Here's a possible vitamin D link to H1N1 complications.
From Science Daily (Dec. 16, 2009):
First Immunological Clue to Why Some H1N1 Patients Get Very Ill or Die (http://www.sciencedaily.com/releases/2009/12/091215102109.htm)
An international team of Canadian and Spanish scientists have found the first potential immunological clue of why some people develop severe pneumonia when infected by the pandemic H1N1 virus.
The study analyzed different levels of regulating molecules for 20 hospitalized patients, 15 outpatients and 15 control subjects in 10 Spanish hospitals during the first pandemic wave in July and August 2009. Researchers from the Hospital Clinico Universitario de Valladolid in Spain and the University Health Network found high levels of a molecule called interleukin 17 in the blood of severe H1N1 patients, and low levels in patients with the mild form of the disease.
Interleukin 17 is produced by the body and is important in the normal regulation of white blood cells which fight infection and disease. In certain circumstances, the molecule becomes "out of control," leading to inflammation and autoimmune diseases. The research paper titled, "Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza" is published in the December issue of the Journal of Critical Care.
"In rare cases, the virus causes lung infections requiring patients to be treated in hospital. By targeting or blocking TH17 in the future, we could potentially reduce the amount of inflammation in the lungs and speed up recovery," says Dr. David Kelvin, the leader of the Canadian team, Head of the Experimental Therapeutics Division, Toronto General Hospital Research Institute, University Health Network and Professor of Immunology, University of Toronto. Dr. Kelvin added that the clinical applications of this work is still many years away.
Dr. Kelvin did note, however, that a test to determine who has high levels of the molecule is possible in the near future. "A diagnostic test could let us know early who is at risk for the severe form of this illness quickly," he said, adding that high levels would indicate a failure of the immune system to eliminate the virus, similar to what happened during the 1918 Spanish flu when huge numbers of deaths occurred due to a deadly influenza A virus strain of subtype H1N1.
Dr. Jesus Bermejo-Martin, the coordinator of the Spanish team, thinks that identifying drugs able to regulate the activity of IL-17 may provide alternative treatments for patients with severe H1N1.
From PubMed:
Calcitriol suppresses antiretinal autoimmunity through inhibitory effects on the Th17 effector response (http://view.ncbi.nlm.nih.gov/pubmed/19342637)
Tang J, Zhou R, Luger D, Zhu W, Silver PB, Grajewski RS, Su SB, Chan CC, Adorini L, Caspi RR.
Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
J Immunol. 2009 Apr 15;182(8):4624-32.
Experimental autoimmune uveitis (EAU) serves as a model for human autoimmune uveitis and for cell-mediated autoimmunity in general. EAU induced in mice by immunization with the retinal Ag interphotoreceptor retinoid-binding protein in CFA is driven by the Th17 response. Oral calcitriol (1,25-dihydroxyvitamin D3) prevented as well as partly reversed disease and suppressed immunological responses.
In vitro, calcitriol directly suppressed IL-17 induction in purified naive CD4+ T cells without inhibiting Th17 lineage commitment, as reflected by unaltered RORgammat, STAT3, and FoxP3 expression. In contrast, in vivo treatment with calcitriol of mice challenged for EAU impaired commitment to the Th17 lineage, as judged by reduction of both RORgammat and IL-17 in CD4+ T cells. Innate immune response parameters in draining lymph nodes of treated mice were suppressed, as was production of IL-1, IL-6, TNF-alpha, and IL-12/IL-23p40, but not IL-10, by explanted splenic dendritic cells (DC). Finally, supernatants of calcitriol-conditioned bone marrow-derived DC had reduced ability to support Th17 polarization of naive CD4+ T cells in vitro and in vivo.
Thus, calcitriol appears to suppress autoimmunity by inhibiting the Th17 response at several levels, including the ability of DC to support priming of Th17 cells, the ability of CD4+ T cells to commit to the Th17 lineage, and the ability of committed Th17 T cells to produce IL-17.
The above research into autoimmunity (http://en.wikipedia.org/wiki/Autoimmunity) suggests that calcitriol, the active form of vitamin D, inhibits Th17 and its ability to produce interleukin 17. IL-17 is linked with severe pneumonia in H1N1. A low vitamin D level could be a factor for H1N1 complications.
This hypothesis may be tested in the next couple of months. Vitamin D levels are at their lowest in the UK in February and March. If a 3rd H1N1 wave occurs during these months (and if low vitamin D is a factor) then there will be higher number of complications (as a percentage) than during the 2nd wave (which hit in the autumn when vitamin D levels were higher).
Canada are checking the vitamin D levels of their H1N1 patients. Their findings when published may corroborate vitamin D's influence (or not).
No news from Canada, but an RCT from Japan has found that vitamin D3 supplementation reduces the incidence of influenza in children. It also reduced asthma attacks too.
Urashima, M. et al. Randomized trial of vitamin d supplementation to prevent seasonal influenza a in schoolchildren. The American journal of clinical nutrition (2010). URL http://dx.doi.org/10.3945/ajcn.2009.29094.
Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren.
BACKGROUND: To our knowledge, no rigorously designed clinical trials have evaluated the relation between vitamin D and physician-diagnosed seasonal influenza.
OBJECTIVE: We investigated the effect of vitamin D supplements on the incidence of seasonal influenza A in schoolchildren.
DESIGN: From December 2008 through March 2009, we conducted a randomized, double-blind, placebo-controlled trial comparing vitamin D(3) supplements (1200 IU/d) with placebo in schoolchildren. The primary outcome was the incidence of influenza A, diagnosed with influenza antigen testing with a nasopharyngeal swab specimen.
RESULTS: Influenza A occurred in 18 of 167 (10.8%) children in the vitamin D(3) group compared with 31 of 167 (18.6%) children in the placebo group [relative risk (RR), 0.58; 95% CI: 0.34, 0.99; P = 0.04]. The reduction in influenza A was more prominent in children who had not been taking other vitamin D supplements (RR: 0.36; 95% CI: 0.17, 0.79; P = 0.006) and who started nursery school after age 3 y (RR: 0.36; 95% CI: 0.17, 0.78; P = 0.005). In children with a previous diagnosis of asthma, asthma attacks as a secondary outcome occurred in 2 children receiving vitamin D(3) compared with 12 children receiving placebo (RR: 0.17; 95% CI: 0.04, 0.73; P = 0.006).
CONCLUSION: This study suggests that vitamin D(3) supplementation during the winter may reduce the incidence of influenza A, especially in specific subgroups of schoolchildren. This trial was registered at https://center.umin.ac.jp as UMIN000001373.