After natural killer immune cells kill virus-infected cells, T and B immune cells produce cytokines. This makes the immune reaction stronger and results in the cytokine storm associated with severe COVID-19 infection.
People with the Alzheimer's associated ApoE e4e4 gene have increased vulnerability to developing severe symptoms of COVID-19 if they become infected with the virus. Findings suggest those with the dementia-related gene have double the risk of developing severe coronavirus symptoms compared to those who those with the common e3e3 form of the APOE gene.
Researchers have identified 6,822 mutations of SARS-CoV-2 across a global dataset. 273 mutations have occurred repeatedly and independently. Of those, researchers investigated 31 mutations that have occurred at least ten times during the current pandemic. They found no evidence that any of the common mutations are increasing the ability of the virus to be transmitted. Some common mutations are neutral, but most are mildly detrimental to the virus. New evidence also suggests the viral spike protein, D614G, is not associated with increased viral transmission.
Researchers isolated live SARS-CoV-2, the virus responsible for COVID-19, from the feces of patients who died as a result of coronavirus infection. Antigens to the virus were also found in post-mortem gastrointestinal surface cells. Isolating the live virus from fecal matter indicates evidence of the infectious virus in feces is a common manifestation of COVID-19. Researchers also found SARS-CoV-2 RNA on surfaces and bedding samples in hotel rooms used by two presymptomatic people who were later diagnosed with COVID-19.
Treating coronavirus patients with alpha-blockers may help prevent the cytokine storm associated with severe COVID-19 infection. Alpha-blockers interfere with the cell signaling that triggers cytokine storms. Mice with bacterial infections that were treated with alpha-blockers experienced reduced cytokine storms and decreased death rates.
Coronavirus patients treated with chloroquine or hydroxychloroquine are significantly more likely to experience ventricular arrhythmias than those who were treated with other medications. The study also revealed that out of 100,000 COVID-19 patients who were hospitalized, the 15,000 who received hydroxychloroquine were more likely to have worse health outcomes than those treated with other drugs.
The placentas of sixteen women who contracted COVID-19 during pregnancy showed evidence of significant injury, a new study reports. The placental injuries were consistent with abnormal blood flow between mother and baby in-utero, suggesting another complication of coronavirus infection in pregnant women.
SARS-CoV-2, the virus responsible for COVID-19, enters human cells by attaching to ACE2 and utilizing TMPRSS2. Drugs that block ACE2 or inhibit the enzyme could help treat the coronavirus, but only during early infection. As the infection progresses, SARS-CoV-2 becomes engulfed in human cells, reducing the number of ACE2 receptors on a cell and leading to an increase of angiotensin II in the blood. Angiotensin II triggers an inflammatory pathway, providing a positive feedback cycle, named IL-6 amplifier, resulting in excessive immune activation and the cytokine storm associated with severe COVID-19.
A new study reveals the recommended 6 foot of distance to help prevent the transmission of COVID-19 may not be enough. Researchers report that even with a slight breeze of 4 KPH, saliva and cough droplets travel 18 feet per 5 seconds.
The current national death rate among those infected with coronavirus is 1.3%. The comparable rate of death for seasonal flu is 0.1%. The study estimates that if the same number of people are infected with COVID-19 by the end of the year as are infected with flu, roughly 33.5 million people in 20018-19, almost 500,000 people will die as a result of coronavirus infection. However, COVID-19 is more infectious than the seasonal flu. Current conservative estimates suggest 20% of the US population will be infected by the end of 2020, leading to a possible 1.2 million deaths.
Interferon-a2b an antiviral treatment shows promise in helping to speed up the recovery of patients with severe COVID-19 infections. IFN-a2b improves viral clearance and decreases the levels of inflammatory markers in coronavirus patients.
S309, a neutralizing antibody first identified in blood samples from a patient who recovered from SARS in 2003, shows promise for the treatment of COVID-19.