The central thesis examined herein is that the prodromal phase of viral infection—the first 24 to 48 hours—represents a critical window where metabolic manipulation can decisively tip the balance in favor of the host. By inducing a catabolic state via fasting, the host suppresses anabolic signaling pathways (specifically mTOR) that viruses hijack for replication, while simultaneously upregulating autophagy (xenophagy) to clear intracellular pathogens. Furthermore, by avoiding the postprandial hyperglycemic spikes associated with “comfort foods,” the host preserves the phagocytic capacity of neutrophils and prevents the competitive inhibition of critical antioxidants like ascorbate.

This analysis synthesizes evidence from evolutionary biology, molecular virology, and clinical pharmacology. It dissects the “opposing effects” of bacterial versus viral metabolism, the “selfish” nature of the activated immune system, and the pharmacodynamics of supraphysiological nutrient delivery. The findings suggest that “starving a cold” is not merely folklore, but a biologically sophisticated maneuver to induce a state of enhanced viral resistance.

The Bioenergetics of Immunity: The “Selfish” Immune System

To understand the rationale for fasting during infection, one must first quantify the exorbitant cost of immunity. The immune system is not a passive entity; it is a voracious consumer of energy that competes aggressively with other vital organs—specifically the brain and muscles—for metabolic substrates during an active challenge.

The Metabolic Cost of the Acute Phase Response

When a pathogen breaches the mucosal barrier, the body initiates the Acute Phase Response (APR). This systemic reaction is orchestrated by pro-inflammatory cytokines, primarily Interleukin-6 (IL-6), Interleukin-1β (IL-1β), and Tumor Necrosis Factor-alpha (TNF-α). The APR is metabolically expensive. In humans, the induction of a fever (pyrexia) raises the Basal Metabolic Rate (BMR) by approximately 10–13% for every 1°C increase in core body temperature. During a fulminant infection, the glucose utilization by the immune system alone can account for over 60% of the body’s total glucose turnover, rivaling the brain’s consumption.

This energy expenditure is allocated to three primary defensive pillars:

1. Biosynthetic Demand: T and B lymphocytes must undergo rapid clonal expansion. A single naïve T-cell can generate thousands of daughter cells within days. This proliferation requires the de novo synthesis of DNA, RNA, proteins, and lipid membranes, a process that places immense demand on the Pentose Phosphate Pathway (PPP) for nucleotide precursors and NADPH.

2. Effector Functions: Neutrophils and macrophages engage in energy-intensive activities such as chemotaxis (migration), phagocytosis (engulfment), and the respiratory burst (generation of reactive oxygen species). The respiratory burst alone consumes vast amounts of oxygen and ATP to fuel the NADPH oxidase complex.

3. Thermogenesis: The generation and maintenance of a fever create a non-permissive thermal environment for viral replication but require significant caloric oxidation by brown adipose tissue and skeletal muscle (shivering).

The “Selfish Immune System” Hypothesis

In a state of health, the human brain is the “selfish” organ, consuming approximately 50% of the daily glucose intake despite representing only 2% of body weight. However, during an acute infection, the immune system engages a resource-reallocation program described by Straub et al. as the “selfish immune system.” To secure the fuel necessary for the APR, the immune system effectively “hijacks” the body’s glucose supply.

Implication for Feeding: This bioenergetic reality challenges the utility of feeding during the acute phase. Ingesting food, particularly carbohydrates, stimulates the release of insulin. Insulin’s primary function is to drive glucose into storage tissues (anabolism). This directly antagonizes the immune system’s effort to induce insulin resistance and keep glucose available for immune cells. By forcing food intake, one may inadvertently disrupt the “selfish” reallocation of energy that the immune system is attempting to orchestrate, potentially forcing the immune system to compete with the host’s own storage tissues for fuel.

The energy required for digestion is not trivial. The specific dynamic action (SDA) of food processing requires significant blood flow to the splanchnic bed (gut, liver, pancreas). During an infection, hemodynamic resources are needed in the periphery (mucosal surfaces, lymph nodes) to transport immune cells. Feeding diverts this blood flow. Furthermore, the synthesis of digestive enzymes and the mechanical motility of the gut consume ATP.

Evolutionary Biology of Sickness Behavior: Why We Stop Eating

The most compelling argument for the proposed protocol lies in the evolutionary conservation of sickness behaviors. If “feeding a cold” were the biologically superior strategy, natural selection would have vigorously selected for the maintenance of appetite during illness. Instead, we observe the exact opposite across the animal kingdom.

Sickness-Associated Anorexia (SAA)

Sickness-associated anorexia—the profound loss of appetite during infection—is observed in virtually every class of animals, from mammals and birds to reptiles and even invertebrates like Drosophila. This universality suggests that SAA is an ancient, highly conserved, and adaptive trait. It is not a passive symptom of feeling unwell; it is an active, orchestrated physiological response.

Evolutionary biologists propose several adaptive advantages to this self-imposed starvation:

1. Behavioral Conservation: Foraging for food requires locomotion, cognitive alertness, and exposure to predation. In a weakened state, an animal is vulnerable. Anorexia suppresses the drive to forage, encouraging the animal to seek shelter and rest (lethargy), thereby conserving energy for the internal metabolic battle against the pathogen.

2. Nutritional Immunity (Iron Sequestration): Many pathogens, particularly bacteria but also viruses, require free iron for replication. The host defends against this by sequestering iron. The liver produces hepcidin, which blocks iron absorption from the gut and locks iron inside macrophages (via ferroportin degradation). Continued feeding would introduce dietary iron into the system, potentially bypassing this blockade. Anorexia cooperates with hepcidin to starve the pathogen of essential micronutrients.

3. Reducing Substrate for Pathogens: As detailed later, viruses are obligate intracellular parasites that rely on host metabolites. By restricting exogenous intake, the host lowers the concentration of circulating amino acids and glucose spikes, potentially throttling the resources available for viral assembly.

The Paradox of “Starve a Fever”

The protocol challenges the second half of the adage “Feed a cold, starve a fever,” arguing instead to stop eating for both (or specifically for viral colds). The historical origin of this aphorism (John Withals, 1574) suggested that fasting cures fever by cooling the body (reducing the thermic effect of food). While the thermal mechanism is simplistic, the behavioral instinct remains sound.

The “Opposing Effects” Model: Bacterial vs. Viral Metabolism

A sophisticated analysis of the literature reveals a critical dichotomy in how the body handles bacterial versus viral infections. This distinction is vital for validating the protocol, which specifically targets “colds and flus” (viral).

The seminal paper by Wang, Medzhitov, et al. (Cell, 2016) titled “Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation” is the cornerstone of this discussion. This study is often misinterpreted as evidence to “feed a virus.” A granular look at the data reveals why it actually supports the focus on early intervention.

• Bacterial Infection: Fasting was potently protective. Mice that were force-fed glucose died. Survival depended on ketogenesis; the production of beta-hydroxybutyrate (BHB) protected the brain from ROS-mediated damage. Glucose feeding suppressed ketogenesis, leading to fatal oxidative stress in the brain.

• Viral Infection: In this lethal model of influenza, mice that were fed glucose survived better than those that were fasted or given 2-deoxyglucose (a glycolysis inhibitor). The mechanism was identified as tolerance. Viral inflammation caused Endoplasmic Reticulum (ER) stress and the Unfolded Protein Response (UPR) in the brain. Glucose was required to resolve this ER stress and prevent neuronal apoptosis.

Resistance vs. Tolerance: The Clinical Distinction

1. Resistance: The ability to reduce the pathogen load (i.e., killing the virus or stopping replication).

2. Tolerance: The ability to endure the tissue damage caused by the infection without necessarily reducing the pathogen load.

Human vs. Murine Metabolic Flexibility

A critical limitation of the mouse model is metabolic fragility. Mice have very high metabolic rates and low glycogen reserves. A 24-hour fast in a mouse is a near-lethal starvation event causing deep hypoglycemia and torpor. Humans, by contrast, are metabolically flexible. A 24–48 hour fast in a human does not deplete glucose to dangerous levels; the liver maintains euglycemia via glycogenolysis and gluconeogenesis.

Therefore, humans can likely reap the benefits of fasting (low insulin, high autophagy, mTOR inhibition) without suffering the catastrophic brain starvation seen in fasted mice. We can maintain enough glucose for the brain (tolerance) via internal reserves while creating a systemic environment hostile to the virus (resistance).

Hyperglycemia and the “Sugar Coma”: Innate Immune Paralysis

The assertion that “eating (especially sugar) works against your immune system” is scientifically robust, grounded in the immediate deleterious effects of hyperglycemia on neutrophil function. Neutrophils are the “first responders” of the innate immune system, and their efficacy is inversely correlated with blood glucose spikes.

The Sanchez Effect: Acute Immunosuppression

This refers to a “classic” finding, referencing the work of Sanchez et al. (1973), often colloquially termed the “sugar coma” study. This study demonstrated that the ingestion of 100g of simple carbohydrates (glucose, fructose, sucrose, honey, or orange juice) significantly depressed the phagocytic index of neutrophils.

• Magnitude: The capacity of neutrophils to engulf bacteria dropped by approximately 50%.

• Time Course: The suppression began within 30 minutes, peaked at 2 hours, and persisted for at least 5 hours.

• Control: Ingestion of complex starch did not produce this effect, isolating the rapid spike in blood glucose (and insulin) as the causative factor.

Molecular Mechanisms of Neutrophil Paralysis

Modern immunobiology has elucidated several mechanisms explaining why hyperglycemia paralyzes neutrophils:

Competitive Inhibition of Vitamin C (The AA/DHA Competition)

Neutrophils accumulate Vitamin C (ascorbate) against a concentration gradient, achieving intracellular levels 50–100 times higher than plasma. This high concentration is vital for protecting the neutrophil from the oxidative burst (superoxide, hypochlorous acid) it generates to kill pathogens. Without sufficient intracellular Vitamin C, the neutrophil suffers oxidative damage and undergoes premature apoptosis (cell death).

Crucially, the oxidized form of Vitamin C (Dehydroascorbic Acid, DHA) enters the cell via the GLUT1 and GLUT3 transporters—the same transporters used for glucose.

• The Mechanism: In a hyperglycemic state (e.g., after drinking juice or eating crackers), glucose floods the bloodstream and competitively inhibits the transport of DHA into the neutrophil.

• The Result: The neutrophil becomes “internally scorbutic” (Vitamin C deficient) despite adequate plasma levels. It loses its antioxidant shield, rendering its “gunpowder” (oxidative burst) dangerous to itself. Motility slows, and phagocytosis stalls.

For a neutrophil to fight infection, it must migrate from the blood vessel into the tissue. This requires a precise sequence of rolling, adhesion, and transmigration (diapedesis). Hyperglycemia alters the expression of adhesion molecules (ICAM-1, VCAM-1) on the endothelium and integrins (CD11b/CD18) on the neutrophil.

• Effect: Neutrophils become “sticky.” They adhere too tightly to the vessel wall or aggregate non-specifically, failing to migrate effectively toward the chemical distress signals (chemokines) of the virus.

Glycation of Immunoglobulins

Acute and chronic hyperglycemia promotes the non-enzymatic glycation of proteins. The Fc region of antibodies (immunoglobulins) is susceptible to glycation. When glycated, antibodies lose their efficiency in opsonization—tagging the virus for destruction. This blinds the neutrophil to the pathogen, further reducing phagocytic efficiency.

The Paradox of Neutrophil Glycolysis (The Warburg Effect)

It is important to note a nuance: Neutrophils are strictly glycolytic cells. They possess few mitochondria and rely almost exclusively on glycolysis for ATP, even in the presence of oxygen (aerobic glycolysis). They need glucose to function.

• The Nuance: The neutrophil’s requirement is met by homeostatic glucose levels (70–90 mg/dL). Fasting does not drop glucose to zero; the liver maintains sufficient levels for neutrophil function. The dysfunction arises from excess (hyperglycemic) glucose, which triggers the competitive inhibition and oxidative stress pathways described above.

Cellular Rewiring: The mTOR vs. Autophagy Axis

The most sophisticated argument for fasting lies in intracellular signaling. The cell operates in a binary mode: it is either in a state of Growth (Anabolism) or Repair/Defense (Catabolism). These states are mutually exclusive, governed by the antagonism between mTOR (The Mammalian Target of Rapamycin) and Autophagy.

mTORC1 (mTOR Complex 1) is the master regulator of protein synthesis and cell growth. It is activated by:

1. Insulin/IGF-1: Signals the presence of carbohydrates.

2. Amino Acids: Signals the presence of protein (specifically leucine).

3. Energy Status: High ATP levels.

• Mechanism: The Influenza A virus protein NS1 interacts with the host’s PI3K/Akt pathway. Phosphorylated Akt activates mTORC1, keeping the cell in a high-protein-synthesis state. This ensures the rapid production of viral capsids and replication enzymes.

• Implication: If the host eats protein and carbs, they provide the exogenous signal (Insulin + Amino Acids) that synergizes with the virus’s internal signal to maximally activate mTOR. This effectively turns on the “printer” that the virus is trying to use.

Autophagy: The Intracellular “Trash Compactor”

Autophagy (“self-eating”) is a catabolic process where the cell degrades its own components to recycle energy. It is the primary mechanism of cellular quality control.

• Xenophagy: A specialized form of autophagy, xenophagy, is dedicated to the detection, engulfment, and lysosomal destruction of intracellular pathogens (viruses and bacteria).

• Mechanism: The cell forms a double-membrane vesicle (autophagosome) around the viral particle. This fuses with a lysosome, where acidic hydrolases degrade the virus.

• Antigen Presentation: The viral debris is not wasted; the peptides are loaded onto MHC Class I and II molecules and presented to T-cells, jumpstarting the adaptive immune response.

Fasting as the Trigger: Fasting is the most potent physiological activator of autophagy.

• AMPK Activation: As glucose drops, the cellular AMP:ATP ratio rises. This activates AMPK (AMP-activated protein kinase).

• The Switch: AMPK directly phosphorylates and inhibits mTORC1. It also phosphorylates ULK1, the initiator of the autophagy cascade.

By fasting for 24–48 hours, the host actively suppresses the viral “printer” (mTOR) and turns on the viral “shredder” (Autophagy). This creates a cellular environment that is fundamentally hostile to viral replication. The claim that fasting “rewires the immune system” is a scientifically accurate description of this AMPK-mediated metabolic switch.

The Clinical Dovetail: Parenteral Micronutrient Pharmacology

The protocol distinguishes itself from simple starvation by advocating for “intelligent layering” of fluids and specific nutrients via IV or IM routes. This bypasses the gastrointestinal tract, avoiding the insulin/mTOR activation associated with digestion while delivering supraphysiological doses of immune-critical cofactors.

Intravenous Vitamin C (Ascorbate)

The recommendation for IV Vitamin C (10–25g) targets a pharmacological effect distinct from oral supplementation.

• Pharmacokinetics: Oral Vitamin C absorption is tightly regulated by the intestinal transporter SVCT1. Absorption is saturable; doses above 200mg result in rapidly diminishing returns, capping plasma levels at ~80–100 µmol/L regardless of intake.

• Pharmacodynamics (IV): Intravenous administration bypasses this gut limit, achieving plasma concentrations in the millimolar range (10,000–20,000 µmol/L).

• The Pro-Oxidant Mechanism: At these supraphysiological concentrations, Vitamin C acts as a pro-drug for the generation of Hydrogen Peroxide (H2O2) in the extracellular fluid. The ascorbate radical donates an electron to transition metals (like iron) in the interstitial fluid (Fenton reaction), generating H2O2.

• Virucidal Effect: H2O2 diffuses into cells. Healthy host cells have robust catalase enzymes to neutralize it. However, virus-infected cells and viral particles often lack sufficient catalase defense. The peroxide exerts a direct oxidative stress on the virus, damaging viral RNA and capsid proteins.

• Clinical Evidence: Trials in sepsis and ARDS (e.g., the CITRIS-ALI trial) have shown that high-dose IVC can reduce mortality and the duration of ICU stays. The Riordan Clinic data suggests a reduction in viral antibody titers (EBV) correlating with high-dose IVC therapy.

• Safety (G6PD): The protocol correctly notes the absolute contraindication of G6PD Deficiency. Patients with this genetic enzyme defect cannot generate enough NADPH to reduce glutathione and neutralize the H2O2, leading to severe hemolytic anemia. Screening is mandatory.

The Vitamin D “Hammer” (Stoss Therapy)

The recommendation involves a single high dose (e.g., 50,000 IU) of Vitamin D. This approach is known in medical literature as Stoss Therapy.

• Rationale: Vitamin D is a secosteroid hormone precursor, not just a vitamin. It modulates the expression of over 1,000 genes. Standard daily dosing (1,000–2,000 IU) takes weeks or months to elevate serum 25(OH)D to therapeutic levels (>50 ng/mL). In an acute infection, time is the limiting factor.

• Mechanism: Vitamin D binds to the Vitamin D Receptor (VDR) on macrophages and bronchial epithelial cells. The VDR translocates to the nucleus and triggers the transcription of Cathelicidin (LL-37) and Beta-defensins.

• Antimicrobial Peptides: LL-37 is a potent broad-spectrum antiviral. It physically disrupts viral envelopes (acting like a detergent) and can inhibit the replication of Influenza and RSV.

• Safety: Systematic reviews of Stoss therapy (doses up to 600,000 IU) in children and adults confirm it is generally safe, with a low risk of hypercalcemia compared to chronic high-dose toxicity. The “hammer” provides the rapid genomic signal needed to arm the mucosal barrier.

Zinc and Magnesium: The Synergists

• Intravenous Zinc: Zinc is a direct inhibitor of the viral RNA-dependent RNA Polymerase (RdRp), the enzyme RNA viruses use to copy their genetic material. However, zinc is an ion that struggles to cross cell membranes. High serum levels (via IV) increase the concentration gradient, driving passive diffusion or facilitating uptake via ZIP transporters.

• Intravenous Magnesium: Magnesium is the counter-ion for ATP; biologically active ATP is actually Mg-ATP. Immune cells, engaging in high-energy turnover, are magnesium-dependent. Furthermore, magnesium stabilizes mast cells (preventing histamine release) and mitigates the vein irritation (phlebitis) that can be caused by the hyperosmolarity of high-dose Vitamin C infusions.

Clinical Protocol Synthesis and Recommendations

The “Prodromal Window” Strategy

The scientific validity of this protocol hinges on timing. The interventions are designed for the prodromal phase—the first signs of “feeling off,” scratchy throat, or malaise.

• Action: Immediate cessation of caloric intake (fasting) for 24–48 hours.

• Support: Hydration with water and electrolytes (no sugar).

• Intervention: Administration of IV/IM nutrient therapy (Vitamin C, D, Zinc, Mg).

Why This Works (Summary Mechanism)

1. Fasting drops insulin and activates AMPK.

2. AMPK shuts down mTOR (viral protein synthesis) and activates Autophagy (viral clearance).

3. Low Glucose prevents neutrophil paralysis and ensures Vitamin C transport into immune cells.

4. IV Nutrients provide the pharmacological “ammunition” (H2O2, LL-37, RdRp inhibition) that the now-optimized immune system uses to destroy the pathogen.

This synergistic approach transforms the host from a “fertile incubator” (high sugar, high mTOR) into a “hostile environment” (low sugar, high autophagy, high antimicrobial peptides).

Limitations and Contraindications

While scientifically robust for healthy adults, this protocol requires medical supervision.

• Type 1 Diabetics: Fasting can induce ketoacidosis; insulin management is complex.

• Pregnant/Breastfeeding Women: Caloric restriction is generally contraindicated.

• Eating Disorders: Fasting may trigger relapse.

• G6PD Deficiency: Absolute contraindication for high-dose IV Vitamin C.

• Renal Impairment: High-dose Vitamin C can cause oxalate nephropathy; magnesium accumulation can be toxic.

The article and proposed protocol are not merely “scientifically robust”; they represent a sophisticated application of systems biology. By integrating the evolutionary logic of anorexia, the molecular biology of the mTOR/Autophagy switch, and the pharmacology of parenteral nutrition, the protocol offers a mechanistic blueprint for enhancing host resistance in the critical early hours of viral infection. It validates the shift from a passive “supportive care” model (soup and crackers) to an active “metabolic intervention” model (fasting and IVs), rightly identifying that in the war against viruses, the terrain is just as important as the pathogen.

Data Tables

Table 1: Metabolic & Immune Effects of Feeding vs. Fasting in Acute Viral Infection

Table 2: Comparative Pharmacokinetics of Oral vs. IV/IM Micronutrients

References

1. Straub RH. The selfish immune system and the selfish brain. Sci Rep. 2014;89891.

2. Wang A, Huen SC, Luan HH, et al. Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation. Cell. 2016;166(6):1512-1525.e12.

3. Deretic V, Saitoh T, Akira S. Autophagy in infection, inflammation and immunity. Nat Rev Immunol. 2013;13(10):722-737.

4. Sanchez A, Reeser JL, Lau HS, et al. Role of sugars in human neutrophilic phagocytosis. Am J Clin Nutr. 1973;26(11):1180-1184.

5. Straub RH, Cutolo M, Buttgereit F, Pongratz G. Energy regulation of the immune system and the brain during infectious and inflammatory diseases. Brain Behav Immun. 2010;24(1):1-10.

6. Baracos VE, Whitmore B, Gale R. The metabolic cost of fever. Can J Physiol Pharmacol. 1987;65(6):1248-1254.

7. Pearce EL, Poffenberger MC, Chang CH, Jones RG. Fueling immunity: insights into metabolism and lymphocyte function. Science. 2013;342(6155):1242454.

8. Borregaard N. Neutrophils, from marrow to microbes. Immunity. 2010;33(5):657-670.

9. Freemerman AJ, Johnson AR, Sacks GN, et al. Metabolic reprogramming of macrophages: glucose transporter 1 (GLUT1)-mediated glucose metabolism drives a proinflammatory phenotype. J Biol Chem. 2014;289(11):7884-7896.

10. Secor SM. Specific dynamic action: a review of the postprandial metabolic response. J Comp Physiol B. 2009;179(1):1-56.

11. Exton MS. Infection-induced anorexia: active host defence strategy. Appetite. 1997;29(3):369-383.

12. McCarthy DO. Anorexia during infection: is it part of the host defense response? Biol Res Nurs. 2000;2(4):284-294.

13. Ganz T. Hepcidin and iron regulation, 10 years later. Blood. 2011;117(17):4425-4433.

14. Withals J. A Shorte Dictionarie for Yonge Begynners. London, England; 1574.

15. Wang A, Medzhitov R. Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation. Cell. 2016;166(6):1512-1525.

16. Washko PW, Wang Y, Levine M. Ascorbic acid recycling in human neutrophils. J Biol Chem. 1993;268(21):15531-15535.

17. Turina M, Fry DE, Polk HC Jr. Acute hyperglycemia and the innate immune system: clinical, cellular, and molecular aspects. Crit Care Med. 2005;33(7):1624-1633.

18. Borregaard N, Herlin T. Energy metabolism of human neutrophils during phagocytosis. J Clin Invest. 1982;70(3):550-557.

19. Kuss-Duerkop SK, Wang J, Mena I, et al. Influenza virus differentially activates mTORC1 and mTORC2 signaling to maximize late stage replication. PLoS Pathog. 2017;13(9):e1006635.

20. Levine B, Kroemer G. Autophagy in the pathogenesis of disease. Cell. 2008;132(1):27-42.

21. Kim J, Kundu M, Viollet B, Guan KL. AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1. Nat Cell Biol. 2011;13(2):132-141.

22. Levine M, Padayatty SJ, Espey MG. Vitamin C: a concentration-function approach yields pharmacology and therapeutic discoveries. Adv Nutr. 2011;2(2):78-88.

23. Chen Q, Espey MG, Krishna MC, et al. Pharmacologic ascorbic acid concentrations selectively kill cancer cells: action as a pro-drug to deliver hydrogen peroxide to tissues. Proc Natl Acad Sci U S A. 2005;102(38):13604-13609.

24. Mikirova N, Hunninghake R. Effect of high dose vitamin C on Epstein-Barr viral infection. Med Sci Monit. 2014;20:725-732.

25. Fowler AA 3rd, Truwit JD, Hite RD, et al. Effect of Vitamin C Infusion on Organ Failure and Biomarkers of Inflammation and Vascular Injury in Patients With Sepsis and Severe Acute Respiratory Failure: The CITRIS-ALI Randomized Clinical Trial. JAMA. 2019;322(13):1261-1270.

26. Liu PT, Stenger S, Li H, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006;311(5768):1770-1773.

27. McNally JD, Menon K, Chakraborty P, et al. The association of vitamin D status with acute respiratory infection in children: a systematic review. Pediatr Pulmonol. 2013;48:106.

28. Schwalfenberg GK. Vitamin D for influenza. Can Fam Physician. 2015;61(6):507.

29. te Velthuis AJ, van den Worm SH, Sims AC, et al. Zn(2+) inhibits coronavirus and arterivirus RNA polymerase activity in vitro and zinc ionophores block the replication of these viruses in cell culture. PLoS Pathog. 2010;6(11):e1001176.