Aerosol and Surface Stability of SARS-CoV-2 In this research letter, investigators report on the stability of SARS-CoV-2 and SARS-CoV-1 under experimental conditions. The viability of the two virus...

https://www.nejm.org/doi/pdf/10.1056/NEJMc2004973?articleTools=true

Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1.

Prospective Cohort Study

Correlation between weather and Covid-19 pandemic in Jakarta, Indonesia.

Potential sources, modes of transmission and effectiveness of prevention measures against SARS-CoV-2.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8719928

Mitigating Covid-19 in the face of emerging virus variants, breakthrough infections and vaccine hesitancy

Since the outbreak of the novel SARS-like coronavirus (SARS-CoV-2) in Wuhan, China, more than 4,000,000 cases have been reported globally. Recently, a large number of reports have been published to discuss the possible roles of environmental factors in transmission of the novel coronavirus. They have focused especially on the impact of two air parameters, temperature and humidity, on the spread of SARS-CoV-2.

/pdf/do-humidity-and-temperature-impact-the-spread-of-the-novel-3mp1valph8.pdf

Do Humidity and Temperature Impact the Spread of the Novel Coronavirus

Highly pathogenic virus infections usually trigger cytokine storms, which may have adverse effects on vital organs and result in high mortalities. The two cytokines interleukin (IL)-4 and interferon (IFN)-γ play key roles in the generation and regulation of cytokine storms. However, it is still unclear whether the cytokine with the largest induction amplitude is the same under different virus infections. It is unknown which is the most critical and whether there are any mathematical formulas that can fit the changing rules of cytokines. Three coronaviruses (SARS-CoV, MERS-CoV, and SARS-CoV-2), three influenza viruses (2009H1N1, H5N1 and H7N9), Ebola virus, human immunodeficiency virus, dengue virus, Zika virus, West Nile virus, hepatitis B virus, hepatitis C virus, and enterovirus 71 were included in this analysis. We retrieved the cytokine fold change (FC), viral load, and clearance rate data from these highly pathogenic virus infections in humans and analyzed the correlations among them. Our analysis showed that interferon-inducible protein (IP)-10, IL-6, IL-8 and IL-17 are the most common cytokines with the largest induction amplitudes. Equations were obtained: the maximum induced cytokine (max) FC = IFN-γ FC × (IFN-γ FC/IL-4 FC) (if IFN-γ FC/IL-4 FC > 1); max FC = IL-4 FC (if IFN-γ FC/IL-4 FC < 1). For IFN-γ-inducible infections, 1.30 × log2 (IFN-γ FC) = log10 (viral load) - 2.48 - 2.83 × (clearance rate). The clinical relevance of cytokines and their antagonists is also discussed.

/pdf/quantification-of-cytokine-storms-during-virus-infections-5cag5u5zhh.pdf

Quantification of Cytokine Storms During Virus Infections.

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threatening hypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation-perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacements and ethanol-oxygen vapor therapy hypothetically) may be greatly helpful for reducing the occurrences of severe cases. Given that late mechanical ventilation may cause mucus (edema fluid) to be blown deep into the small airways, oxygen therapy should be given at the early stages. The optimal time and blood oxygen saturation (SpO2) threshold for oxygen therapy are also discussed.

https://www.mdpi.com/2073-4409/10/8/1897/pdf

The Role of Alveolar Edema in COVID-19.

Acute respiratory distress syndrome (ARDS) and the serious complications are the most frequent causes of death of SARS-CoV-2 infection. We bring out a hypothesis that early low-flow oxygen inhalation would maintain the hypoxic pulmonary vasoconstriction (an essential protection mechanism of the lung that optimize gas exchange) and accelerate the re-absorption of pulmonary edema fluid. The optimal time for oxygen therapy was analyzed and four comments are proposed: (1) Finger SpO2 should be measured at home simultaneously with the first-time nucleic acid test. (2) If the patient's SpO2 was lower than the reference value by 2% or more, it is suggested to be hospitalized immediately for standard low-flow oxygen inhalation. (3) If it was not possible to be admitted to hospital immediately, the patient is recommended to take oxygen in the home. (4) The Patients with low SpO2 are advised to use prone position as much as possible.

https://www.preprints.org/manuscript/202004.0360/v1/download

Early Oxygen Inhalation to Prevent SARS-CoV-2-Induced Acute Respiratory Distress Syndrome

The 2019 novel SARS-like coronavirus (SARS-CoV-2) entry depends on the host membrane serine protease TMPRSS2, which can be blocked by some clinically-proven drugs. Here we analyzed spatial relevance between glycosylation sequons and antibody epitopes and found that, different from SARS-CoV S, most high-surface-accessible epitopes of SARS-CoV-2 S are blocked by the glycosylation, and the optimal epitope with the highest surface accessibility is covered by the S1 cap. TMPRSS2 inhibitor treatments may prevent unmasking of this epitope and therefore prolong virus clearance and may induce antibody-dependent enhancement. Interestingly, a heparin-binding sequence immediately upstream of the S1/S2 cleavage site has been found in SARS-CoV-2 S but not in SARS-CoV S. Binding of SARS-CoV-2 with heparins may lead to exposure of S686, which then facilitates the S1/S2 cleavage, induces exposure of the optimal epitope, and therefore increases the antibody titres. A combination of heparin and vaccine (or convalescent serum) treatments thus is recommended.

/pdf/tmprss2-protease-inhibitors-may-prolong-but-heparins-2trwvsx6rh.pdf

Si-Cong Jiang

Papers

Do Humidity and Temperature Impact the Spread of the Novel Coronavirus

Quantification of Cytokine Storms During Virus Infections.

The Role of Alveolar Edema in COVID-19.

Early Oxygen Inhalation to Prevent SARS-CoV-2-Induced Acute Respiratory Distress Syndrome

TMPRSS2 Protease Inhibitors May Prolong But Heparins Accelerate SARS-CoV-2 Clearance