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The potential antiviral mechanism of vitamin D against DENV has yet not been fully explored; however, certain reports support the proposal that vitamin D could perform anti-DENV effects and immunoregulatory functions on innate immune responses [ 10 — 12 ]. In line with this, the effect of vitamin D treatment of human monocytic cell lines on DENV infection was recently reported [ 72 ]. The molecular mechanisms by which vitamin D can elicit an antiviral and anti-inflammatory role towards DENV have not been fully described, and although we observed that monocyte-derived macrophages differentiated in the presence of 1,25 OH 2 D 3 are less susceptible to DENV infection and express lower levels of mannose receptor restricting binding of DENV to target cells manuscript in preparation , further studies are required to confirm that vitamin D treatment confers both anti-inflammatory and antiviral responses.
Besides the members of the let-7 family, other miRs have also been associated with suppression of DENV infection and the inflammatory responses against the virus, as discussed below. Viruses strictly depend on cellular mechanisms for their replication; therefore, there is an obligatory interaction between the virus and the host RNA silencing machinery. Although virus-derived small interfering RNAs may induce changes in cellular mRNA and miR expression profiles to induce replication, cellular miRs can also target viral sequences or induce antiviral protein expression to inhibit viral replication and translation [ ].
Indeed, during DENV infection, several cellular miRs have been reported to have an effect on the replicative activity of the virus and the permissiveness of the host cells. The expression levels of different miRs regulated during DENV infection have been screened in the hepatic cell line Huh This approach identified miR let-7c as a key regulator of the viral replicative cycle that affects viral replication and the oxidative stress immune response through the protein Heme Oxygenase-1 HO-1 by activating its transcription factor BACH1 Basic Leucine Zipper Transcription Factor-1 [ 68 ].
This antiviral effect was explained by the fact that miR targets the DENV-2 E protein gene sequence, downregulating its expression and therefore acting as an antiviral regulator [ 78 ]. This antiviral effect induced by signaling of type I IFN is also promoted by miR that has been reported to control virus-induced immune responses in models of infection with other members of the Flavivirus genus such as HCV [ — ].
This observation is in accordance with a study in which elevated expression of miR in patients with DHF was correlated with suppression of SOCS-1 expression in monocytes [ 80 ] that in turn could be linked to the fact that vitamin D controls inflammatory responses through modulation of SOCS by downregulating miR [ 20 ]. Although it has remained unclear whether endogenous miRs can interfere with viral replicative activity by targeting DENV sequences or viral mRNAs, some experimental approaches have shown the importance of miRs in restricting viral replication through this mechanism [ 85 , — ].
Some artificial miRs amiRs have been described as targeting the highly conserved regions of the DENV-2 genome and promoting efficient inhibition of virus replication [ ]. Likewise, the insertion of the MRE for the hematopoietic specific miR into the DENV-2 genome restricts replication of the virus in DCs and macrophages, highlighting the importance of this hematopoietic miR in dissemination of the virus [ 82 ]. Moreover, overexpression of miR inhibited replication of DENV in an endothelial cell-like cell line. The authors showed that miR inhibits DENV by negatively regulating the microtubule destabilizing protein stathmin 1 STMN-1 that is crucial for reorganization of microtubules and later replication of the virus.
Although little is known regarding the variations in miR expression in DENV-infected individuals, a recent study showed the expression profile of the miRs in blood samples of DEN-infected patients. The authors report 12 miRs that were specifically altered upon acute dengue and 17 miRs that could potentially be associated with specific dengue-related complications [ ]. In addition, another profiling study reported abundance changes in the expression of some miRs in DENV-infected peripheral blood monocytes.
Importantly, let-7e was among the miRs with the most significant regulation which, besides anti-DENV activity, may be of crucial importance for the modulation of inflammatory responses. Since a link between vitamin D and miR expression has been established, but no reports discuss their combined implications for DENV antiviral and inflammatory response, we hypothesized here a vitamin D and miR interplay that could modulate DENV pathogenesis, opening new horizons in the therapeutic field of dengue disease.
Severe dengue disease symptoms and DENV infection are characterized by overproduction of proinflammatory cytokines driven mainly by activation of several PRRs [ 29 ].
However, a better understanding of these mechanisms is required to provide interesting clues regarding DENV pathogenesis and dengue disease treatment. Certainly, epidemiological and experimental evidence describe an overall positive vitamin D-related immune effect in which increased levels of vitamin D and variants in the VDR receptor are associated with reduction of viral replication, decreased risk of infection, lower disease severity, and better outcome of the dengue symptoms [ 9 — 12 , 72 ].
Additionally, the emerging relationships between vitamin D, the TLR signaling pathway, and its regulation by miRs are beginning to gain critical importance in infectious diseases. Indeed, as discussed above, several DENV infection studies have started to illustrate these vitamin D regulatory features that could be key mechanisms for the control of virus replication and homeostasis of the inflammatory response, thus making this hormone a special candidate for therapeutic strategies [ ]. Although it is important to note that such a global effect on the inflammatory activity could weaken the host response to other opportunistic pathogens, it has been suggested that while vitamin D may reduce inflammatory markers during viral infections, it also exerts protective effects against coinfections with other opportunistic pathogens [ 14 , ].
Moreover, its clinical effectiveness has been tested by improving the overall physical condition of DENV patients and reducing the progression of the disease [ 11 ]. Although incoming supplementary trials are required to fully elucidate the therapeutic relevance of vitamin D, it is evident that this hormone may be an excellent alternative of a natural immune-regulatory agent capable of modulating the innate immune response against DENV, which will provide crucial information to understand and design strategies to treat and control progression of dengue disease.
Although further experimental studies are required to boost the understanding of vitamin D in the regulation of inflammation and antiviral response against DENV infection, the information discussed above highlights the features of vitamin D in immune regulation as an exciting research field and as an efficient and low-cost therapeutic procedure against DENV and possibly other viral infections.
The authors thank Anne-Lise Haenni for reading the paper and for her constructive and valuable comments. Indexed in Web of Science. Subscribe to Table of Contents Alerts. Table of Contents Alerts.
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Abstract Over the last few years, an increasing body of evidence has highlighted the critical participation of vitamin D in the regulation of proinflammatory responses and protection against many infectious pathogens, including viruses. Introduction Activation of innate immune cells results in the release of proinflammatory mediators to initiate a protective local response against invading pathogens [ 1 ]. Vitamin D and miR targets associated with inflammatory response. View at Google Scholar T. South African Journal of Science. The replicator paradigm sheds decisive light on an old but misguided question".
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Herpes simplex virus infections. Herpesvirus latency confers symbiotic protection from bacterial infection. Immune response and tolerance during chronic hepatitis B virus infection. Indian Journal of Medical Microbiology. Highly endemic hepatitis B infection in rural Vietnam. Journal of Gastroenterology and Hepatology.
Reducing the risk of mother-to-child human immunodeficiency virus transmission: The congenital varicella syndrome. Role of herd immunity in determining the effect of vaccines against sexually transmitted disease. The influence of weather conditions on the epidemiology of vector-borne diseases by the example of West Nile fever in Russia.
The British, the Indians, and smallpox: Canadian Bulletin of Medical History. Patterson KB, Runge T. Smallpox and the Native American. The American Journal of the Medical Sciences. The major epidemic infections: The role of epidemic infectious diseases in the discovery of America. New York State Journal of Medicine. Smallpox decimates the Tlingit The geography and mortality of the influenza pandemic.
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Volume 72 Aaron J. Volume 98 Margaret Kielian. Volume 69 Aaron J. Volume 74 Aaron J. Volume 57 Frederick A. Volume 89 Karl Maramorosch. Control of Plant Virus Diseases: Volume 90 Nikolaos Katis.