Enveloped virus infection (RSV, coronavirus, HIV, etc.) 1.5X more likely if poor Vitamin D Receptor – meta-analysis Dec 2018

Vitamin D Receptor polymorphisms and risk of enveloped virus infection: A meta-analysis

Gene Volume 678, 15 December 2018, Pages 384-394 https://doi.org/10.1016/j.gene.2018.08.017
Marina Laplana1b José Luis Royo 2

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Respiratory viral infection (RSV) and low vitamin D - many studies

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Highlights

  • Meta-analysis underlines FokI as a risk polymorphism for enveloped virus infection.
  • Worldwide incidence of RSV infection and FokI allele frequency show a common trend.
  • FokI should be considered a genetic factor when describing worldwide RSV incidence.

Introduction
Vitamin-D plays a role regulating the immune response against to viral infection. In this sense, vitamin-D deficiency may confer increased susceptibility to enveloped virus infection such as

  • HIV,
  • Hepatitis,
  • Dengue and
  • Respiratory Syncytial virus infection,

among others. Vitamin D activity is mediated by its receptor (VDR), which acts as a transcription factor modulating the expression of genes triggering the response against viruses. To date, six major VDR polymorphisms (Cdx, A1012G, FokI, BsmI, ApaI and TaqI) have been studied in the context of viral infection susceptibility. Reported studies show controversial results probably due to statistical lack of power and population genetic differences.

Aims
To do a systematic review of the published data and to perform a meta-analysis examining the role of six VDR polymorphisms on infection susceptibility to enveloped virus.

Results
From all markers and virus considered an association of FokI polymorphism with RSV infection emerges as significant. The worldwide distribution of risk T-allele reveals a lower prevalence in African populations that runs parallel with the relative lower incidence of RSV-associated severe ALRI in children <1 year described in African samples.

Conclusion
The results disclose FokI polymorphism as a relevant variant capturing the association of VDR polymorphisms with viral infection.

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