|Proteins||Human cross-sectional study||23 elderly patients subjected to influenza vaccination and measurement of their nutrient status. ||Total protein status (determined by questionnaire) was slightly lower (p < 0.05) in influenza vaccine non-responders vs. responders (66 vs. 69 g/L).|
Similar results were found for iron, proposing that immune-response was compromised by poor nutrient status in this elderly population.
|Fulop et al., 1999  |
|Animal study (mice)||Group receiving a diet adequate in protein (AP; 18% of energy) vs. group receiving very low protein (VLP; 2%) for 3 weeks.|
Both groups were subjected to influenza infection.
|Higher mortality in the VLP group (p < 0.001) vs. AP, 25 d post infection (p.i.).|
The AP vs. the VLP group showed a decreased virus titer by day 9 (p < 0.001) and an efficient clearance within 12 d (p < 0.001).
%age of NK cells in lungs were reduced (p < 0.01) in VLP vs. AP group with higher (p < 0.001) neutrophil proportions in response to infection with influenza virus in each group, respectively.
The VLP group had less influenza NP-specific CD8+ T cells at days 8 (p < 0.05), 15 (p < 0.05), and 30 (p = 0.001).
Switching VLP to AP diet improved CD4+ and CD8+ T cell subset levels on days 8 (p < 0.01), 15 (p < 0.01), and 30 (p < 0.01) and increased IFN-γ (p < 0.001).
|Taylor et al., 2013  |
|Animal study (mice)||Mycobacteria-infected mice fed 2% protein diet vs. control group receiving 20% protein diet for up to 30 days.||100% of malnourished mice (fed 2% protein diet) succumbed to M. tuberculosis infection within 66 d p.i.|
Malnourished mice had a reduced expression of IFN-γ, TNF-α, and iNOS in the lungs.
A mortal infection of M. tuberculosis in malnourished animals was reversed upon re-feeding with the 20% protein diet.
|Chan et al., 1996 |
|Lipids||Animal study (mice)||Mice infected with H5N1 virus treated with omega-3 polyunsaturated fatty acid-derived lipid mediator protectin D1 (PD1), given 3 times i.v.||H5N1 virus pathogenicity decreased with higher levels of PD1.|
PD1 inhibited virus replication (p < 0.001) via influenza virus nucleoprotein mRNA expression at day 2 p.i.
PD1 treatment within 12 h improved the survival (p < 0.05) and pathology of severe influenza (p < 0.001).
|Morita et al., 2013 |
|Animal study (mice)||Influenza A virus (IAV) infected mice fed with a high-fat (HF, 40% of energy) vs. low-fat (LF, 12% of energy) diet for 10 weeks.||HF mice were more susceptible to respiratory disease after IAV infection than were LF mice, with lower blood oxygen saturation (p < 0.05) and an increase in pulmonary viral load (p < 0.05).|
Decreased pro-inflammatory response to IAV in the serum of HF mice vs. LF for IL-6, IFN-γ, IFN-α, and IP-10 (p < 0.05).
Antiviral response in the heart was reduced in HF mice after IAV infection, where higher viral loads were detected in the hearts of HF vs. LF mice (p < 0.05).
Correlation between IAV-infected HF mice and viral infection in the heart, left ventricular mass, and thickening of the left ventricular wall, characterized by increased HIF-1α compared to LF group (p < 0.05).
|Siegers et al., 2020 |
|Animal study (mice)||High-fat diet (HFD) 60% or regular-fat diet (RFD) 5% fat, administered to 4-week old mice for 10 weeks.|
Influenza vaccination was conducted after 10 weeks.
|Functionality of macrophages was diminished after diet-induced obesity (p < 0.001) via lower CD86-expressing macrophages, lower release of IL-6 and TNF-α, increased Th1 cell subpopulation, and reduced proportion of Treg cells.|
Vaccination-induced antibody production was decreased in animals receiving HFD vs. RFD (p < 0.001)
|Cho et al., 2016 |
|Lipids, carbo-hydrates||Animal study (mice)||Feeding mice with ketogenic, i.e., low carbohydrate diet (KD, 90% fat) vs. standard high-fat (60% fats, 20% lipids) diet (HFD) for 7 d before influenza A virus (IAV) infection.||KD protected mice from lethal IAV infection and disease (p < 0.05) compared to HFD-fed mice.|
KD resulted in an expansion of T-cells (p < 0.001), compared with the HFD group.
KD-fed mice had better blood O2 saturation (p < 0.001).
KD diet was significantly related to improved antiviral resistance (p < 0.001).
|Goldberg et al., 2019 |
|Fiber||Prospective human cohort study||Study evaluating dietary fiber intake versus health outcomes. n = 219,123 men and 168,999 women, aged 50–71 y. 9 y follow-up. ||Consumption of dietary fiber correlated with lowered mortality from infectious and respiratory diseases.|
Per 10 g/d increase in dietary fiber, the multivariate RRs for infectious and respiratory diseases were 0.66 (CI: 0.52–0.84) and 0.82 (CI: 0.74–0.93) in men and 0.61 (CI: 0.44–0.85) and 0.66 (CI: 0.56–0.78) in women, respectively.
|Park et al., 2011  |
|Animal study (mice)||High-fiber diet (HFD)-fed mice vs. control group, subjected to viral influenza infection||Intake of dietary fiber improved influenza by prolonged survival (p < 0.05) and ameliorated clinical scores (p < 0.001).|
After 7 d, HFD-fed mice with high-dose infection had better lung function as shown by reduced pulmonary resistance (p > 0.01) and enhanced compliance in response to methacholine (p > 0.01).
In HFD-fed mice, the excessive neutrophil influx into the airways was inhibited by blunted levels of CXCL1, produced by lung monocytes and macrophages (p < 0.001) vs. controls.
Increased antiviral immunity by dietary fiber through CD8+ T cell activation (p < 0.01) vs. controls.
(HFD)-fed mice showed enhanced adaptive immunity by changed CD8+ T cell metabolism (p < 0.05).
|Trompette et al., 2018 |
|Animal study (mice)||Fiber-free diet group (LFD) vs. control group for up to 40 d, subjected to infection with mucosal pathogen Citrobacter rodentium||Low fiber intake resulting in increases in mucus-degrading microbiota and enhanced lethal colitis cases (p < 0.05). ||Desai et al., 2017 |
|Vitamin A||Meta-analysis of RCTs.||Effects of vitamin A supplementation on acute lower respiratory tract infections (LRTI). 10 studies (n = 33,179 children). ||Though some individual studies demonstrated a positive effect of vitamin A supplementation on LRTI, in pooled analyses, there was no effect of vitamin A supplementation on acute LRTI incidence or prevalence of symptoms.||Chen et al., 2008 |
| ||Meta-analysis of RCTS.||Assessment of vitamin A supplementation on acute respiratory infection. 5 studies (n = 2177 children (1067 children under intervention, 1110 control). ||Faster recovery from infection symptoms due to vitamin A, no differences in the placebo group: fever: OR: 0.03, CI: −0.10–0.17; oxygen requirement: OR: −0.08, CI: −0.31–0.16; increased respiratory rate: OR: −0.09, CI: −0.38 –0.19; hospital stay duration: OR: −0.06, CI: −0.52–0.40.||Brown and Roberts 2004 |
|Vitamin D||Retrospective human study||Study determining mortality patterns of COVID-19 and associated factors: Special focus on vitamin D status. 2 cohorts of 780 cases with confirmed infection of SARS-CoV-2 in Indonesia.||Vitamin D status is strongly associated with COVID-19 mortality (adjusted for age, sex, and comorbidity) (p < 0.001). Individuals with insufficient vitamin D status were ca. 12.6 as likely to die (OR 12.55).||Reharusun et al., 2020 |
|Meta-analysis of RCTs||Assessment of vitamin D supplementation on respiratory tract infections. 5 clinical trials (n = 964 participants). ||Significantly fewer respiratory tract infections were observed following a vitamin D supplementation. (OR: 0.58, CI: 0.417–0.812). In clinical trials there were beneficial effects on events of infections due to vitamin D supplementation in children (OR: 0.58, CI: 0.416–0.805) and adults (OR: 0.65, CI: 0.472–0.904).||Charan et al., 2012 |
|Meta-analysis of RCTs||Assessment of vitamin D supplementation on respiratory tract infection (RTI). 11 placebo-controlled studies (RTCs) (n = 5660 patients). ||Vitamin D had protective effects against RTI (OR: 0.64; CI, 0.49- 0.84). This was more pronounced by individual daily dosing compared to bolus doses (OR = 0.51 vs. OR = 0.86, p = 0.01).||Bergman et al., 2013 |
|Vitamin E ||Humans, RCT ||Assessment of vitamin E supplementation and community acquired pneumonia. n = 7469|
men 50–69 y.
|Lower incidence of pneumonia in individuals receiving vitamin E supplements (RR: 0.28; CI: 0.11–0.69).||Hemila, 2016 |
|Vitamin C||Meta-analysis of RCTs||Supplementation trials with vitamin C and observation of cold symptoms.|
9 randomized controlled trials (n = 5500) in children (3 months–18 y of age).
|Daily supplementation in vitamin C with extra doses reduced the time of having a common cold (mean difference = −0.56, 95% confidence interval (CI) (−1.03, −0.10)), fever (mean difference = −0.45, 95% CI (−0.78, −0.11)) and chest pain (mean difference = −0.40, 95% CI (−0.77, −0.03)).||Ran et al., 2018  |
|B-vitamins||Human cross-sectional study||Observation of inflammation markers and nutrient status.|
HIV infected participants (n = 180 men, 134 women; 18–60 y).
|Serum CRP concentrations were inversely associated with increased vitamin B intake including niacin, pyridoxine, and cobalamin (p for trend p < 0.01, p < 0.05 and p = 0.037, respectively) in men. Trends were observed in women.||Poudel-Tandukar et al., 2016 |
|Zinc||Human double-blinded RCT||Patients in the zinc group (n = 50) received lozenges (13.3 mg of zinc gluconate) as long as they showed cold symptoms. Patients in the placebo group (n = 50) received 5% calcium lactate pentahydrate.||A faster decrease of the cold symptoms (median, 4.4 d vs. 7.6 d; p < 0.001), e.g., fewer days with coughing (median, 2 d compared with 4.5 d; p < 0.05), hoarseness (2 and 3 d; p < 0.05), headache (2 and 3 d; p < 0.05), nasal congestion (4 and 6 d; p < 0.01), and sore throat (1 and 3 d; p < 0.001) were found in the intervention group, supplemented with zinc, in comparison with the placebo group. ||Mossad et al., 1996 |
|Iron ||Animal trial (Wistar rats)||Administration of low iron diet (4–5 mg powder), medium iron diet (15 mg), control group (35 mg) and normal iron intake diet group. At week 4, rats received injection of inactivated porcine influenza vaccine (HswIN1).||Following immunization, anemic rats exhibited decreased (p < 0.05) antibody titer vs. controls. Antibody synthesis was preserved in moderate iron deficiency, but was hampered by severe anemia.||Dhur et al., 1990 |
|Selenium ||Human randomized, double-blinded RCT||Evaluation of response to influenza vaccine. 12-weeks follow up. n = 119 (50–64y)|
6 intervention groups:
50, 100, or 200 mgSe/day, meals with Se-enriched onions (50 mg se/day), unenriched onions and placebo.
|SEPS1 mRNA (marker of inflammation) increased (p < 0.05) after one week of vaccine administration, being dependent on the dose of Se per each intervention arm.||Goldson 2011 |
|Polyphenols||Animal study (mice)||Evaluation of effect of polyphenol extract from Cistus Incanus on avian influenza Aviurs (H7N7).|
Inbred female Balb/c and C57Bl/6 mice at the age of 6–8 weeks.
|The polyphenol extract helped mice to not contract avian influenza, and to not alter bronchiole epithelial cells, as well as to keep constant the body temperature and the gross motor activity.||Droebner et al., 2007  |
|Carotenoids||Longitudinal study with infants||Observation of β-carotene in plasma.|
194 HIV-infected infants.
|β-Carotene was related to increased risk of death during HIV infection (OR: 3.16, CI: 1.38 to 7.21; p < 0.01).||Melikian et al., 2001 |