Coronavirus expert Christian Drosten joins Vincent to provide a view from Germany on COVID-19 and SARS-CoV-2.
Host: Vincent Racaniello
Guest: Christian Drosten
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Links for this episode
- Das Coronavirus podcast 1:00
- Identification of SARS-CoV in Germany (NEJM) 3:13
- 29 nt deletion in genome of SARS-CoV (Sci Rep) 34:20
- 382 nt deletion in genome of SARS-CoV-2 (bioRxiv) 38:00
- Virological assessment of COVID-19 patients (Nature) 26:29
- Timestamps by Jolene. Thanks!
Intro music is by Ronald Jenkees.
Send your virology questions and comments to email@example.com
Update there are now claims that Vitamin C could be used to Treat COVID-19
With the 2019 novel coronavirus (2019-nCoV) outbreak now spreading across the world, people are seeking ways in which to potentially protect themselves from the virus or to alleviate its effects once caught. One such means that is being touted online and in the media is vitamin C.
Vitamin C is best known for its antioxidant properties, being able to scavenge damaging reactive oxygen species, thus protecting the body’s cells and tissues from oxidative damage and dysfunction. However, the vitamin also has numerous other important functions within the body, many of which are known to support healthy immune function. During infection, vitamin C levels can become depleted and a person’s requirement for vitamin C increases with the severity of the infection . In severe cases, this may require intravenous administration of gram doses in order to achieve high enough levels in the body to compensate for the enhanced turnover of the vitamin.
As of February 2020, the clinical characteristics of patients hospitalized with COVID-19-related pneumonia indicated that 26% were transferred to the ICU because of complications such as ARDS and shock . A recently published RCT carried out in the USA in 167 patients with sepsis-related ARDS indicated that administration of ~ 15 g/day of IV vitamin C for 4 days may decrease mortality in these patients . An earlier IV vitamin C trial of patients admitted to the ICU with pneumonia included hydrocortisone administration , however, systemic corticosteroid treatment has not been shown to have significant benefits in patients with COVID-19 .
Just recently registered on clincialtrials.gov (Identifier: NCT04264533), a new clinical trial to investigate vitamin C infusion for the treatment of severe 2019-nCoV infected pneumonia has begun in Wuhan, China. This is one of the first RCTs to test the effects of IV vitamin C in patients infected with this virus. In this trial, the investigators will treat 140 patients with a placebo control or intravenous vitamin C at a dose of 24 g/day for 7 days. They will assess requirements for mechanical ventilation and vasopressor drugs, organ failure scores, ICU length of stay and 28-day mortality.
I was reading about the Minimal Infectious Dose (MID), the dose of virus that is not snuffed out by the innate immunity and develops into an infection, but clearly the number is all over the map. It’s like if you try to calculate average wealth by asking random people in the streets of Seattle how much they are worth and you run into Bill Gates — with him in the tally your number will be useless.
But what about *individual* MID for SARS-Cov-2? Would an immunocompromised person need fewer virus particles to get infected than a 20-something who is strong like an ox and eats a dozen cloves of garlic every day? I imagine it varies even for the same individual — they are weaker if they have not slept or if they drank alcohol. But is there still a concept of individual MID (probably a range since probability plays a role, maybe even at a quantum level) which applies to a given person at a given time, for a given virus?
If so, what if that person were first administered an extremely low dose of the coronavirus, and then after a few days (in quarantine) checked for infection, then administered a higher dose and so on, until their innate immunity can’t take out all of the virus anymore and they develop an infection. Would it be reasonable to assume it would turn to be a mild disease? Would their adaptive immunity learn to defend against the virus? Would that protect them if they receive a higher dose in the wild? Is there possibly some regimen (sleep, nutrition, supplements, drugs) that could keep the infection level stable — low but still persistent enough for the antibodies to develop?
It’s something like an iterative live virus vaccine. I imagine the answer to some of those questions would be “no” or “we don’t know” or “it’s unknowable” for the same reason it’s hard to control a fire, but I have a feeling it would be very educational to hear experts discuss it.
I didn’t say how much I love your videos and podcasts because I think by now you know we do.
What do you think about this article talking about “brain infections” with SARS COV2? Not sure if the neurons express the ACE2 receptor or weather this is just part of the cytokine storm?
Thanks for all the great information!
you guys used some abbreviations that I had not idea what they are. If I understood correctly, the virus trasmits because of its high levels in the throat esp. through days 1-5 after onset of symptoms. What data do we have for pre-symptomatic or asymptomatic tranmission though? I didn’t understand. He said that transmission through surfaces is not as considerable. So do asymptomatic and symptomatic individuals transmit to the same degree? Can we ask him when he “comes back”? I hope he does. this was great!
Yes, he mentioned in his German podcast from today that a study done in Italy (I believe the city Vo), that A) 40% seemed to have been asymptomatic B) viral load was basically the same in symptomatic and asymptomatic and c) (maybe different study) viral load was highest one day before onset of symptoms) don’t quite me…;) Going back to the Go study may be the best bet
when I listened I had thought Drosten were probably wrong about the containment and it went
to Italy and >50% of the world just from that Shanghai-woman via Webasto/Munich.
But I checked again …
@c_drosten , Apr 13 … sequences from Germany … https://civnb.info/sequences/
and someone had anonymously leaked the semi-secret GISAID-mutations until mid-March (thanks a lot)
And then I read the Vo-paper.
@cmyeaton [Vo-paper] … full of interesting results…. [compare with Drosten’s Munich cluster]
The 3 Shanghai-Webasto mutations are C00241T,C03037T,A23403G.
Then somewhere,somehow C14408T joined the 3 and is now seen everywhere.
Italy Feb19;France Feb20,NL,CH,I Feb23;D-BW,Brazil,Finland,Spain Feb24,England,Ireland Feb25
Maybe some other airplane from Shanghai with a C14408T superspreader.
They really should have checked all these airplane contacts including the Shanghai-Webasto flight.
They should also have asked in Vo about fever+cough in Jan or China/Germany travel history
btw. I just saw this : [add to the Drosten immune podcasts]
@florian_krammer Excellent review of human immune responses to coronaviruses!
The best one I found so far. I already cited it https://medrxiv.org/content/10.110