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Neurological phenotype induced by SARS-CoV-2 spike protein in neurons

Neurological phenotype induced by SARS-CoV-2 spike protein in neurons


In a recent study posted on Bio Rxiv*Preprint Server, Researchers Investigated Link to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) spike protein and neuronal burst activity.

Image credit: whitehoune/

study: SARS-CoV-2 spike protein reduces neuronal bursting activity measured by microelectrode arrayImage credit: whitehoune/

*Important Notices: Bio Rxiv We publish a non-peer-reviewed, preliminary scientific report and should not be viewed as conclusive, to guide clinical practice/health-related actions, or to be treated as established information.


The major components of the SARS-CoV-2 structure are the envelope (E), spike (S), membrane (M), and nucleocapsid (N) proteins. This study focuses on the effects of the S protein. The S protein facilitates virus attachment and entry into host cells. The S1 subunit interacts with the angiotensin-converting enzyme 2 (ACE2) receptor present in intestinal and lung cells.

Within the brain, ACE2 is expressed primarily in the brainstem and regions whose primary function is to regulate blood pressure and cardiovascular function. Although neurological signs have been documented in some but not all COVID-19 patients, the exact mechanism by which the virus affects nerve cells is still unknown and therefore the subject of investigation It is

About research

In the present study, researchers quantified the neurological phenotype induced in neurons by the SARS-CoV-2 S protein.

In this study, the S1 and S2 subunits of the spike protein were evaluated separately to determine whether they elicit neurological phenotypes putative by microelectrode arrays (MEA). On day zero, neurons obtained from newborn P1 mice were treated with recombinant SARS-CoV-2 S protein and S1 and S2 S2 subunits. The team evaluated the data using an in-house devised algorithm. Characteristics such as the number of bursts per electrode, their duration, frequency and the number of spikes per burst depending on the treatment condition were also quantified.

The team also determined whether the S1 subunit affected mature neurons during cell exposure. Neurons were treated with similar S1 concentrations on day 12. This was followed by exposure to the same S1 concentration for 7 consecutive days. The team then performed rescue experiments to see if this neuronal phenotype was reversible. Human monoclonal anti-S1 antibodies were sampled and neutralized using antibodies prior to administration of S1 to neurons on day 0. To test the hypothesis that the S1 receptor binding domain (RBD) may be responsible for the burst reduction, the team collected and evaluated purified recombinant His RBD.


In this study, the number of pulses per electrode was identified to be the most prominent feature that differentiated wells treated with spike protein from control wells. The S1 subunit significantly reduced the number of bursts per electrode, whereas the S2 subunit did not show a comparable reduction. This study suggests that S1 is responsible for the decreased bursting activity of neuronal populations when cells are exposed early in development. However, there was no discernible difference in bursting activity between S1-treated and control wells. Thus, the data indicated that the S1 subunit affected neurons only when the cells were exposed early in development.

Antibody-neutralized S1 did not result in a significant reduction in burst activity compared to controls, whereas conventional S1 treatment on day 0 reduced burst activity. The data and p-values ​​suggest that anti-S1 antibody reversed the effect of S1 on bursting activity. Overall, rescue experiments provided compelling evidence that S1 was able to suppress burst activity when exposed to cells early in development. Compared to S1 data, the team identified a significant reduction in surge activity. This result strongly suggests that the RBD itself is sufficient to suppress surge activity.


The results of this study demonstrate a causal link between the SARS-CoV-2 S1 protein and the in vitro bursting propensity in neuronal populations, which can be reversed by antibody treatment. The study also pointed out that RBD may be involved in the inhibition of nerve signals. This study also showed that neutralizing S1 restored neuronal discharge activity to control levels. Furthermore, antibody rescue experiments confirmed the role of S1 in suppressing burst activity, highlighting the protective function of anti-S1 antibodies and the importance of RBD in regulating neuronal phenotype.

The researchers believe that the results of this study provide new insights into the activities of the SARS-CoV-2 S protein beyond its well-established functions in viral attachment and entry. This finding may shed light on important aspects of SARS-CoV-2 infection, patient care methods, and future vaccine and antiviral development.

*Important Notices: Bio Rxiv We publish a non-peer-reviewed, preliminary scientific report and should not be viewed as conclusive, to guide clinical practice/health-related actions, or to be treated as established information.




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