Epidemic influenza and vitamin D. Epidemiol Infect

Boston University, Boston, Massachusetts, United States
Epidemiology and Infection (Impact Factor: 2.54). 01/2007; 134(6):1129-40. DOI: 10.1017/S0950268806007175
Source: PubMed


In 1981, R. Edgar Hope-Simpson proposed that a 'seasonal stimulus' intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity. 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the 'oxidative burst' potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection. Volunteers inoculated with live attenuated influenza virus are more likely to develop fever and serological evidence of an immune response in the winter. Vitamin D deficiency predisposes children to respiratory infections. Ultraviolet radiation (either from artificial sources or from sunlight) reduces the incidence of viral respiratory infections, as does cod liver oil (which contains vitamin D). An interventional study showed that vitamin D reduces the incidence of respiratory infections in children. We conclude that vitamin D, or lack of it, may be Hope-Simpson's 'seasonal stimulus'.

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    • "There is a considerable amount of research on cell and tissue levels investigating sun radiance effects through vitamin D-dependent and independent pathways in the regulation of immune system-driven diseases, and proposing that these pathways complement each other in imunoregulation[20]. Also, multiply observational studies show that vitamin D deficiency predisposes children to respiratory infections , while ultraviolet radiation (either from artificial sources or from sunlight) and vitamin supplementation reduces the incidence of viral respiratory infections in children[28]. Prenatal or early childhood infections may both protect from the T1D and accelerate autoimmunity[29,30]. According to the results of the previously conduced Danish study, neonatal infection increased theT1D risk in boys, but not in in girls[31]. "
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    ABSTRACT: Background: We aimed to assess the association between exposure to sunshine during gestation and the risk of type 1 diabetes (T1D) in Danish children. Methods: The study population included 331,623 individuals born in Denmark from 1983 to 1988; 886 (0.26%) developed T1D by the age of 15 years. The values of sunshine hours were obtained from the Danish Meteorological Institute. Gestational exposure to sunshine was calculated by summing recorded monthly sunshine hours during the full 9 months prior to the month of birth. The linear variable then was split into two categories separated by the median value. Results and conclusions: Cox regression models showed that more sunshine during the third gestational trimester was associated with lower hazards (HR) of T1D at age 5-9 years in males: HR (95% CI): 0.60 (0.43-0.84), p=0.003. Our results should be considered in the context of evidence-based recommendations to the public about skin protection from the sun.
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    • "Our study recorded high detection rates of HCoVs in the harmattan and the wet seasons compared to the other seasons. Possible explanations for this include seasonal variations in host immune status to infection [47] and changes in humidity which increase viral survival in the environment [48]. In the harmattan season for instance humidity is extremely low with heavy amount of dust that could injure the respiratory system thus exposing individuals to infection [49]. "
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    ABSTRACT: Background Acute respiratory tract infections (ARI) are the leading cause of morbidity and mortality in developing countries, especially in Africa. This study sought to determine whether human coronaviruses (HCoVs) are associated with upper respiratory tract infections among older children and adults in Ghana. Methods We conducted a case control study among older children and adults in three rural areas of Ghana using asymptomatic subjects as controls. Nasal/Nasopharyngeal swabs were tested for Middle East respiratory syndrome coronavirus (MERS-CoV), HCoV-22E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1 using Reverse Transcriptase Real-Time Polymerase Chain Reaction. Results Out of 1,213 subjects recruited, 150 (12.4%) were positive for one or more viruses. Of these, single virus detections occurred in 146 subjects (12.0%) and multiple detections occurred in 4 (0.3%). Compared with control subjects, infections with HCoV-229E (OR = 5.15, 95%CI = 2.24–11.78), HCoV-OC43 (OR = 6.16, 95%CI = 1.77–21.65) and combine HCoVs (OR = 2.36, 95%CI = 1.5 = 3.72) were associated with upper respiratory tract infections. HCoVs were found to be seasonally dependent with significant detections in the harmattan season (mainly HCoV-229E) and wet season (mainly HCoV-NL63). A comparison of the obtained sequences resulted in no differences to sequences already published in GenBank. Conclusion HCoVs could play significant role in causing upper respiratory tract infections among adults and older children in rural areas of Ghana.
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    • "In patients with sepsis, circulating 25D levels have been shown to correlate directly with serum concentrations of CAMP, and inversely with critical illness in these patients (Jeng et al., 2009). Low serum 25D has also been linked to upper respiratory infections such as influenza (Cannell et al., 2006), and in patients with CKD low serum is associated with increased risk of infection and mortality (Gombart et al., 2009a). "
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    ABSTRACT: Immunomodulatory responses to the active form of vitamin D (1,25-dihydroxyvitamin D, 1,25D) have been recognized for many years, but it is only in the last 5 years that the potential role of this in normal human immune function has been recognized. Genome-wide analyses have played a pivotal role in redefining our perspective on vitamin D and immunity. The description of increased vitamin D receptor (VDR) and 1α-hydroxylase (CYP27B1) expression in macrophages following a pathogen challenge, has underlined the importance of intracrine vitamin D as key mediator of innate immune function. It is now clear that both macrophages and dendritic cells (DCs) are able to respond to 25-hydroxyvitamin D (25D), the major circulating vitamin D metabolite, thereby providing a link between the function of these cells and the variations in vitamin D status common to many humans. The identification of hundreds of primary 1,25D target genes in immune cells has also provided new insight into the role of vitamin D in the adaptive immune system, such as the modulation of antigen-presentation and T cells proliferation and phenotype, with the over-arching effects being to suppress inflammation and promote immune tolerance. In macrophages 1,25D promotes antimicrobial responses through the induction of antibacterial proteins, and stimulation of autophagy and autophagosome activity. In this way variations in 25D levels have the potential to influence both innate and adaptive immune responses. More recent genome-wide analyses have highlighted how cytokine signaling pathways can influence the intracrine vitamin D system and either enhance or abrogate responses to 25D. The current review will discuss the impact of intracrine vitamin D metabolism on both innate and adaptive immunity, whilst introducing the concept of disease-specific corruption of vitamin D metabolism and how this may alter the requirements for vitamin D in maintaining a healthy immune system in humans.
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