Understanding how a virus damage human cells and organs give us clues for developing a more effective therapy. Viruses cause infections that are often associated with redox modification leading to oxidative stress. Changes in redox homeostasis in infected cells are one of the key events in the pathogenesis of respiratory viral infections in all phases of the disease, contributing to severe inflammatory reaction and subsequent tissue damage. Redox changes to an oxidised state also play a critical role in the activation of numerous cell pathways that are hijacked by viruses to replicate and to suppress the patient’s immune response.
Viruses use several strategies to manipulate host cell to their advantage. Among these, the imbalance of intracellular redox state caused by viruses could play an important role in modulating the activity of several signaling pathways. Oxidative imbalance caused by viral infections, ligand–receptor binding or cytokine storm could result in localised oxidation of reactive residues of redox-sensitive proteins. Increased oxidative stress leads to a systemic inflammatory response due to increased production of cytokines, contributing to ARDS, the key pathology in the high mortality of acute respiratory viral infections. Despite the antiviral role of cytokines in respiratory infections, their overproduction during the cytokine storm is more damaging to lung tissue than the viruses themselves.
As a common immunological defense mechanism, immune cells respond to foreign infection by producing large quantities of reactive oxygen species to destroy invading organisms. Previous pathological and histological examinations showed that coronaviruses and influenza induced significant down regulation of the airway antioxidant system, leading to lethal lung injury and death from ARDS due to oxidative damage.
C reactive protein (CRP) is raised in many acute viral infections which suggest increased oxidative stress.
Role of vitamin C in viral infection:
Viruses
like influenza, corona and rhino viruses increase oxidative stress in the body
leading to cellular and tissue damage. In addition to standard
conventional supportive treatments, administration of vitamin C (ascorbic acid
or ascorbate), has been shown to be a safe and effective therapy for
respiratory viral infections.
Implementation
of high-dose vitamin C therapy could dramatically reduce the need for high
doses of corticosteroids, antibacterials and antiviral drugs that may be
immunosuppressive, adrenal depressive and toxic, complicating the disease
course. In order to effectively fight the stubborn viruses, medical
professionals should explore readily available pharmaceutical and nutritional
therapeutic agents with proven antioxidant, anti-inflammatory and
immunosupportive properties.
Vitamin
C has many properties that make it a valuable therapeutic agent for respiratory
infections. It is a potent antioxidant with anti-inflammatory and immune
supportive properties. Vitamin C is a small, water-soluble molecule that
readily acts as a one- or two-electron reducing agent for many free radicals
and oxidants. Almost all mammals, except for humans, primates and
guinea pigs, can synthesise vitamin C in their livers, with increased
production during stress. Vitamin C is an essential vitamin that acts as a
cofactor for several enzymes and facilitates the production of catecholamines,
vasopressin, l‐carnitine,
collagen neurotransmitters and cortisol, which are central to cellular function
and homeostasis. Additionally, vitamin C plays a significant role in viral
infection, including attenuation of the pro-inflammatory response, enhancement
of epithelial barrier function, increased alveolar fluid clearance, and
prevention of sepsis-associated coagulation abnormalities.
This
essential vitamin has a huge role in antiviral activity and immune enhancement.
It has been shown that vitamin C is an essential factor in the production of
type I interferons during the antiviral immune response. Vitamin C has also
been shown to upregulate natural killer cell and cytotoxic T-lymphocyte
activity. Other studies have used this vitamin as an inactivating agent both
for RNA and DNA viruses, lessening viral infectivity. In addition, vitamin C
can detoxify viral products that produce pain and inflammation. Evidence has
shown the effectiveness of vitamin C in treating pneumonia and infection owing
to its direct inhibitory effects on pathogens. Also, vitamin C is present in
the epithelial lining of the respiratory tract where it functions as a local
mucosal protecting agent, helping to ameliorate symptoms of upper respiratory
tract infection.
A
high dose of vitamin C may be a proven therapeutic agent that not only
ameliorates oxidative stress and inflammation during acute virus infection, but
also suppresses viral replication and improves antiviral immune defense and
adrenal function.
Supplemental
vitamin C may also provide additional benefits for the prevention of viral infection,
shorten the disease course and lessen complications of the disease.