on July 22, 2026
The management of acute viral respiratory tract diseases represents one of the most complex challenges in modern medicine. In the face of highly mutable viruses, particularly retroviruses and RNA viruses belonging to the Coronaviridae or Orthomyxoviridae families, conventional symptomatic pharmacological treatment often shows evident structural limitations. The routine use of paracetamol, corticosteroids, and antibiotics does not directly act on the elimination of the virion: antibiotics are ineffective against viral structures and risk altering the intestinal microbiota, while corticosteroids, if administered early, can delay viral clearance. At the same time, specific antiviral options often present a non-negligible toxicity profile with a benefit/risk ratio that must be carefully evaluated, just as the use of off-label drugs (such as hydroxychloroquine or IL-6 inhibitors like tocilizumab) has shown heterogeneous responses and potential severe adverse reactions.
A crucial pathophysiological aspect concerns the role of chronic medications and their interference with the virus's cellular entry mechanisms. The angiotensin-converting enzyme 2 (ACE2) receptor, expressed on type II alveolar epithelial cells, constitutes the cellular entry point for several coronaviruses. Clinical and molecular studies have documented how the prolonged use of specific antihypertensives (ACE inhibitors and sartans) and widely used NSAIDs such as ibuprofen can modulate ACE2 expression. Although the clinical balance is complex, it is evident that the accumulation of pharmacological treatments in elderly and multimorbid patients can paradoxically alter the host's physiological barriers.
Viruses are acellular microorganisms and obligate intracellular parasites. Lacking an autonomous metabolism, they consist of genetic material (DNA or RNA) enclosed in a protein coating (capsid) and sometimes a lipid membrane (pericapsid). Their biological survival depends on the ability to infect a host cell without causing its immediate death before replication has occurred; hence the evolutionary pressure toward mutations that optimize the balance between transmissibility and virulence. Viruses also represent a powerful agent of Horizontal Gene Transfer (HGT), a mechanism by which genetic material is exchanged between non-descendant organisms, increasing genomic diversity.
Once it has penetrated the target cell through the specific interaction between viral ligands and membrane receptors, the virus loses its structural individuality, hijacking the host's biosynthetic machinery. From an epigenetic perspective, viral nucleotide sequences resonate with pre-existing gene programs, acting as true biological information capable of activating the pericellular connective tissue and triggering inflammatory enzymatic cascades necessary for the drainage of the cellular toxic load. Coronaviruses (from SARS-CoV identified in 2002 to MERS-CoV in 2012 and emerging variants) show a marked tendency for interspecies jumps (spillover) from animal reservoirs (skunks, dromedaries, bats) to humans, highlighting the impossibility of permanently eradicating such viral families from the environment.
The main mechanism of defense and restoration of tissue homeostasis is represented by physiological inflammation. When a pathogen penetrates the primary barriers (skin, intestinal mucosa, respiratory epithelium), the innate immune system recruits cytokines and cellular effectors to contain the insult. However, if acute and resolving response inflammation transforms into a chronic low-intensity process (low-grade inflammation), tissue integrity is compromised.
In Italy, the higher lethality found in certain patient cohorts during pandemic waves is closely related to the demographic structure (advanced average age) and the high prevalence of metabolic and cardiovascular comorbidities (type 2 diabetes mellitus, arterial hypertension, chronic obstructive pulmonary disease, renal failure, and cognitive decline). In this context of frailty and polypharmacy, viral infection acts as the triggering factor on a biological ground already severely compromised.
The structural integrity of the respiratory epithelium plays a role of primary importance. Cigarette smoke and chronic exposure to atmospheric particulate matter (PM10 and PM2.5) paralyze and damage the mucociliary apparatus, preventing the mechanical clearance of virions and facilitating the pathogen's access to the deep airways. Similarly, states of obesity, insulin resistance, sedentary lifestyle, and chronic psycho-neuro-endocrine stress alter the HPA axis and suppress the cell-mediated immune response.
To optimize the immune response and reduce the baseline inflammatory state, scientific literature highlights the importance of precise lifestyle changes:
· Diet rich in phytonutrients: Daily consumption of fresh fruit and vegetables, sources of natural antioxidants capable of neutralizing oxidative stress induced by infections.
· Glycemic load control: Elimination of refined sugars and high-glycemic-index flours to prevent insulin spikes that fuel systemic inflammatory pathways.
· Moderate and regular physical activity: At least 30 minutes a day of brisk walking or outdoor running to stimulate lymphatic circulation and the recruitment of NK lymphocytes.
· Respiratory and environmental hygiene: Complete cessation of cigarette smoking, reduction of exposure to crowded and poorly ventilated indoor spaces, and frequent hand washing.
· Sleep hygiene and stress management: Adequate nighttime rest to promote melatonin secretion and the regulation of the cortisol response.
To support immune defenses, several micronutrients possess solid biological and clinical evidence:
· Vitamin C (Ascorbic Acid): A powerful water-soluble antioxidant, it stimulates neutrophil function and interferon production.
· Vitamin D3 (Cholecalciferol): Regulates the expression of antimicrobial peptides (cathelicidins and defensins) and modulates the cytokine response, reducing the risk of acute respiratory tract infections.
· Vitamin A (Retinol): Essential for maintaining mucosal integrity and for the cytotoxic activity of Natural Killer (NK) cells.
· Trace Elements (Zinc, Copper, Manganese): Zinc inhibits viral RNA polymerase in vitro and is effective in reducing the duration of respiratory symptoms if taken early; Copper and Manganese act as enzymatic cofactors of the superoxide dismutase (SOD) enzyme.
· Microbiota and Probiotics: Strains of Lactobacillus and Bifidobacterium reinforce the intestinal barrier (GALT) through the production of bacteriocins and competition for the ecological niche, modulating the systemic immune response through the gut-lung axis.
Although there are no phytotherapeutic treatments with a preventive or specific curative indication for SARS-CoV-2 validated by definitive clinical trials, the study of pharmacognostic literature identifies several medicinal plants with immunomodulating, indirect antiviral, and adaptogenic actions:
· Echinacea (Echinacea angustifolia / purpurea): Increases the Th1 response and phagocytic activity, demonstrating efficacy in reducing the incidence and severity of viral respiratory infections.
· Astragalus (Astragalus membranaceus): The root has a bronchial anti-inflammatory and immunostimulating action, increasing antibody production and lymphocyte proliferation.
· Uncaria tomentosa and Elderberry (Sambucus nigra): Extracts rich in flavonoids capable of interfering with viral adhesion to host cells and modulating the inflammatory cascade.
· Licorice (Glycyrrhiza glabra) and Geranium (Pelargonium sidoides): Glycyrrhizic acid shows direct antiviral properties in vitro, while Pelargonium is widely documented in the treatment of acute viral bronchitis.
· Tea Tree Essential Oil (Melaleuca alternifolia) and Propolis: Agents with pronounced antiseptic and local disinfectant activity for the upper airways.
Chronic stress significantly alters the cellular immune response through the hyperactivation of the sympathetic system and the hypothalamus-pituitary-adrenal axis. To counteract anxiety and psychophysical fatigue, the use of adaptogenic plants and herbs with muscle-relaxant and anxiolytic action is of primary support:
· Major adaptogens: Withania somnifera (Ashwagandha) and Rhodiola rosea modulate cortisol levels, improve stress resilience, and, together with Curcuma longa (Curcumin), support neuroinflammation and the synthesis of neurotrophins (BDNF).
· Anxiolytics and sleep regulators: Scutellaria baicalensis, Passiflora incarnata, Melissa officinalis, Valeriana officinalis, Lavandula officinalis, and Humulus lupulus offer a phytotherapeutic synergy aimed at reducing neuromuscular excitability and restoring physiological and emuntorial sleep.
Bibliographic References and Scientific Studies
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