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SARS - CoV-2 , the computer virus that causes COVID-19 , may preferentially use a " back threshold " into cells to taint the brain , a new mouse study paint a picture .
The finding could partly explicate why many people haveneurological symptomssuch as fatigue , dizziness , brain fog , or loss of smell or gustatory perception during or after a bust with the virus . scientist think these symptoms may arise when SARS - CoV-2enters the cardinal nervous system of rules , but how and why the virus move from the respiratory tract to the brain was n’t clear until now .
A new study in mice shows that a mutation on the spike protein may help SARS-CoV-2 better infect the brain.
In an clause write Aug. 23 in the journalNature Microbiology , research worker discovered mutations inthe virus ’s spike protein , which it uses to enter human cells by hold to amolecule call ACE2on the cell ' surface .
" The SARS - CoV-2 spike protein coat the exterior of the virus and allows it to move into a electric cell , " study co - authorJudd Hultquist , an adjunct prof of infectious diseases at Northwestern University in Chicago , tell apart Live Science in an email . " unremarkably , the virus can enter the cell in two agency : either at the mobile phone surface ( through the front door ) or internally after it is take up into the cubicle ( through the back door ) . "
Part of the spike protein , called thefurin segmentation site , aid the virus inscribe through the front door . If this site is mutated or removed , the virus can only apply the backdoor route .
" Cells in the upper airways and lungs are extremely susceptible to SARS - CoV-2 , which can enter these cells through the front and back doors , " Hultquist said . " To reach and replicate successfully in the psyche , it seems like the virus has to enter through the back door . delete the furin cleavage site makes the virus more likely to employ this pathway — and more likely to taint brain cells . "
To study this , the research worker used genetically engineered shiner whose cells make human ACE2 . After infecting these mice with SARS - CoV-2 , they call for computer virus samples from lung and brain tissue paper and sequence the viral genomes .
" We found that mice infect with normal SARS - CoV-2 had some infection in the brain but that there were a mickle more septic cadre when the virus had a variation in the furin cleavage site , " Hultquist read . Although it ’s not yet possible to say whether these infected cellular phone are responsible for COVID-19 ’s neurological symptom , Hultquist and his workfellow saw gamey rates of contagion in cells of thehippocampusand premotor cortex , which are connect with memory and apparent motion , respectively .
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However , the study was done only in mouse , so more inquiry is need to determine out whether SARS - CoV-2 has similar requirements for infect the human mind .
" It is important to survey this report up with human sample to see if the same variation are found in human beings as in mice,“Matthew Frieman , a University of Maryland professor of microbiology and immunology who was not involve in the study , evidence Live Science . " As researchers target neuronal inflammation for therapy against longsighted - COVID symptom , understanding how the virus replicates there in the first place is of critical grandness . "
Hultquist also wants to do it more about why furin cleavage land site mutations make the computer virus more likely to enter the brain . " We show in the study that normal SARS - CoV-2 can replicate in the mind if it is direct inject , which suggests that departure of the furin cleavage site is crucial for travel to the brain , " Hultquist said . " How just this do work remains a enigma . "
Even so , this research could position the fundament for process the neurologic effects of COVID-19 .
" know that the virus needs the back room access to infect the brain provides unique opportunities to stop [ it ] , " Hultquist suppose . " Small molecules that block this nerve tract may be peculiarly efficient at forestall infection of the brain and the complications that arise . The next challenge will be to figure out not only which drugs may be best able-bodied to do this , but also which ones can get to the learning ability . "
