HIV Background Correspondence: Birhanu Ayelign Email Human immunodeficiency virus (HIV) disease is one of the main risks of developing tuberculosis (TB) disease.1,2 Tuberculosis is the leading cause of death in HIV-infected individuals in Africa.3 Globally in 2017, the best estimate is that 10.0 million people (9.0–11.1 million) developed TB disease, 9% having TB/HIV coinfection. In 2017, TB caused an estimated 1.6 million deaths and there were 300 000 deaths from TB/HIV co-infection.4 TB/HIV co-infection accelerates the sudden deterioration of the immune system that causes premature death. In sub-Saharan African countries up to 70% of HIV-positive patients are estimated to be co-infected with Mycobacterium tuberculosis(Mtb). The immune suppression associated with HIV infection is an aggravating factor for the development of latent tuberculosis to vigorous disease and finally leads to death.5 Human immunodeficiency virus infection has contributed to a doubling of the number of tuberculosis cases in some African countries during the past decade. Thus, the double burden due to co-infection increased difficulties in tuberculosis diagnosis, an increased frequency of the treatment side-effects, and higher relapse and reinfection 111 submit your manuscript | www.dovepress.com Infection and Drug Resistance 2020:13 111–118 DovePress © 2020 Ayelign et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms. php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). http://doi.org/10.2147/IDR.S228336 Powered by TCPDF (www.tcpdf.org) REVIEW Infection and Drug Resistance downloaded from https://www.dovepress.com/ by 153.229.40.219 on 03-Jun-2020 For personal use only. Ayelign et al rates.6 Even though we are unable to understand the exact mechanism of TB/HIV co-infection, they have a positive correlation to one another.7 The management of HIV and TB co-infection is challenging and usually associated with favorable treatment outcome. The emergency and dissemination of drug-resistant Mtb strains contribute to its epidemicity. In addition to drug resistance strains, both clinical and public health management problems are other reasons. Some studies showed that HIV testing and drug susceptibility (DST) capacity for MtB is robust, 40–80% of TB patients with multidrug-resistant and extensive drug resistance TB are HIV infected.8 As a result, vitamin D (Vit-D) supplementation can overcome the challenge and inhibit HIV and replication and growth. Cathelicidin, which is part of the innate immune system, plays a critical role in the fight against TB. Mycobacterium tuberculosis binds to toll-like receptors (TLR2/1) on macrophages and leads to upregulation of 1α-hydroxylase gene expression. Intracellular 1,25 (OH)2D binds to the vitamin D receptor to activate production of cathelicidin that has antimicrobial effects. In the same way, Vit-D also activates T helper cells through activation of VDR gene-encoded PLC-y, which also results in upregulation of PLC-y1 by 75-fold for good activation of the TCR.9 The Immunological Interaction Between Mycobacterium Tuberculosis And HIV Infection Immunocompetent individuals have a 5–10% chance to develop active TB in a lifetime, but patients with HIV have a chance to develop TB of up to 15% per year. Epidemiological studies showed that the risk of TB increases in HIV-1-infected people due to a decline in CD4 count and advanced clinical stages of disease (WHO stages 3/4). Although unsuppressed HIV-1 viral load during ART treatment has been linked with increased risk of TB in a large retrospective study, others have not shown it to be an independent risk factor.10–12 The initial cellular targets of HIV-1 infection are the mucosal CD4 T cells, dendritic cells, and local macrophages; final results are the depletion of these cells. The exhaustion of CD4+ T cells, which is the most important characteristic of HIV/AIDS, is entirely a significant contributor to the increased risk of reactivation of latent TB and vulnerability to new infection. The other mechanisms are 112 Powered by TCPDF (www.tcpdf.org) submit your manuscript | www.dovepress.com DovePress Dovepress also that in HIV-positive individuals there is upregulat (...truncated)