A Potential Therapy for SARS-Cov-2 Virus Deactivation: Carbon Dioxide Management

Correspondence: papers@team.qeios.com — Qeios will forward to the authors

COVID-19, a severe acute respiratory syndrome caused by SARS-CoV-2 virus, requires long-term multi-variant strategic plans especially with the increase in the number of impacted cases. As of February 12^th, 2021, more than 108 million coronavirus cases were reported with about 25.5 million of currently infected patients^[1]. The associated death toll is on the rise exceeding 2.4 million cases^[1]. With the positive news on the effectiveness of several vaccines towards SARS-COV-2 control directed toward minimizing illness and death, we may be far from ending COVID-19 pandemic as a public health issue. We should expect several associated challenges in the future^[2]. Although the vaccines are expected to be effective at reducing the risk of severe Covid-19 cases, the vaccinated people may still be infected and transmit the virus without showing the symptoms^[2]. The coverage levels, which is essential step to achieve a herd immunity by vaccination, may also be a challenge in many countries due to economical or cultural factors^[2]. Another challenge is associated with the lack of information on the long-term side effects of such vaccines. The effectiveness of these vaccines in protecting people may be time limited especially with the observed mutations in the virus; therefore, there may be a need for repeated vaccinations in order to control this pandemic^[2]. The vaccine manufacturer will be required to provide answers and continue to improve the effectiveness of the currently licensed COVID-19 vaccines beyond the emergency use authorization^[2]. At the same time, the scientific community should continue their research on alternative medicines for treatment and prevention. In this letter, we are proposing a potential treatment method.

In many cases of COVID-19, patients develop different symptoms range from mild to severe, including sore throat, body aches, coughing, fever, and may escalate to reach respiratory failures. In critically ill patients, when the lung get infected with SARS-Cov-2 virus, a respiratory response in form of hyperventilation is developed where the amount of CO₂ exhaled is more than the amount of O₂ inhaled. This will lead to increase in the breathing rate with less O₂ and CO₂ supply in the blood stream to organs^[3]. This may become an issue among elderly COVID-19 patients with other comorbidities as hypertension or diabetes. In those cases, the infection is associated with severe respiratory illness termed as Acute Respiratory Distress Syndrome (ARDS), which imposes hypoxia and hypocapnia (hypocapnea) similar to the ones observed in hyperventilation cases^[4][5]. Those cases require prolonged period of recovery and admission to ICU. The Estimated Oxygen Saturation (SpO₂) in these cases are low. 

 Hypoxia is a major indicator of the illness severity, which is defined as lower levels of oxygen circulated in the blood to body tissues. This is  measured by SpO₂ using the pulse oximeter. Healthy level of SpO₂ should exceed 95% in order to maintain normal metabolic functions in the body, while a reading of less than 90% indicates a serious illness in these functions including breathing problems. The symptoms of hypoxia depend on the severity of the case and may include shortness of breath, rapid breathing, and tachycardia in acute cases. In severe cases, the symptoms are confusion, inability to communicate and possibility of coma and death^[6]. Cerebral hypoxia attacks brain tissues and may lead to brain damage and death. The severity of cerebral hypoxia is measured by monitoring CBF status, which is measured by cerebrovascular reactivity (CVR-CO₂)^[7]. CO₂ has a reversible effect on cerebral blood flow (CBF), and its stability is highly sensitive to changes in PaCO₂ ^[8].

 In patients with COVID-19, a cytokine storm takes place, where cytokine bodies increase in the blood serum. It has been found that a similarity in the inflammatory response in the cases reported for both of COVID-19 and in patients with unstable CBF (vasculitis, stroke, traumatic brain injury, seizures and cognitive decline), where a reaction of cytokine storm leads to the release of interleukins   IL-1, Il-6, IL-2r and,IL-8 ^[7][9][10].  Maintaining healthy level of CBF during CO₂ fluctuation in COVID-19 patients would maintain stable breathing process in the body; hence, it will provide a chemo reflex control of breathing. Normal CBF in adults is maintained at ~ 50ml/100g of brain tissue/ min. As reported, there is a linear relationship between CO₂ and CBF demonstrated in humans where inhalation of 5% CO₂ will increase the CBF by 50 %. On the other hand, inhalation of 7% CO₂ is expected to increase CBF by 100%^[11]. Therefore, the use of CO₂ may have potential for treating moderate to severe cases of Covid-19, especially when breathing difficulties and hypoxia are present. By elevating the partial pressure of arterial CO₂ (PaCO₂), CBF increases resulting in the stabilization of the breath by increasing the oxygen supply in the body tissues. This will help in stabilizing the release of interleukins and in suppressing the cytokine storm reaction where the CO₂ gas is diffused in body tissues about 20 times more than O₂ ^[12]. In patients admitted to ICU with severe symptoms of COVID-19, severe hypoxia was found to trigger the respiratory response for hypocapnia (low PaCO₂) ^[3][13]; hence, leading to a favorable environment for bacterial and viral growth. Inhalation of CO₂ gas would reduce the release of interleukins by lowering the pH to 5.5, as CO₂ gas possess anti-inflammatory, antimicrobial and anti-cytokine features.

CO₂ plays a vital role in improving oxygenation of blood and body organs. Based on the above discussions, we suggest administering a heated warmed and humidified CO₂ in order to lower PH to around 4.2. This acidic medium increases the cell membrane permeability to CO₂ leading to a decrease in the viral growth rate inside the cell and ultimately the deactivation of the viral process. This suggestion aligns with a recent article, which showed the inactivation of viruses and bacteria by CO₂ bubbles in solution^[13]. In addition, Dense Phase Carbon Dioxide (DPCD) treatment may be applied for the deactivation of the virus. This high density of warmed CO₂ molecules enter the virus capsid and binds to the protein sites to form CO₂-protein binding complex which results in the deactivation of the virus action as well.