Precursor Forms of Vitamin D Reduce HIV-1 Infection In Vitro

Aguilar-Jiménez, Wbeimar; Villegas-Ospina, Simón; González, Sandra; Zapata, Wildeman; Saulle, Irma; Garziano, Micaela; Biasin, Mara; Clerici, Mario; Rugeles, Marı́a Teresa

doi:10.1097/qai.0000000000001150

Cited by 19 publications

(36 citation statements)

References 57 publications

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“…[204][205][206][207] This effect may be partially explained by the fact that sufficient VitD levels can reduce inflammation and T cell activation, restrain HIV-1 infection in T cells, and promote the proliferation of CD4 + T cells induced by APCs. 207,208 These observations suggest that the baseline metabolic characteristics may be associated with impaired immune reconstitution in HIV-1-infected individuals during ART.…”

Section: Host Metabolic Factorsmentioning

confidence: 91%

“…Several studies have demonstrated that baseline VitD deficiency in HIV‐1‐infected individuals was associated with diminished CD4 + T‐cell recovery after ART initiation . This effect may be partially explained by the fact that sufficient VitD levels can reduce inflammation and T cell activation, restrain HIV‐1 infection in T cells, and promote the proliferation of CD4 + T cells induced by APCs . These observations suggest that the baseline metabolic characteristics may be associated with impaired immune reconstitution in HIV‐1‐infected individuals during ART.…”

Section: Potential Mechanisms Of Incomplete Immune Reconstitutionmentioning

confidence: 99%

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Incomplete immune reconstitution in HIV/AIDS patients on antiretroviral therapy: Challenges of immunological non-responders

Yang

Zhang

et al. 2020

Journal of Leukocyte Biology

212

214

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The morbidity and mortality of HIV type‐1 (HIV‐1)‐related diseases were dramatically diminished by the grounds of the introduction of potent antiretroviral therapy, which induces persistent suppression of HIV‐1 replication and gradual recovery of CD4+ T‐cell counts. However, ∼10–40% of HIV‐1‐infected individuals fail to achieve normalization of CD4+ T‐cell counts despite persistent virological suppression. These patients are referred to as “inadequate immunological responders,” “immunodiscordant responders,” or “immunological non‐responders (INRs)” who show severe immunological dysfunction. Indeed, INRs are at an increased risk of clinical progression to AIDS and non‐AIDS events and present higher rates of mortality than HIV‐1‐infected individuals with adequate immune reconstitution. To date, the underlying mechanism of incomplete immune reconstitution in HIV‐1‐infected patients has not been fully elucidated. In light of this limitation, it is of substantial practical significance to deeply understand the mechanism of immune reconstitution and design effective individualized treatment strategies. Therefore, in this review, we aim to highlight the mechanism and risk factors of incomplete immune reconstitution and strategies to intervene.

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Section: Host Metabolic Factorsmentioning

confidence: 91%

Section: Potential Mechanisms Of Incomplete Immune Reconstitutionmentioning

confidence: 99%

Incomplete immune reconstitution in HIV/AIDS patients on antiretroviral therapy: Challenges of immunological non-responders

Yang

Zhang

et al. 2020

Journal of Leukocyte Biology

212

214

View full text Add to dashboard Cite

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“…Vitamin D induces antiviral gene expression, reduces the viral co-receptor CCR5 on CD4+ T-cells, and promotes an HIV-1-restrictive CD38+HLA-DR+ immunophenotype in in vitro assays, leading to HIV-1 infection inhibition in T cells ( 109 ). Likewise, VitD reduces the ability of TNFα to upregulate the transcription of HIV RNA from latently infected CD4+ cells ( 110 ).…”

Section: Vitd and The Immune Systemmentioning

confidence: 99%

Vitamin D in Human Immunodeficiency Virus Infection: Influence on Immunity and Disease

et al. 2018

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People living with human immunodeficiency virus (HIV) infection typically have hypovitaminosis D, which is linked to a large number of pathologies, including immune disorders and infectious diseases. Vitamin D (VitD) is a key regulator of host defense against infections by activating genes and pathways that enhance innate and adaptive immunity. VitD mediates its biological effects by binding to the Vitamin D receptor (VDR), and activating and regulating multiple cellular pathways. Single nucleotide polymorphisms in genes from those pathways have been associated with protection from HIV-1 infection. High levels of VitD and VDR expression are also associated with natural resistance to HIV-1 infection. Conversely, VitD deficiency is linked to more inflammation and immune activation, low peripheral blood CD4+ T-cells, faster progression of HIV disease, and shorter survival time in HIV-infected patients. VitD supplementation and restoration to normal values in HIV-infected patients may improve immunologic recovery during combination antiretroviral therapy, reduce levels of inflammation and immune activation, and increase immunity against pathogens. Additionally, VitD may protect against the development of immune reconstitution inflammatory syndrome events, pulmonary tuberculosis, and mortality among HIV-infected patients. In summary, this review suggests that VitD deficiency may contribute to the pathogenesis of HIV infection. Also, VitD supplementation seems to reverse some alterations of the immune system, supporting the use of VitD supplementation as prophylaxis, especially in individuals with more severe VitD deficiency.

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“…In support of this, VD supplementation attenuated HIV-1 replication and increased the number of circulating leukocytes from 100 VD 3 -fed healthy adults [142]. In in vitro experiments using PBMC infected with HIVBa-L, VD treatment reduced HIV-1 infection in T cells by inducing antiviral gene expression and reducing the levels of viral co-receptor CCR5 [143]. In ex vivo experiments using PBMC from seronegative individuals infected with HIV-1, VD treatment was able to reduce HIV-1 transmission by specifically modulating the activation of T cells and the production of antiviral factors [144].…”

Section: Effect Of Vd On Hi Infection Immune Response Pathogenesismentioning

confidence: 74%

Controversial Effects of Vitamin D and Related Genes on Viral Infections, Pathogenesis, and Treatment Outcomes

Lee

2020

Nutrients

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Vitamin D (VD) plays an essential role in mineral homeostasis and bone remodeling. A number of different VD-related genes (VDRG) are required for the metabolic activation of VD and the subsequent induction of its target genes. They include a set of genes that encode for VD-binding protein, metabolic enzymes, and the VD receptor. In addition to its well-characterized skeletal function, the immunoregulatory activities of VD and the related polymorphisms of VDRG have been reported and linked to its therapeutic and preventive actions for the control of several viral diseases. However, in regards to their roles in the progression of viral diseases, inconsistent and, in some cases, contradictory results also exist. To resolve this discrepancy, I conducted an extensive literature search by using relevant keywords on the PubMed website. Based on the volume of hit papers related to a certain viral infection, I summarized and compared the effects of VD and VDRG polymorphism on the infection, pathogenesis, and treatment outcomes of clinically important viral diseases. They include viral hepatitis, respiratory viral infections, acquired immunodeficiency syndrome (AIDS), and other viral diseases, which are caused by herpesviruses, dengue virus, rotavirus, and human papillomavirus. This review will provide the most current information on the nutritional and clinical utilization of VD and VDRG in the management of the key viral diseases. This information should be valuable not only to nutritionists but also to clinicians who wish to provide evidence-based recommendations on the use of VD to virally infected patients.

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Precursor Forms of Vitamin D Reduce HIV-1 Infection In Vitro

Abstract: VitD reduces HIV-1 infection in T cells possibly by inducing antiviral gene expression, reducing the viral co-receptor CCR5 and, at least at the highest cholecalciferol concentration, by promoting an HIV-1-restrictive CD38HLA-DR immunophenotype.

Cited by 19 publications

References 57 publications

Incomplete immune reconstitution in HIV/AIDS patients on antiretroviral therapy: Challenges of immunological non-responders

Incomplete immune reconstitution in HIV/AIDS patients on antiretroviral therapy: Challenges of immunological non-responders

Vitamin D in Human Immunodeficiency Virus Infection: Influence on Immunity and Disease

Controversial Effects of Vitamin D and Related Genes on Viral Infections, Pathogenesis, and Treatment Outcomes

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