Dermato-Endocrinology 1:6, 307-309; November/December, 2009; © 2009 Landes Bioscience
Johan Moan, 1,2; Arne Dahlback, 2; LiWei Ma 1, and Asta Juzeniene 1, asta.juzeniene at rr-research.no
1 Department of radiation Biology; institute for Cancer research; the Norwegian radium Hospital; oslo University Hospital; Montebello, oslo Norway;
2 institute of physics; University of oslo; Blindern, oslo Norway
OBJECTIVES: Seasonal variations in ultraviolet B (UVB) radiation cause seasonal variations in vitamin D status.
This may influence immune responses and play a role in the seasonality of influenza.
METHODS: Pandemic and non-pandemic influenzas in Sweden, Norway, the USA, Singapore, and Japan were studied. Weekly/monthly influenza incidence and death rates were evaluated in view of monthly UVB fluences.
RESULTS: Non-pandemic influenzas mostly occur in the winter season in temperate regions. UVB calculations show that at high latitudes very little, if any, vitamin D is produced in the skin during the winter. Even at 26°N (Okinawa) there is about four times more UVB during the summer than during the winter. In tropical regions there are two minor peaks in vitamin D photosynthesis, and practically no seasonality of influenza. Pandemics may start with a wave in an arbitrary season, while secondary waves often occur the following winter. Thus, it appears that a low vitamin D status may play a significant role in most influenzas.
CONCLUSIONS: In temperate latitudes even pandemic influenzas often show a clear seasonality. The data support the hypothesis that high fluences of UVB radiation (vitamin D level), as occur in the summer, act in a protective manner with respect to influenza.
Copyright © 2010 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
PMID: 21036090
Text without images from previous 2009 paper by Moan: PDF attached to bottom of this page
Introduction
Nearly all human diseases related to respiratory pathogens exhibit seasonal variations.[1] and [2] However, the reasons for this seasonality are still not known. Among the tested hypotheses are: seasonality of low temperatures, absolute humidity (aerosol transmission), or of dry air, crowding together indoors during the winter, travel patterns, vacations, seasonality of ultraviolet (UV) radiation from the sun that might kill pathogens, circannual rhythms of hormones, such as the ‘dark hormone’ melatonin, etc.[1], [3], [4], [5], [6], [7] and [8] Another founded hypothesis is that seasonal variations in UVB radiation and consequently vitamin D photosynthesis, causing seasonal variations in vitamin D status,[9] and [10] which plays a role in the immune response to infections, may be responsible for the influenza seasonality.[9], [10], [11], [12], [13], [14] and [15] Additionally, the question of whether it is the host or the virus/bacterium that exhibits seasonality arises. However, there are exceptions from seasonality, notably for pandemic influenzas, which often occur outside the winter influenza seasons. Furthermore, in equatorial regions the seasonal pattern is weak.[2] and [16]
In the present work we have compared the seasonality of cases and deaths caused by both pandemic and non-pandemic influenzas with doses of UVB radiation (vitamin D photosynthesis). Influenza may cause death either directly (due to a primary complication caused by the influenza virus) or indirectly (due to secondary non-influenza complications either pulmonary or non-pulmonary in nature).[17] and [18] Recent studies have indicated that the majority of deaths in previous influenza pandemics have been a result of secondary bacterial pneumonias.[18], [19], [20] and [21] In this paper all deaths related to influenza are referred to as ‘influenza deaths’ without further specification.
2. Materials and methods
2.1. Influenza cases and deaths
Data from various sources were used in the present study ([Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5] and [Figure 6]). The numbers of weekly Russian influenza cases in Sweden (Figure 1) are from the publication by Skog et al.22 The monthly death cases from influenza in Norway during 1980–1999 (Figure 2) are from the publication by Moan et al.14 The weekly death rates of the Spanish flu in some American cities (Figure 3) were obtained from the work of Britten.23 Monthly death rates from 10 non-pandemic and two pandemic influenza seasons in the USA during 1941–1976 (Figure 4) are from the publication by Doshi.24 The pattern of monthly influenza cases in Okinawa from 2001 to 2007 (Figure 6) are from Suzuki et al.,25 while the data for Singapore from 1990 to 1994 (Figure 5) are from the publication by Chew et al.26
Figure 1. Numbers of infected persons (?) per Thiessen area in Sweden for each week from 1889 to 1890 during the Russian flu, obtained from Skog et al.22 Weekly photosynthesis of vitamin D (—?—) for a relevant latitude (Oslo, 60°N) was calculated by use of the vitamin D action spectrum, UV measurements, and radiative transfer calculations (see Materials and methods).
----------------------------
Figure 2. The monthly influenza deaths (?) from 1980 to 1999 in Norway, extracted from Moan et al.14 Monthly photosynthesis of vitamin D (—?—) for Oslo (60°N) was calculated by use of the vitamin D action spectrum, UV measurements, and radiative transfer calculations (see Materials and methods).----------------------------
Figure 3. Weekly Spanish influenza death rates in Baltimore (39°N), Augusta (33°N), and San Francisco (37°N) from 1918 to 1919, taken from Britten.23----------------------------
Figure 4. The monthly death rates from two pandemic (A) and 10 non-pandemic (B and C) influenza seasons in the USA during 1941–1976; data from Doshi.24 Monthly photosynthesis of vitamin D for San Francisco (37°N) and Baltimore (39°N) was calculated by use of the vitamin D action spectrum, UV measurements, and radiative transfer calculations (see Materials and methods).
–––––––––––––––––––––––––––––-
Figure 5. The pattern of mean monthly influenza A cases (?) from 1990 to 1994 in Singapore; data from Chew et al.26 Monthly photosynthesis of vitamin D (—?—) for Singapore (1°N) was calculated by use of the vitamin D action spectrum, UV measurements, and radiative transfer calculations (see Materials and methods).----------------------------
Figure 6. The mean number of monthly influenza cases (?) from 2001 to 2007 in Okinawa, adapted from Suzuki et al.25 Monthly photosynthesis of vitamin D (—?—) for Okinawa (26°N) was calculated by use of the vitamin D action spectrum, UV measurements, and radiative transfer calculations (see Materials and methods).
2.2. Solar exposure and seasonal vitamin D synthesis in human skin
The main factors influencing UV irradiance at ground level are solar zenith angle (variable with season, latitude, and time of day), cloud and snow cover, aerosols, and the thickness of the ozone layer.27 In this study, global solar UV irradiances were calculated using a radiative transfer model.[28] and [29] Daily total ozone amounts used in this model were measured by the Total Ozone Mapping Spectrometer (TOMS) onboard the Earth Probe satellite. The daily cloud cover used in our model was derived from reflectivity measurements by TOMS. The errors in ozone derived from TOMS instruments onboard several satellites are generally less than 2%.[30] and [31] Not included in our calculations were atmospheric aerosols, which may potentially have an impact on the solar irradiance reaching the earth's surface.[32], [33] and [34]
The calculated monthly UV exposures were based on the satellite measurements in the period 1997–2004. A cylinder geometry of the human body was used. The arguments for such a choice have been presented previously.[35] and [36]
Results are presented as vitamin D-forming UV doses. The efficiency spectrum for vitamin D production gives the relative effectiveness of solar radiation at different wavelengths in converting 7-dehydrocholesterol (7-DHC) to previtamin D. An efficiency spectrum is calculated by multiplying the intensity of the solar radiation (wavelength by wavelength) with the action spectrum for vitamin D production for the corresponding wavelength. The vitamin D action spectrum was taken from the publication of Galkin and Terentskaya,37 and is similar to that measured by MacLaughlin et al. in ex vivo skin specimens.38 This action spectrum is being used by a large number of investigators, but is not ideal.
3. Results and discussion
3.1. Pandemic and non-pandemic influenzas
There are three types of influenza virus: influenza A virus, influenza B virus, and influenza C virus.39 Influenza A viruses are the most important because they generally cause severe secondary diseases and often cause seasonal epidemics and pandemics.[40] and [41] Influenza B is less common than influenza A, but can periodically cause large epidemics, although not pandemics.40 Influenza C virus is less common than influenza A and B, and diseases caused by this species are generally much milder; it is not thought to cause epidemics.[40] and [42] Influenzas mainly attack weaker persons in a population, such as children, the elderly, and the immune incompetent.39
The best known and documented influenza pandemics are the Russian flu (1889–1890, about 1 million deaths), the Spanish flu (1918–1919, about 50 million deaths worldwide), the Asian flu (1957–1958, about 2 million deaths worldwide), and the Hong Kong flu (1968–1969 about 0.7 million deaths worldwide).[43] and [44] In April 2009, a novel H1N1 influenza A virus, the so-called pandemic H1N1/09 virus (swine influenza, Mexican flu, North American flu) was identified in Mexico.[45], [46] and [47] The virus has since spread throughout the world and has caused an influenza pandemic, but it has not exhibited unusually high pathogenecity.21 The full impact of the current pandemic is not yet clear.[47] and [48] According to the World Health Organization (WHO), more than 209 countries have reported laboratory confirmed cases of pandemic influenza H1N1 2009, and there have been at least 14 142 deaths.49
The spread of Russian pandemic influenza, caused by the influenza A virus subtype H2N2, was extremely rapid. The Russian flu was first detected in Bokara (Central Asia) in May 1889, quickly reached St Petersburg in October, and 6 weeks later was registered in the UK.[22], [44] and [50] In mid-December 1889 the flu was reported in North America and in North and South Africa; in February 1890 it was reported in Latin America and in Asia and in March in New Zealand, Australia, and East Africa.[43] and [51] In Sweden, Russian flu occurred in the winter, with maximal numbers of infected persons between mid-December 1889 and late January 1890 (Figure 1),22 almost coinciding in time with the seasonal (non-pandemic) influenza deaths in Norway (Figure 2).14 We can conclude that in temperate latitudes even pandemic influenzas may appear with a clear winter seasonality of incidence and mortality.
The Spanish flu, caused by influenza A virus subtype H1N1, is sometimes referred to as ‘the mother of all pandemics’, because since 1919 almost all influenza A pandemics have been caused by descendants of this virus.52 It is still uncertain whether the first wave of the Spanish flu occurred in Europe or in America.[44], [53], [54] and [55] The first wave of the pandemic in European countries was in the spring and summer of 1918. It was highly contagious, but caused few deaths.56 The second and largest peak was the most serious and occurred in October 1918.56 The third, most long-lasting pandemic wave started in February 1919.56 Influenza-related mortality rates were high, ranging from 0.2 to 11 deaths per 1000 inhabitants in European countries.56
In the USA, the first wave of the Spanish flu occurred in March 1918.[52], [55] and [57] The second lethal wave peaked in the autumn of 1918, and was responsible for most of the deaths, just as in Europe. However, in Europe, only one autumn wave was seen in most cities, whereas many of the USA cities had two peaks of mortality, spaced by only a few weeks (Figure 3).58 The second wave probably spread from the east coast to the west coast, because the highest death rates were registered on October 19 in Baltimore (39°N, 76°W), on October 26 in Augusta (33°N, 81°W), and on November 5 in San Francisco (37°N, 122°W) (Figure 3).23 The third wave came in the classical influenza season (Figure 3).23 In Baltimore the winter wave was weak and came later, while in the other cities it came in mid-January (Figure 3), i.e., when the vitamin D photosynthesis rate is at its minimum (Figure 4A). One possible mechanism explaining the differences in death rates between the summer, autumn and winter waves of the Spanish flu could be related to serum vitamin D levels and pre-existing heterosubtypic immunity, probably induced by prior exposure to different subtypes of influenza.59
However, this pattern of three waves was not universal: Australia, for example, due to the partial success of a maritime quarantine that delayed the outbreak until early in 1919, experienced a single, longer wave of influenza activity.[60], [61] and [62] The Spanish flu came in two waves in Singapore (1°N), a tropical island city-state: in June–July and in October–November 1918,[63] and [64] i.e., later than the first wave in Europe and in the USA.
Arguments for the role of UVB and vitamin D in Spanish flu in the USA have been reviewed previously.15 The lowest pneumonia and influenza mortality rates were seen in the areas with the highest solar UVB irradiance and lowest latitudes (these being good indicators for high levels of vitamin D), while the highest rates were in the areas with the lowest UVB irradiance and highest latitudes (indicators of low vitamin D levels).15
The Asian pandemic influenza originated in the southwest of China in February 1957 (i.e., in the influenza season).2 It reached Hong Kong in April, and then spread rapidly to Singapore, Taiwan, and Japan. The causative agent, an influenza A H2N2 virus, was first isolated in Japan in May 1957. This virus was found in June 1957 in the UK and in July 1957 in the USA, but the peak of influenza incidence and mortality occurred in October 1957.[2], [54] and [65] This first wave of disease in North America and in Europe was followed by a second wave in January–February 1958, again in the influenza season.[2], [54] and [65]
The Hong Kong influenza A virus subtype H3N2 was first isolated in Hong Kong in July 1968, and in September it was registered in Japan, the USA, England and Wales; it was registered in France in January 1969.66 Despite the rapid and extensive spread of this virus, its impact was not the same in all geographical regions: in North America, the majority of influenza-related deaths occurred during the first pandemic season ((1968/1969), while in Europe most deaths occurred during the second pandemic season (1969/1970). The highest rates of influenza cases and mortality were observed during the winter in all studied countries (the USA, Canada, England and Wales, France, Japan, and Australia).[66] and [67]
Thus, these two pandemics, the Asian flu and the Hong Kong flu, followed an almost classical trend with high winter death rates, similar to non-pandemic seasonal influenzas in the USA (Figure 4, B and C).24 Both of these pandemics occurred in Singapore, which has almost no incidence variations in seasonal influenzas (see below).[64] and [68] The Asian influenza pandemic in Singapore started in May 1957 (earlier than in the USA, Figure 4A), and the Hong Kong influenza pandemic first occurred in August–early September 1968 (also earlier than in the USA, Figure 4A).64
All seasonal influenzas in the period from 1941 to 1976 in the USA followed a similar winter trend, with the exceptions of the 1946–1947 and the 1975–1976 waves, which came late, peaking in March–April (Figure 4, B and C).24 However, these waves also came before the vitamin D levels start to increase after the winter (Figure 4A).
3.2. Seasonal variations in vitamin D photosynthesis and non-pandemics
The monthly variations in vitamin D photosynthesis in human skin in some selected countries were calculated using the action spectrum of Galkin and Terentskaya37 and assuming cylinder geometry.[35] and [36] As shown in our earlier studies of the Nordic countries,69 the vitamin D level is maximal about a month after the time of maximal rate of synthesis, which occurs close to midsummer. This is due to the fact that the vitamin D level here is determined as the concentration of 25-hydroxyvitamin D in serum, and that the formation of this metabolite from previtamin D, via vitamin D (mainly in the liver), takes around one week.70 Above 37° latitude, very low UVB fluences reach the ground during the months of November through February.71 Therefore, very little, if any, vitamin D is produced in the skin during the winter. In fact, the lowest vitamin D levels are found in February–March.71
Seasonal variations in vitamin D photosynthesis decrease as the equator is approached (Figure 5). In fact, as the curve for Singapore (1°N) shows (Figure 5), there are two minor maxima per year, located almost symmetrically around the midsummer minimum. The reasons why the symmetry is not complete are the slight ozone asymmetry and changes in cloud cover, which were both taken into account when we calculated the curves in Figure 5. November and December are the months of the rainy season in Singapore. In this city there is almost no seasonality of influenza,[26], [64] and [72] as might be expected from the small seasonal variation in vitamin D photosynthesis (Figure 5). However, a small seasonal variation in influenza has been observed, with small peaks in June and December–January.[26], [64] and [72] It appears that the influenza waves start during periods of low vitamin D photosynthesis. These peaks may be related to humidity, or possibly to contamination from seasonal influenzas in the southern and northern hemisphere, and to the seasonal variation in vitamin D photosynthesis (Figure 5).
For the subtropical region, influenza data are available for Okinawa (26°N) and Taiwan (23°N).[25] and [73] In both of these places there is a regular, major outbreak of influenza in the winter and a minor outbreak in the summer. This pattern is also characteristic of influenza circulation in other subtropical areas.74 In these places there is significant vitamin D photosynthesis throughout the year, but it should be noted that the winter rate is only a fourth of the summer rate (Figure 6).
In the USA, non-pandemics of influenza typically start during the fall or winter months, but the peak of activity occurs in January–March (Figure 4), just as we have found for Norway (Figure 2). In both countries, very few cases are registered in the summer time. Seasonal variations in immune system responses have been reported in humans75 and such variations may be responsible for the increased incidence of infectious diseases during winter and for the seasonality of non-pandemic influenza. Vitamin D modulates the immune system, essentially strengthening it, in several ways, as reviewed elsewhere.[76], [77], [78], [79] and [80]
Norway is located between 60 and 70°N, while the center of population gravity of the USA is located between 35 and 45°N. The seasonal variations in vitamin D photosynthesis are larger for Norway than for the USA ([Figure 2] and [Figure 4]). Thus, in the USA, as in Norway, the numbers of deaths are small in the season when vitamin D status is best.
3.3. Mechanisms behind seasonality
Being the main source of vitamin D, UVB radiation may affect influenza via the immune system. It was demonstrated in two independent studies[81] and [82] that children who were regularly exposed to artificial UVB radiation had around two times lower incidence rates of upper respiratory tract infections, influenza, and sore throat than non-exposed children, and the phagocytic activity of macrophages increased significantly in all exposed subjects in a dose-dependent manner.
The impact of rurality on morbidity and mortality from the 1918 pandemic influenza in England, Wales, New Zealand, and Japan was investigated.[83], [84] and [85] The influenza morbidity in villages was higher than or similar to that in towns and cities, while the mortality appeared to be lowest in villages, revealing significant differences compared to all cities and towns. The differences in mortality rates between urban and rural regions may be related to many factors, including differences in vitamin D status. People living in rural areas have significantly higher vitamin D levels compared to those living in urban areas.[86] and [87]
3.4. Seasonal variations in host immunity or in pathogen virulence
An argument for the seasonal effect on the host are that outbreaks of genetically similar strains occur simultaneously at similar latitudes across different continents.1 There seems to be, in many cases, a continuous presence of pathogens throughout the year.88 Circadian variations of hormones, like melatonin, change with the season.[88] and [89] This may lead to a seasonal variation in immunity.89 Thus, mice exhibit circadian variations of susceptibility to pathogens, with the highest susceptibility in the morning.90
The same virus strain appears to be present in the hosts over longer periods, two years or more, but leading to manifest disease only under favorable conditions, mainly related to host immune weakening.88 One might expect variations in the immune system to play a major role. The preventive effect of vitamin D supplementation against influenza has also been demonstrated in intervention studies.11 Furthermore, Ginde et al.91 found that serum levels of vitamin D were inversely associated with upper respiratory tract infections.
UV radiation interacts with the immune system in several ways, as already mentioned. We believe that the main mechanism involves vitamin D photosynthesis in the skin.
3.5. The influence of vitamin D on the immune response
Vitamin D plays an important immunomodulatory function in primates. Deficiency has been linked with several autoimmune diseases, the development of cancer, and an increased risk of infection.[92], [93], [94], [95] and [96] Better knowledge of the mechanisms through which vitamin D regulates immune responses is essential for understanding how it may prevent or reduce the impact of an influenza pandemic in humans. Calcitriol, the metabolically active form of vitamin D, influences host immunity in two different important ways: generally it suppresses adaptive immunity, particularly Th1 cellular immune responses, while it stimulates innate non-specific immunity.97
Vitamin D strengthens innate non-specific immunity in several different ways. It up-regulates the expression of antimicrobial proteins (AMPs) like cathelicidins or ?-defensins.[98] and [99] The synthesis of LL-37 antimicrobial peptide (the only human member of the cathelicidin family, an important component of innate defense) in human macrophages is one of the best known mechanisms involving vitamin D.98 In addition to its antimicrobial properties, it is also effective against viruses, including influenza virus.[100], [101] and [102] Moreover, vitamin D induces the production of NF-?B transcription factor inhibitor – I?B?.103 The inhibition of NF-?B signaling may impair influenza virus infection. Nimmerjahn et al.104 showed that human cells with low NF-?B activity were resistant to influenza virus infection.
Other non-specific components of innate immunity regulated by calcitriol are Toll-like receptors (TLRs) that recognize structurally conserved molecules derived from microorganisms such as bacteria, viruses, and fungi, and activate immune responses once an antigen is recognized.105 TLR signaling is strictly linked with vitamin D. Influenza A is a single-stranded (ss)RNA virus. (ss)RNA is a TLR7/8 ligand.[106] and [107] Furthermore, it can induce expression of the gene coding for the LL-37 peptide.102
While vitamin D may strengthen innate, non-specific immune responses and possibly reduce the risk of influenza virus infection, attenuation of adaptive immune responses might be linked with decreased mortality.9 Calcitriol down-regulates secretion of proinflammatory cytokines and up-regulates the release of anti-inflammatory cytokines, hence influences the Th1/Th2 balance.[108] and [109] Moreover, it suppresses antigen presentation by antigen presenting cells (APC) like dendritic cells (DCs) and macrophages.[110] and [111] The mortality caused by the highly pathogenic influenza A virus strains appears to be related to the release of pro-inflammatory mediators.112 Thus, the attenuation of the Th1 immune response by vitamin D might be beneficial for infected patients.
3.6. Use of vitamin D supplementation to prevent influenza
Solar radiation contributes significantly to vitamin D status. In temperate regions vitamin D levels are higher in late summer than in late winter, when the solar radiation contains too little UVB to synthesize enough vitamin D in human skin. Cannell et al.[9] and [10] hypothesized that wintertime vitamin D insufficiency may explain seasonal variation in influenza. Two preliminary studies support this hypothesis.[11] and [113] A randomized controlled trial of bone loss in postmenopausal, black women found that women given vitamin D (800 IU/day) were three times less likely to report cold and flu symptoms than controls given a placebo.11 The intake of high doses of vitamin D (2000 IU/day) for 1 year efficiently protected women against the ‘typical’ winter colds and influenza, since only one patient reported these symptoms.11 Another randomized, double-blind, placebo-controlled trial, comparing vitamin D supplements with placebo in schoolchildren, found that intake of vitamin D (1200 IU/day) during winter and early spring can reduce the incidence of seasonal influenza A by a factor of around two, while this is not true for influenza B.113
4. Conclusions
Non-pandemic influenzas usually arrive in winter/early spring, while the initial wave of pandemic influenzas may occur in any season, but with secondary waves in midwinter. Seasonal waves of all influenzas are small at low latitudes. It seems likely that seasonal variations in the incidence and death rates of both pandemic and non-pandemic influenza are related to seasonal variations in vitamin D status. An argument against this hypothesis might be that influenza death rates start to increase almost 2 months after the vitamin D levels have reached their minimum. Similarly, the death rates start to decrease several months before vitamin D levels start to increase significantly. This is likely to be related to the generation of immunity.
Conflict of interest
We have no personal or financial conflict of interest to declare and have not entered into any agreement that could interfere with our access to the data on the research, or upon our ability to analyze the data independently, to prepare this manuscript, and to publish it.
Acknowledgements
Direct overpass TOMS data were provided by NASA/GSFC.
References
1 S.F. Dowell and M.S. Ho, Seasonality of infectious diseases and severe acute respiratory syndrome—what we don’t know can hurt us, Lancet Infect Dis 4 (2004), pp. 704–708. Article | PDF (127 K) | View Record in Scopus | Cited By in Scopus (34)
2 N.J. Cox and K. Subbarao, Global epidemiology of influenza: past and present, Annu Rev Med 51 (2000), pp. 407–421. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (191)
3 R. Eccles, An explanation for the seasonality of acute upper respiratory tract viral infections, Acta Otolaryngol 122 (2002), pp. 183–191. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (42)
4 E. Lofgren, N.H. Fefferman, Y.N. Naumov, J. Gorski and E.N. Naumova, Influenza seasonality: underlying causes and modeling theories, J Virol 81 (2007), pp. 5429–5436. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (28)
5 M. Lipsitch and C. Viboud, Influenza seasonality: lifting the fog, Proc Natl Acad Sci U S A 106 (2009), pp. 3645–3646. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (12)
6 J. Shaman and M. Kohn, Absolute humidity modulates influenza survival, transmission, and seasonality, Proc Natl Acad Sci U S A 106 (2009), pp. 3243–3248. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (22)
7 J. Shaman, V.E. Pitzer, C. Viboud, B.T. Grenfell and M. Lipsitch, Absolute humidity and the seasonal onset of influenza in the continental United States, PLoS Biol 8 (2010), p. e1000316. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (4)
8 R. Tellier, Aerosol transmission of influenza A virus: a review of new studies, J R Soc Interface 6 (Suppl 6) (2009), pp. S783–S790. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (17)
9 J.J. Cannell, R. Vieth, J.C. Umhau, M.F. Holick, W.B. Grant and S. Madronich et al., Epidemic influenza and vitamin D, Epidemiol Infect 134 (2006), pp. 1129–1140. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (139)
10 J.J. Cannell, M. Zasloff, C.F. Garland, R. Scragg and E. Giovannucci, On the epidemiology of influenza, Virol J 5 (2008), p. 29. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (33)
11 J.F. Aloia and M. Li-Ng, Re: epidemic influenza and vitamin D, Epidemiol Infect 135 (2007), pp. 1095–1096. View Record in Scopus | Cited By in Scopus (17)
12 D.M. Fleming and A.J. Elliot, Epidemic influenza and vitamin D, Epidemiol Infect 135 (2007), pp. 1091–1092. View Record in Scopus | Cited By in Scopus (0)
13 M.R. Goldstein, L. Mascitelli and F. Pezzetta, Pandemic influenza A (H1N1): mandatory vitamin D supplementation?, Med Hypotheses 74 (2009), p. 756.
14 J. Moan, A. Dahlback, L.W. Ma and A. Juzeniene, Influenza, solar radiation and vitamin D, Dermatoendocrinol 1 (2009), pp. 307–309.
15 W.B. Grant and E. Giovannucci, The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918-1919 influenza pandemic in the United States, Dermatoendocrinol 1 (2009), pp. 1–5.
16 C. Viboud, W.J. Alonso and L. Simonsen, Influenza in tropical regions, PLoS Med 3 (2006), p. e89. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (0)
17 J.A. McCullers, Insights into the interaction between influenza virus and pneumococcus, Clin Microbiol Rev 19 (2006), pp. 571–582. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (107)
18 J.F. Brundage and G.D. Shanks, What really happened during the 1918 influenza pandemic? The importance of bacterial secondary infections, J Infect Dis 196 (2007), pp. 1717–1718. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (6)
19 D.M. Morens, J.K. Taubenberger and A.S. Fauci, Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness, J Infect Dis 198 (2008), pp. 962–970. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (151)
20 T. Hussell, E. Wissinger and J. Goulding, Bacterial complications during pandemic influenza infection, Future Microbiol 4 (2009), pp. 269–272. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (5)
21 D.M. Morens, J.K. Taubenberger, H.A. Harvey and M.J. Memoli, The 1918 influenza pandemic: lessons for 2009 and the future, Crit Care Med 38 (2010), pp. e10–20.
22 L. Skog, H. Hauska and A. Linde, The Russian influenza in Sweden in 1889-90: an example of Geographic Information System analysis, Euro Surveill 13 (2008), pp. 1–7.
23 R.H. Britten, The incidence of epidemic influenza, 1918-1919. A further analysis according to age, sex, and color of records of morbidity and mortality obtained in surveys of 12 localities, Pub Health Rep 47 (1932), pp. 303–339. Full Text via CrossRef
24 P. Doshi, Trends in recorded influenza mortality: United States, 1900-2004, Am J Public Health 98 (2008), pp. 939–945. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (12)
25 Y. Suzuki, K. Taira, R. Saito, M. Nidaira, S. Okano, H. Zaraket and H. Suzuki, Epidemiologic study of influenza infection in Okinawa, Japan, from 2001 to 2007: changing patterns of seasonality and prevalence of amantadine-resistant influenza A virus, J Clin Microbiol 47 (2009), pp. 623–629. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (4)
26 F.T. Chew, S. Doraisingham, A.E. Ling, G. Kumarasinghe and B.W. Lee, Seasonal trends of viral respiratory tract infections in the tropics, Epidemiol Infect 121 (1998), pp. 121–128. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (95)
27 S. Madronich, R.L. McKenzie, L.O. Bjorn and M.M. Caldwell, Changes in biologically active ultraviolet radiation reaching the Earth's surface, J Photochem Photobiol B 46 (1998), pp. 5–19. Abstract | PDF (1866 K) | View Record in Scopus | Cited By in Scopus (383)
28 A. Dahlback and K. Stamnes, A new spherical model for computing the radiation field available for photolysis and heating rate at twilight, Planet Space Sci 39 (1991), pp. 671–683. Abstract | PDF (1203 K) | View Record in Scopus | Cited By in Scopus (149)
29 K. Stamnes, S.C. Tsay, W.J. Wiscombe and K. Jayaweera, Numerically stable algorithm for discrete-ordinate-method radiative transfer in multiple scattering and emitting layered media, Appl Opt 27 (1988), pp. 2502–2509. Full Text via CrossRef
30 McPeters RD, Bhartia PK, Krueger AJ, Herman JR, Wellemeyer CG, Seftor CJ, et al. Earth Probe Total Ozone Mapping Spectrometer (TOMS) data products user's guide. Greenbelt, Maryland: NASA Technical Publication, NASA Goddard Space Flights Center; 1998, p. 1–64.
31 K. Vanicek, Differences between ground Dobson, Brewer and satellite TOMS-8, GOME-WFDOAS total ozone observations at Hradec Kralove, Czech. Atmos Chem Phys 6 (2006), pp. 5163–5171. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (11)
32 K.V. Badarinath, S.K. Kharol, D.G. Kaskaoutis and H.D. Kambezidis, Influence of atmospheric aerosols on solar spectral irradiance in an urban area, J Atmos Sol Terr Phys 69 (2007), pp. 589–599. Article | PDF (879 K) | View Record in Scopus | Cited By in Scopus (19)
33 Bais AF, Lubin D. Surface ultraviolet radiation: past, present, and future. In: Ennis CA, editor. Scientific assessment of ozone depletion: 2006. Global Ozone Research and Monitoring Project Report No. 50. Geneva, Switzerland: World Meteorological Organization; 2007, p. 7.1–7.53.
34 van der Leun J, Bornman JF, Tang X., Environmental effects of ozone depletion and its interactions with climate change. Progress Report. United Nations Environment Programme; 2009, p. 1–52.
35 J. Moan, A. Dahlback and A.C. Porojnicu, At what time should one go out in the sun?, Adv Exp Med Biol 624 (2008), pp. 86–88. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (3)
36 J. Moan, A. Dahlback, Z. Lagunova, E. Cicarma and A.C. Porojnicu, Solar radiation, vitamin D and cancer incidence and mortality in Norway, Anticancer Res 29 (2009), pp. 3501–3509. View Record in Scopus | Cited By in Scopus (5)
37 O.N. Galkin and I.P. Terenetskaya, ‘Vitamin D’ biodosimeter: basic characteristics and potential applications, J Photochem Photobiol B 53 (1999), pp. 12–19. Article | PDF (330 K) | View Record in Scopus | Cited By in Scopus (33)
38 J.A. MacLaughlin, R.R. Anderson and M.F. Holick, Spectral character of sunlight modulates photosynthesis of previtamin D3 and its photoisomers in human skin, Science 216 (1982), pp. 1001–1003. View Record in Scopus | Cited By in Scopus (130)
39 J. Chen and Y.M. Deng, Influenza virus antigenic variation, host antibody production and new approach to control epidemics, Virol J 6 (2009), p. 30. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (0)
40 J.K. Taubenberger and D.M. Morens, The pathology of influenza virus infections, Annu Rev Pathol 3 (2008), pp. 499–522. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (76)
41 T. Kuiken and J.K. Taubenberger, Pathology of human influenza revisited, Vaccine 26 (Suppl 4) (2008), pp. D59–66.
42 S.A. Harper, J.S. Bradley, J.A. Englund, T.M. File, S. Gravenstein and F.G. Hayden et al., Seasonal influenza in adults and children—diagnosis, treatment, chemoprophylaxis, and institutional outbreak management: clinical practice guidelines of the Infectious Diseases Society of America, Clin Infect Dis 48 (2009), pp. 1003–1032. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (79)
43 B.A. Cunha, Influenza: historical aspects of epidemics and pandemics, Infect Dis Clin North Am 18 (2004), pp. 141–155. Abstract | Article | PDF (218 K) | View Record in Scopus | Cited By in Scopus (32)
44 E. Tognotti, Influenza pandemics: a historical retrospect, J Infect Dev Ctries 3 (2009), pp. 331–334. View Record in Scopus | Cited By in Scopus (2)
45 C. Del Rio and M. Hernandez-Avila, Lessons from previous influenza pandemics and from the Mexican response to the current influenza pandemic, Arch Med Res 40 (2009), pp. 677–680. Article | PDF (84 K) | View Record in Scopus | Cited By in Scopus (0)
46 J.W. Tang, P.A. Tambyah, F.Y. Lai, H.K. Lee, C.K. Lee and T.P. Loh et al., Differing symptom patterns in early pandemic vs seasonal influenza infections, Arch Intern Med 170 (2010), pp. 861–867. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (0)
47 N.M. Scalera and S.B. Mossad, The first pandemic of the 21st century: a review of the 2009 pandemic variant influenza A (H1N1) virus, Postgrad Med 121 (2009), pp. 43–47. Full Text via CrossRef
48 Presanis AM, De Angelis D, Hagy A, Reed C, Riley S, Cooper BS, et al. The severity of pandemic H1N1 influenza in the United States, from April to July 2009: a Bayesian analysis. PLoS Med 2009; 6:e1000207.
49 World Health Organization. Pandemic (H1N1) 2009—update 84. Geneva: World Health Organization; 2009. Available at: http://www.who.int/csr/don/2010_01_22/en/index.html. (accessed February 26, 2010).
50 A.J. Valleron, S. Meurisse and P.Y. Boelle, Historical analysis of the 1889-1890 pandemic in Europe, Int J Infect Dis 12 (2008), p. e95.
51 F.B. Smith, The Russian influenza in the United Kingdom, 1889-1894, Soc Hist Med 8 (1995), pp. 55–73. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (12)
52 J.K. Taubenberger and D.M. Morens, 1918 Influenza: the mother of all pandemics, Emerg Infect Dis 12 (2006), pp. 15–22. View Record in Scopus | Cited By in Scopus (246)
53 J.M. Barry, The site of origin of the 1918 influenza pandemic and its public health implications, J Transl Med 2 (2004), p. 3. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (Cool
54 C.W. Potter, A history of influenza, J Appl Microbiol 91 (2001), pp. 572–579. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (88)
55 D.R. Olson, L. Simonsen, P.J. Edelson and S.S. Morse, Epidemiological evidence of an early wave of the 1918 influenza pandemic in New York City, Proc Natl Acad Sci U S A 102 (2005), pp. 11059–11063. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (47)
56 S. Ansart, C. Pelat, P.Y. Boelle, F. Carrat, A. Flahault and A.J. Valleron, Mortality burden of the 1918-1919 influenza pandemic in Europe, Influenza Other Respi Viruses 3 (2009), pp. 99–106. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (6)
57 J.M. Barry, C. Viboud and L. Simonsen, Cross-protection between successive waves of the 1918-1919 influenza pandemic: epidemiological evidence from US Army camps and from Britain, J Infect Dis 198 (2008), pp. 1427–1434. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (18)
58 M.C. Bootsma and N.M. Ferguson, The effect of public health measures on the 1918 influenza pandemic in U.S. cities, Proc Natl Acad Sci U S A 104 (2007), pp. 7588–7593. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (68)
59 J.D. Mathews, E.S. McBryde, J. McVernon, P.K. Pallaghy and J.M. McCaw, Prior immunity helps to explain wave-like behaviour of pandemic influenza in 1918-9, BMC Infect Dis 10 (2010), p. 128. Full Text via CrossRef
60 N.P. Johnson and J. Mueller, Updating the accounts: global mortality of the 1918-1920 ‘Spanish’ influenza pandemic, Bull Hist Med 76 (2002), pp. 105–115. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (281)
61 P. Curson and K. McCracken, An Australian perspective of the 1918-1919 influenza pandemic, N S W Public Health Bull 17 (2006), pp. 103–107. View Record in Scopus | Cited By in Scopus (3)
62 M.A. McLeod, M. Baker, N. Wilson, H. Kelly, T. Kiedrzynski and J.L. Kool, Protective effect of maritime quarantine in South Pacific jurisdictions, 1918-19 influenza pandemic, Emerg Infect Dis 14 (2008), pp. 468–470. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (9)
63 V.J. Lee, M.I. Chen, S.P. Chan, C.S. Wong, J. Cutter, K.T. Goh and P.A. Tambyah, Influenza pandemics in Singapore, a tropical, globally connected city, Emerg Infect Dis 13 (2007), pp. 1052–1057. View Record in Scopus | Cited By in Scopus (15)
64 V.J. Lee, C.S. Wong, P.A. Tambyah, J. Cutter, M.I. Chen and K.T. Goh, Twentieth century influenza pandemics in Singapore, Ann Acad Med Singapore 37 (2008), pp. 470–476. View Record in Scopus | Cited By in Scopus (4)
65 W.P. Glezen, Emerging infections: pandemic influenza, Epidemiol Rev 18 (1996), pp. 64–76. View Record in Scopus | Cited By in Scopus (212)
66 C. Viboud, R.F. Grais, B.A. Lafont, M.A. Miller and L. Simonsen, Multinational impact of the 1968 Hong Kong influenza pandemic: evidence for a smoldering pandemic, J Infect Dis 192 (2005), pp. 233–248. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (49)
67 D.L. Miller, M.S. Pereira and M. Clarke, Epidemiology of the Hong Kong-68 variant of influenza A2 in Britain, Br Med J 1 (1971), pp. 475–479. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (7)
68 V.J. Lee, J. Yap, J.B. Ong, K.P. Chan, R.T. Lin and S.P. Chan et al., Influenza excess mortality from 1950-2000 in tropical Singapore, PLoS One 4 (2009), p. e8096. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (2)
69 J. Moan, A.C. Porojnicu, T.E. Robsahm, A. Dahlback, A. Juzeniene, S. Tretli and W. Grant, Solar radiation, vitamin D and survival rate of colon cancer in Norway, J Photochem Photobiol B 78 (2005), pp. 189–193. Article | PDF (195 K) | View Record in Scopus | Cited By in Scopus (57)
70 M.F. Holick, The cutaneous photosynthesis of previtamin D3: a unique photoendocrine system, J Invest Dermatol 77 (1981), pp. 51–58. View Record in Scopus | Cited By in Scopus (64)
71 W.B. Grant and M.F. Holick, Benefits and requirements of vitamin D for optimal health: a review, Altern Med Rev 10 (2005), pp. 94–111. View Record in Scopus | Cited By in Scopus (126)
72 S. Doraisingham, K.T. Goh, A.E. Ling and M. Yu, Influenza surveillance in Singapore: 1972–86, Bull World Health Organ 66 (1988), pp. 57–63. View Record in Scopus | Cited By in Scopus (27)
73 S.R. Shih, G.W. Chen, C.C. Yang, W.Z. Yang, D.P. Liu and J.H. Lin et al., Laboratory-based surveillance and molecular epidemiology of influenza virus in Taiwan, J Clin Microbiol 43 (2005), pp. 1651–1661. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (24)
74 C.K. Li, B.C. Choi and T.W. Wong, Influenza-related deaths and hospitalizations in Hong Kong: a subtropical area, Public Health 120 (2006), pp. 517–524. Article | PDF (152 K) | View Record in Scopus | Cited By in Scopus (12)
75 E. Haus and M.H. Smolensky, Biologic rhythms in the immune system, Chronobiol Int 16 (1999), pp. 581–622. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (89)
76 Garssen J, van Loveren H. Effects of ultraviolet exposure on the immune system. Crit Rev Immunol 2001; 21:359–97.
77 M.T. Cantorna, Y. Zhu, M. Froicu and A. Wittke, Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system, Am J Clin Nutr 80 (2004), pp. 1717S–1720S.
78 Mathieu C, van Etten E, Decallonne B, Guilietti A, Gysemans C, Bouillon R, Overbergh L., Vitamin D and 1,25-dihydroxyvitamin D3 as modulators in the immune system. J Steroid Biochem Mol Biol 2004; 89–90:449–52.
79 D.D. Bikle, Vitamin D and the immune system: role in protection against bacterial infection, Curr Opin Nephrol Hypertens 17 (2008), pp. 348–352. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (25)
80 E. van Etten, K. Stoffels, C. Gysemans, C. Mathieu and L. Overbergh, Regulation of vitamin D homeostasis: implications for the immune system, Nutr Rev 66 (2008), pp. S125–S134. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (Cool
81 A.I. Andrianova, [Prophylactic ultraviolet irradiation of preschool children of Moscow.], Gig Sanit 35 (1970), pp. 30–33. View Record in Scopus | Cited By in Scopus (1)
82 T.P. Bezberkhaia, [The toughening of boarding school students by ultraviolet irradiation.], Gig Sanit 28 (1963), pp. 94–97. View Record in Scopus | Cited By in Scopus (1)
83 K. McSweeny, A. Colman, N. Fancourt, M. Parnell, S. Stantiall and G. Rice et al., Was rurality protective in the 1918 influenza pandemic in New Zealand?, N Z Med J 120 (2007), p. U2579. View Record in Scopus | Cited By in Scopus (5)
84 G. Chowell, L.M. Bettencourt, N. Johnson, W.J. Alonso and C. Viboud, The 1918-1919 influenza pandemic in England and Wales: spatial patterns in transmissibility and mortality impact, Proc Biol Sci 275 (2008), pp. 501–509. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (10)
85 H. Nishiura and G. Chowell, Rurality and pandemic influenza: geographic heterogeneity in the risks of infection and death in Kanagawa, Japan (1918–1919), N Z Med J 121 (2008), pp. 18–27.
86 M.H. Gannage-Yared, R. Chemali, N. Yaacoub and G. Halaby, Hypovitaminosis D in a sunny country: relation to lifestyle and bone markers, J Bone Miner Res 15 (2000), pp. 1856–1862. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (122)
87 J.J. McGrath, M.G. Kimlin, S. Saha, D.W. Eyles and A.V. Parisi, Vitamin D insufficiency in south-east Queensland, Med J Aust 174 (2001), pp. 150–151. View Record in Scopus | Cited By in Scopus (56)
88 S.F. Dowell, Seasonal variation in host susceptibility and cycles of certain infectious diseases, Emerg Infect Dis 7 (2001), pp. 369–374. View Record in Scopus | Cited By in Scopus (115)
89 R.J. Nelson and D.L. Drazen, Melatonin mediates seasonal adjustments in immune function, Reprod Nutr Dev 39 (1999), pp. 383–398. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (51)
90 Feigin RD, San Joaquin VH, Haymond MW, Wyatt RG., Daily periodicity of susceptibility of mice to pneumococcal infection. Nature 1969; 224:379-80.
91 A.A. Ginde, J.M. Mansbach and C.A. Camargo Jr., Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey, Arch Intern Med 169 (2009), pp. 384–390. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (53)
92 W.B. Grant, Epidemiology of disease risks in relation to vitamin D insufficiency, Prog Biophys Mol Biol 92 (2006), pp. 65–79. Article | PDF (219 K) | View Record in Scopus | Cited By in Scopus (60)
93 A.F. Embry, L.R. Snowdon and R. Vieth, Vitamin D and seasonal fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in multiple sclerosis, Ann Neurol 48 (2000), pp. 271–272. View Record in Scopus | Cited By in Scopus (70)
94 R. Lin and J.H. White, The pleiotropic actions of vitamin D, Bioessays 26 (2004), pp. 21–28. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (80)
95 J.M. Lappe, D. Travers-Gustafson, K.M. Davies, R.R. Recker and R.P. Heaney, Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial, Am J Clin Nutr 85 (2007), pp. 1586–1591. View Record in Scopus | Cited By in Scopus (280)
96 I. Laaksi, J.P. Ruohola, P. Tuohimaa, A. Auvinen, R. Haataja, H. Pihlajamaki and T. Ylikomi, An association of serum vitamin D concentrations < 40 nmol/L with acute respiratory tract infection in young Finnish men, Am J Clin Nutr 86 (2007), pp. 714–717. View Record in Scopus | Cited By in Scopus (46)
97 L.A. Armas, Vitamin D, infections and immune-mediated diseases, Int J Clin Rheumatol 4 (2009), pp. 89–103. View Record in Scopus | Cited By in Scopus (0)
98 P.T. Liu, S. Stenger, D.H. Tang and R.L. Modlin, Cutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin, J Immunol 179 (2007), pp. 2060–2063. View Record in Scopus | Cited By in Scopus (107)
99 T.T. Wang, F.P. Nestel, V. Bourdeau, Y. Nagai, Q. Wang and J. Liao et al., Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression, J Immunol 173 (2004), pp. 2909–2912. View Record in Scopus | Cited By in Scopus (214)
100 J. Harder, R. Glaser and J.M. Schroder, Human antimicrobial proteins effectors of innate immunity, J Endotoxin Res 13 (2007), pp. 317–338. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (14)
101 D.M. Laube, S. Yim, L.K. Ryan, K.O. Kisich and G. Diamond, Antimicrobial peptides in the airway, Curr Top Microbiol Immunol 306 (2006), pp. 153–182. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (36)
102 S.K. Krutzik, P. Hong, A. Robles, K. Corcoran, R.L. Modlin and B. Lee, HIV-1 ssRNA triggers a vitamin D-dependent anti-viral pathway in human monocytes, FASEB J 22 (672) (2008), p. 22.
103 S. Hansdottir, M.M. Monick, N. Lovan, L. Powers, A. Gerke and G.W. Hunninghake, Vitamin D decreases respiratory syncytial virus induction of NF-kappaB-linked chemokines and cytokines in airway epithelium while maintaining the antiviral state, J Immunol 184 (2010), pp. 965–974. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (2)
104 F. Nimmerjahn, D. Dudziak, U. Dirmeier, G. Hobom, A. Riedel and M. Schlee et al., Active NF-kappaB signalling is a prerequisite for influenza virus infection, J Gen Virol 85 (2004), pp. 2347–2356. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (48)
105 S. Akira, Toll-like receptor signaling, J Biol Chem 278 (2003), pp. 38105–38108. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (287)
106 J.M. Lund, L. Alexopoulou, A. Sato, M. Karow, N.C. Adams and N.W. Gale et al., Recognition of single-stranded RNA viruses by Toll-like receptor 7, Proc Natl Acad Sci U S A 101 (2004), pp. 5598–5603. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (606)
107 F. Heil, H. Hemmi, H. Hochrein, F. Ampenberger, C. Kirschning and S. Akira et al., Species-specific recognition of single-stranded RNA via toll-like receptor 7 and 8, Science 303 (2004), pp. 1526–1529. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (1190)
108 B.D. Mahon, A. Wittke, V. Weaver and M.T. Cantorna, The targets of vitamin D depend on the differentiation and activation status of CD4 positive T cells, J Cell Biochem 89 (2003), pp. 922–932. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (83)
109 F.E. Nashold, K.A. Hoag, J. Goverman and C.E. Hayes, Rag-1-dependent cells are necessary for 1,25-dihydroxyvitamin D(3) prevention of experimental autoimmune encephalomyelitis, J Neuroimmunol 119 (2001), pp. 16–29. Article | PDF (254 K) | View Record in Scopus | Cited By in Scopus (50)
110 E. van Etten and C. Mathieu, Immunoregulation by 1,25-dihydroxyvitamin D3: basic concepts, J Steroid Biochem Mol Biol 97 (2005), pp. 93–101. View Record in Scopus | Cited By in Scopus (132)
111 C. Daniel, N.A. Sartory, N. Zahn, H.H. Radeke and J.M. Stein, Immune modulatory treatment of trinitrobenzene sulfonic acid colitis with calcitriol is associated with a change of a T helper (Th) 1/Th17 to a Th2 and regulatory T cell profile, J Pharmacol Exp Ther 324 (2008), pp. 23–33. View Record in Scopus | Cited By in Scopus (43)
112 P.C. Doherty, S.J. Turner, R.G. Webby and P.G. Thomas, Influenza and the challenge for immunology, Nat Immunol 7 (2006), pp. 449–455. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (92)
113 M. Urashima, T. Segawa, M. Okazaki, M. Kurihara, Y. Wada and H. Ida, Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren, Am J Clin Nutr 91 (2010), pp. 1255–1260. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (Cool