SARS-CoV-2, the virus responsible for COVID-19, can infect human neural progenitor cells and brain organoids. The findings back previous research, finding coronavirus can infect the human brain. Read More
Infection of non-neuronal supporting cells in the nose and forebrain may be responsible for the olfactory problems associated with COVID-19. Findings suggest olfactory sensory neurons are not vulnerable to coronavirus infection as they do not express ACE2. Read More
Cholesterol-lowering statins show promise for the treatment of severe coronavirus infections. Statins lowered the death rate and decreased the need for mechanical ventilation in patients hospitalized for severe COVID-19. Read More
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. Read More
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. Read More
Smoking increases the gene expression of ACE2, a protein that binds to SARS-CoV-2, increasing the risk of coronavirus infection. Findings suggest long-term smokers could have an increase of ACE2 in the lungs, leading to higher rates of morbidity in COVID-19 patients. Read More
From losing the sense of taste or smell to developing an increased risk of stroke, researchers investigate both the known and potential long-term implications of COVID-19 infection in the brain. Read More
ACE2 and TMPRSS2, two proteins required for SARS-CoV-2 entry, are produced in cells in the nasal cavity that contribute to odor detection. The findings may explain why people with coronavirus often describe the loss of the sense of smell as a symptom of the virus. Read More
Men have higher concentrations of ACE2 in their blood than women. As ACE2 enables coronavirus to infect cells, the findings may explain why men are more susceptible to COVID-19 infection than women. Read More
SARS-CoV-2, the virus that causes COVID-19, can infect intestinal cells and multiple in the gastrointestinal system. When researchers added SARS-CoV-2 to intestinal organoids, they noticed rapid infection. Researchers say in addition to nasal and throat swabs, rectal swabs and stool samples could be key for coronavirus testing. Read More
Smoking remodels the gene expression of lung cells so that the ACE2 gene is more highly expressed in goblet cells. The effects of smoking on ACE2 pulmonary expression indicates an increase in the overall entry points for coronavirus and increases the risk for viral binding and entry of COVID-19 into the lungs. Read More
Males who contract COVID-19 have 2.5 times the death rate of women. Being males is a significant risk factor for worse disease severity, regardless of age. Researchers found a similar trend in data from the 2003 SARS outbreak. The study speculates the reason why males are more prone to negative outcomes of coronavirus is due to levels of ACE2, which is significantly higher in males than females. Read More
