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.
SARS_CoV_2, the virus responsible for COVID-19, can directly enter the nervous system. The virus can infect the brain, causing alterations in blood vessels and directly disrupt oxygen supply to the organ.
MIT researchers have identified a protein fragment that may inhibit COVID-19's ability to enter human lung cells. The new peptide can bind to the viral protein and potentially disarm it.
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.
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.
Some viral infections could increase intercellular spreading of protein aggregates associated with neurodegenerative disorders, increasing the risk for developing Alzheimer's, Parkinson's, and other neurodegenerative diseases.
A new study seeks to explain why men infected by coronavirus generally show more severe symptoms and have an increased risk of death over women. Focusing on ACE2 receptors, researchers found the testes, along with the lungs and kidneys, were among areas of the body with the highest ACE2 expression. ACE2 could not be detected in ovarian tissue. The findings back up a previous study that reported male COVID-19 patients experienced impaired testicular function. This suggests the testes may be significantly affected when men develop coronavirus.
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.
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.
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.
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.
Researchers confirm ACE inhibitors and ARBS medications may increase the risk of patients with COVID-19 developing more severe symptoms.
