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.
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.
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.
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.
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.
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.
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, 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.
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.
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.
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.