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.
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.
The receptor protein ACE2 and the TMPRSS2 protease that can activate SARS-CoV-2 entry are expressed in cells on the inner lining of the nose. Mucus producing goblet cells and ciliated cells in the nose have the highest levels of both proteins, making them the most likely initial infection route for coronavirus. Additional key entry points were found in the cells of the eye's cornea and the intestines. This suggests other points of infection could be via the tear ducts and through fecal-oral transmission.
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.
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.
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.
Using over a century of data from other pandemics, and applying knowledge about the current COVID-19 infection, researchers predict the long term effects coronavirus will have on the brain and nervous system.
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.
Researchers have mapped the interaction between SARS-CoV-2 proteins and human cells, showing which proteins are being activated and deactivated by coronavirus. The findings reveal how the virus can spread through the human body.
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.
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.
Researchers have identified specific cell types that appear to be the main targets of SARS-CoV-2, the virus that causes COVID-19. Using existing data on the RNA found in different types of cells, researchers were able to identify cells that expressed ACE2 and TMPRSS2, two proteins that assist coronavirus to enter human cells. Cells in the lungs, nasal passage and intestines appear to be the main targets for SARS-CoV-2.
