Researchers confirm ACE inhibitors and ARBS medications may increase the risk of patients with COVID-19 developing more severe symptoms.
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 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.
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.
Certain progenitor cells in the bronchi are mainly responsible for producing coronavirus receptors. These cells normally develop into respiratory tract sells linked with cilia, that clear bacteria out of the lungs.
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.
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.
Previous studies report COVID-19 may be present in the testes. Researchers report coronavirus is unlikely to spread via semen, and the chances of the infection being spread through sexual transmission are remote.
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.
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.
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.
