Second ‘key’ used by the SARS-CoV-2

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  • Sun, Oct 25, 2020 - 12:26pm

    #1
    The Finn

    The Finn

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    Second ‘key’ used by the SARS-CoV-2

Open Ses­ame! Re­search­ers dis­covered the second ‘key’ used by the SARS-CoV-2 virus to enter into hu­man cells

https://www.helsinki.fi/en/news/health-news/open-sesame-researchers-discovered-the-second-key-used-by-the-sars-cov-2-virus-to-enter-into-human-cells

To efficiently infect human cells, SARS-CoV-2, the virus that causes COVID-19, is able to use a receptor called Neuropilin-1, which is very abundant in many human tissues including the respiratory tract, blood vessels and neurons. The breakthrough discovery was made by a German-Finnish team of researchers led by neuroscientists Mika Simons, Technical University of Munich, Germany and virologist Giuseppe Balistreri, Faculty of Biological and Environmental Sciences, University of Helsinki, Finland.

 

  • Tue, Oct 27, 2020 - 03:38pm

    #2

    000

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    I can now stop looking for dead mice.

There has been an increasing number of patients who have been suffering from a weird condition after a brush with COVID-19: parosmia – a lingering, foul-smelling scent almost everywhere.

https://www.sciencetimes.com/articles/27750/20201018/parosmia-foul-smelling-effect-covid-19.htm

  • Thu, Oct 29, 2020 - 08:49am

    #3
    tbp

    tbp

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    Neuropilin; parosmia

Regarding neuropilin-1, this one was already known, it seems there’s nothing new here, except maybe this:

“We could determine that neuropilin-1, at least under the conditions of our experiments, promotes transport into the brain, but we cannot make any conclusion whether this is also true for SARS-CoV-2. It is very likely that this pathway is suppressed by the immune system in most patients”, Simons says.

They even seem to backtrack a bit from previous studies:

Neuropilin-1 facilitates SARS-CoV-2 cell entry and provides a possible pathway into the central nervous system [June]

Here, we found that the cellular receptor neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, which was inhibited by a monoclonal blocking antibody against the extracellular b1b2 domain of NRP1. NRP1 is abundantly expressed in the respiratory and olfactory epithelium, with highest expression in endothelial cells and in the epithelial cells facing the nasal cavity. Neuropathological analysis of human COVID-19 autopsies revealed SARS-CoV-2 infected NRP1-positive cells in the olfactory epithelium and bulb. In the olfactory bulb infection was detected particularly within NRP1-positive endothelial cells of small capillaries and medium-sized vessels. Studies in mice demonstrated, after intranasal application, NRP1-mediated transport of virus-sized particles into the central nervous system. Thus, NRP1 could explain the enhanced tropism and spreading of SARS-CoV-2.

As for the parosmia, as with anosmia (loss of sense of smell), as the article points out, it’s not unique: “Patel tells the Smithsonian that there are a number of viruses that can cause this condition aside from coronaviruses, like rhinoviruses and influenza viruses.”

What causes it though, I’m still not sure. One factor is NRP1 or ACE2 smell/taste-related cell destruction and slow regeneration, and another is zinc deficiency effects lasting longer than you’d except. The complex biochemical processes involved in the sense of smell and taste can take a long time to regenerate, it seems.

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