Study reports SARS-CoV-2, the virus that causes COVID-19, was well suited to making the jump from animals to humans by shapeshifting as it gained the ability to infect human cells. The virus's ability to infect humans occurred via exchanging gene fragments from a coronavirus that infected pangolins. The species-to-species transmission was a result of the ability of SARS-CoV-2 to bind to host cells through alterations to its genetic material.
Researchers have identified 6,822 mutations of SARS-CoV-2 across a global dataset. 273 mutations have occurred repeatedly and independently. Of those, researchers investigated 31 mutations that have occurred at least ten times during the current pandemic. They found no evidence that any of the common mutations are increasing the ability of the virus to be transmitted. Some common mutations are neutral, but most are mildly detrimental to the virus. New evidence also suggests the viral spike protein, D614G, is not associated with increased viral transmission.
Researchers isolated live SARS-CoV-2, the virus responsible for COVID-19, from the feces of patients who died as a result of coronavirus infection. Antigens to the virus were also found in post-mortem gastrointestinal surface cells. Isolating the live virus from fecal matter indicates evidence of the infectious virus in feces is a common manifestation of COVID-19. Researchers also found SARS-CoV-2 RNA on surfaces and bedding samples in hotel rooms used by two presymptomatic people who were later diagnosed with COVID-19.
MicroRNAs that should attack SARS-CoV-2, the virus that causes COVID-19, diminish with age, and due to chronic health problems. The findings shed light on why those who are older, and those with health conditions are more susceptible to coronavirus.
The ability to extinguish fear memories may rely on the flexibility of a person's DNA.
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.
Researchers have identified the structural basis for SARS-CoV-2 inhibition by the drug Remdesivir. The findings reveal a potential binding pattern that offers support for the design of new, more efficient, and specific anti-COVID-19 drugs.
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.
Long non-coding RNAs (lncRNAs) are significantly altered in depression in both sex and brain site-specific manners. The LINC00473 gene is downregulated in the prefrontal cortex of depressed females, but not males. Findings reveal the role of LINC00473 in sex-specific depression and may explain why females are more vulnerable to depressive symptoms than males.
Remdesivir, a drug initially developed to fight Ebola and currently being fast-tracked into trials for COVID-19, is highly effective at stopping the replication mechanism of coronavirus. The drug tricks the virus by mimicking its building blocks, causing the inhibitor to get incorporated repeatedly, and preventing replication of SARS-CoV-2.
Newly discovered modifications of the coronavirus RNA offers clues for combatting COVID-19. The findings also shed light on the lifecycle of the SARS-CoV-2 virus.
Researchers identify genetic variations in the prefrontal cortex during different stages of development to assess how psychiatric conditions, such as autism and schizophrenia, may arise in individuals.