TWiV 690: This is your brain on SARS-CoV-2

December 6, 2020

TWiV reviews the difficulties in predicting species susceptibility to SARS-CoV-2 infection by only examining the ACE2 protein, and the olfactory mucosa as a portal of entry into the central nervous system in COVID-19 patients.

Hosts: Vincent Racaniello, Dickson Despommier, Alan Dove, and Rich Condit

Guest: Amy Rosenfeld

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Intro music is by Ronald Jenkees

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5 comments on “TWiV 690: This is your brain on SARS-CoV-2

  1. Make Amy a permanent member of the TWiV crew, if she wants to and can.

  2. The CNS includes the spinal cord… just saying.

    ACE2 receptors are not as prevalent on the axon or dendrites but present I think. I will have to relisten but I think there was confusion on that.

    Here is a PubMed link with some helpful info as well…,SARS%2DCoV%2D2%20infection.

    I’d offer a wild guess (as a reader and listener not a scientist) that the speed of the neural firing is affected here wrt brain fog, arrhythmia, and even anosmia (with the clearly compromised epithelial cells) and not the connectivity. The brain issues with CoVid 19 are curious … I’d like to here this paper in TWiN.

    • Hmm… I’ve read more on this including the work referenced by Amy by Laura Pelegrini and Madeline Lancaster (“SARS-CoV-2 Infects the Brain Choroid Plexus and Disrupts the Blood-CSF Barrier in Human Brain Organoids”:

      Hmm… neuron to neuron transmission is not likely if present. I’m very much more inclined to read on to the epithelial barriers in and around the brain.

      I’m still interested in CoVid19 patients with hypertension. I would very much like to know if the neural symptoms are more prevalent in these patients. I’m not sure what that would mean, what the impact of ACE2 inhibitors would be in these patients or for that matter how the CNS is affected here.

      I’m wondering if CSF can be sampled post mortem and if so why this study didn’t do that.

  3. Janet Dec 10, 2020

    CNS effects may be via olfactory bulb, as found with S Pyogenes

    I know: recurrent bacterial infection (and mice)- but this sort of infection also has asymptomatic carriers/spreaders so here too the pathology is determined by the beholder of the antigen, I guess.

    It also makes me think of Kleine-Levin Syndrome which is a more-or-less stuporous state occurring in episodes which often follow infections/stressful events…unknown aetiology but some hypothesise an auto-immune/-inlammatory mechanism as in narcolepsy

    So CNS effects of bacterial and viral infections without viraemia or neurotropism could be through auto-immune/autoinflammatory mechanisms.
    Maybe something like this-concurrent or consecutive infections- would also explain some variation in severity of Covid 19.
    I think it is one possible mechanism of CNS effects for a significant minority of people and maybe swabbing for GAS could be helpful. I know Dr Griffin reminds us of pointlessness of antibiotics in therapy of Covid 19 itself but preventing auto-immune sequalae would be worthwhile if so.
    Maybe somebody could collect the data on Covid 19 patients who also received antibiotics to see if it modulates either long-term Covid 19 or new autoimmune disease-including new psychiatric disorder- diagnoses e.g:

  4. Janet Dec 11, 2020
    Cardiac surgeon with transplantexpertise theorises molecular mimicry leading to myocarditis- perhaps there is also a similar mechanism to neurological symptoms and long-term covid 19?
    Are the mRNA platforms more or less likely to lead to this sort of thing? What effect would separating the exposure to spike protein presence from whole virus in time and space (when eventual exposure to viral infection occurs) have on the likelihood of this hypothesised auto-immune/-inflammatory outcome? Too soon to tell. I worry about bystander activation and misidentification of self-proteins as potentially pathological due to immune activation without whole virus presence. I am not sure we can guarantee such a finely tuned and highly selective immune response, limited only to the spike on APCs…
    Were people with autoimmune disorders and atopy/CFS excluded from the trials ?
    The two cases of anaphylaxis so far in the UK healthcare workers rollout has lead to those with history of anaphylaxis being excluded from now on.