A way to end the pandemic — an update

Back on 5 April I wrote a post suggesting that we might be able to end the current coronavirus pandemic by infecting people with a cocktail of the 4 coronaviruses known to cause the common cold.  That post appears verbatim after the *** , along with a comment from a follower and my reply.

In the most recent Science (https://science.sciencemag.org/content/368/6493/809) — Science  22 May 2020: Vol. 368, Issue 6493, pp. 809-810 the following appeared

” The La Jolla team studied stored blood samples collected between 2015 and 2018, well before the current pandemic began, and detected these cross-reactive helper T cells in about half of them. The researchers think these cells were likely triggered by past infection with one of the four human coronaviruses that cause colds; proteins in these viruses resemble those of SARS-CoV-2.”

This is exactly what I was hoping for by giving the cocktail.  So there is cross reactivity. The quoted material  was tantalizingly brief, so I’ve written the people in La Jolla for more information, but it’s Memorial Day tomorrow.

A degree of immunity, however small, may explain some of the confounding aspects of the epidemic. First off, based on the presence of antibodies to the pandemic coronavirus (SARS-CoV-19), well over 90% of people with them simply aren’t sick. Second, given that 33% of the people in the Bronx have these antibodies, why doesn’t everyone?  Surely the 67% of the Bronx population lacking the antibodies have come in contact with someone who was infected, yet in some way they were immune.  Third, given enough exposure for a long enough time just about everyone gets infected — see some of the horrible examples in the excellent website — https://www.erinbromage.com/post/the-risks-know-them-avoid-them.

Susceptibility to clinical illness due to SARS-CoV-19 might be analogous to susceptibility to epilepsy.  We know that given enough electrical stimulation, every brain will convulse (see electroconvulsive therapy — ECT). 2% of children and 1% of adults do have spontaneous convulsions (epilepsy). Differential susceptibility to electrically induced convuslions is exactly how Dilantin (phenytoin), one of the first anticonvulsants was discovered in 1938.  All sorts of compounds were thrown at hapless experimental animals, and the amount of electricity needed to convulse them was measured.  An animal given Dilantin required more.

It’s important to note that the Science article wasn’t talking about antibodies, but something else called cellular immunity.  Hopefully the folks in La Jolla will write back and I’ll have more for you on these points in the near future.

Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology

 

 

****

A way to end the pandemic

Could infecting people with the four or so coronaviruses that cause the common cold protect them against the new coronavirus causing the pandemic?   The official name for the new virus is SARS-CoV-2, the name for the disease is COVID-19.

“According to Marie-Louise Landry, MD, an infectious disease expert at Yale Medical School and the Director of the Yale Clinical Virology Laboratory, four common human coronaviruses cause 15-30% of common colds”

https://www.health.com/condition/infectious-diseases/coronavirus/coronavirus-symptoms-vs-cold

Now ask yourself how she could make a statement like this.  I’m going to try to get in touch with her tomorrow, but it is very likely that these cold causing coronaviruses are detected by measuring antibodies to them, carried in the blood of people who have been infected by them in the past.

Could one coronavirus (even a benign one) give partial immunity to others?  It’s possible and it’s time to find out.  We could know  in a few weeks.

Assume the test to measure the antibodies to cold coronaviruses exists.  Then measure them in our real, honest to God, modern day heroes on the front lines  — the nurses, docs, EMTs, orderlies, housekeeping, cops, etc. etc.  who are exposed every day to COVID-19.

Every hospital in the country could at least draw blood on them, look to see if antibodies are present and wait.   I doubt that many would refuse the test.

Sadly, it wouldn’t be long before some of them became infected with SARS-CoV-2.  Then investigators couldlook to see if those with the antibodies to the cold causing coronaviruses were protected.

If so, then make a cocktail of the 4 or so coronaviruses and give it to everyone.   It would be Edward Jenner and the cowpox all over again — https://en.wikipedia.org/wiki/Edward_Jenner

Even if the protection was only partial, decreasing the number of susceptible individuals would be enough to slow the pandemic and possibly even stop it.

  • loupgarous On April 18, 2020 at 12:32 am

    Not afraid of a dengue fever-type antibody-dependent enhancement problem?

Loupgarous: I’m not worried about this with the coronaviruses causing colds. People are worried about immune enhancement with vaccine development for dengue, SARS and RSV and now SARS-CoV-2 [ Proc. Natl. Acad. Sci. vol. 1176 pp. 8218 – 8221 ’20 ]. Immune enhancement definitely happens with clinical dengue (http://www.denguevirusnet.com/antibody-dependent-enhancement.html).

Why no worries? Because we’ve all had colds, lots of them, probably multiple ones with coronaviruses and no one has seen immune enhancement with colds (of any type). Naturally occurring cold causing coronaviruses are what I’d use if the experiment described in the post showed protection.

However, it is possible that such has happening with coronavirus caused colds, and we’ve been misdiagnosing it as influenza (which does kill a lot of people every year). This seems pretty remote.

Thanks for commenting. I really hadn’t considered this.

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Comments

  • Ashby  On May 25, 2020 at 9:22 pm

    I’ve been wondering about something that’s related to your idea. If you use cloning techniques to replace the spike protein of a common-cold coronavirus with the spike of the SARS-CoV-2 virus, do you get another nasty version of the SARS-CoV-2 virus, or do you get a mild cold virus with SARS-CoV-2 spikes that might generate antibodies to SARS-CoV-2. If it’s the latter, could you deliberately infect people with the recombinant common-cold virus to generate immunity to the SARS-CoV-2 virus?

    • luysii  On May 27, 2020 at 7:52 am

      Interesting idea. Whether it works or not depends on the 15 or so nonStructural proteins of SARS-CoV-2 and the cold viruses — are they the same or no?. Most of the SARS-CoV-2 genome codes tor these nonStructural proteins.

      I don’t know why it takes so long for comments to show up — yours was approved 2 days ago

  • Handles  On May 25, 2020 at 9:28 pm

    As I understand it, antibody-dependent enhancement occurs when immunity from previous exposure fades, and protective antibodies are diluted to sub-neutralising titres. I would modify your proposed experiment as follows:dont just measure presence or absence of antibodies in your frontline workers, but quantify them, and look at the rate of hospitalisation at various antibody titres. If people with few antibodies remaining suffer more serious disease on re-exposure, then you might suspect ADE.

    From reading https://smw.ch/article/doi/smw.2020.20249, immunity from cross-reactive antibodies fades more quickly than immunity from a primary infection, but I dont know if this is a general thing or just specific to Dengue. Exposure to one Dengue subtype gives you lifelong immunity to that subtype, and two months of cross-reactive immunity to the other 3 subtypes. As this fades over 2 years your chance of ADE and severe disease increases.

    So one hypothesis to explain why some people under 40 die from COVID-19 while others are asymptomatic, is that the unlucky ones were infected with a cold at just the right time in the past, and their cross-reactive immunity has faded. The first SARS virus with sub-neutralising levels of bound antibody can infect cells in vitro via Fcy receptor instead of ACE, which could lead to infection in intestinal epithelia, kidney, and endothelial cells where this receptor is expressed in high levels, matching some of the clinical outcomes (see same ref above).

    In my naive opinion your plan could work if the pandemic is stamped out, but might cause trouble under certain circumstances if the disease becomes endemic?

    • luysii  On May 26, 2020 at 10:52 am

      Handles: Quite reasonable. I hope to contact the La Jolla people later today. Even better would be to test the first responders for cellular immunity to SARS-CoV-2 as well as antibodies and see if they are resistant. This is more complicated, but it would tell us if cellular immunity to SARS-CoV-2 in people without antibodies to it (e.g. never infected) was protective.

  • PJ  On May 27, 2020 at 9:30 am

    > Second, given that 33% of the people in the Bronx have these antibodies, why doesn’t everyone?

    FYI: Currently, SARS-COV2 tests have around 30% sensitivity and specificity [1]. Yes, eeks.

    [1] internal numbers from German federal health departments.

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