K, it's Saturday evening and I am tired of working. So how about a little light history. I've seen some speculation as to the origin of Moderna's name. People have gotten close, but I haven't seen anyone quite get it right. On this, I admit to a bit of insider info.
My friend Derrick Rossi is the original founder of the company, and his wife was the one who came up with the name--it is a play on 'modified RNA.' Derrick (who exited from Moderna years ago) is a stem cell biologist, not an immunologist. This began when his lab wanted to find a
better way to make induced pluripotent stem cells. These are somatic cells that are reprogrammed with transcription factors to become like an embryonic stem cell. At the time, people were doing this with retroviruses, which integrate into host DNA. He explicitly wanted to avoid
these remnants, and thought, hey, why not just transfect RNA which can't go backwards? Well, as immunologists know, synthetic RNA differs from normal mRNA and triggers host sensors like RIG-I. It kills the cells and triggers a huge IFN response. The proteins never get made.
So what Derrick's group did was modify the nucleosides to make the mRNA a bit more 'normal' and avoid these sensors. Thus, Mod(ified)RNA. It isn't perfect, so you still get some pattern recognition receptors triggered. But that is actually a perfect adjuvant for vaccines.
This is his original paper that started it: sciencedirect.com/science/articl…
And some history of how Derrick knew what specific mRNA modifications to make. Important work by UPenn scientists.

h/t @g_d_williams

statnews.com/2020/11/10/the…

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More from @deeptabhattacha

23 Nov
Two questions on vaccine efficacy keep coming up: 1) How long will immunity last? 2) Will it limit overall infections/transmission, and not just symptomatic disease? Q1 is exactly what my lab works on, but is tough to know (thread later). So on to Q2…
In macaque challenges pneumonia was prevented, but infections still occurred. I am going to pretend I'm a Vegas oddsmaker and take you through my (possibly incorrect) logic on why the macaque data likely underestimates efficacy against overall infections. biorxiv.org/content/10.110…
This article by @KatherineJWu explains the issue nicely. Infections start in the upper respiratory tract, which is protected by a mucus and epithelial cell layer. The barrier goes both ways--it limits things from getting in...nytimes.com/2020/07/14/hea….
Read 13 tweets
1 Nov
I received this email from someone last week that I can't stop thinking about. I probably received this since I have been openly optimistic about vaccine efforts. So I wanted to explain exactly why I am glass half-full.
Many of the grim posts about predicted efficacy (only 50%) have used the flu vaccine as a comparison. But as with many aspects of the pandemic (e.g. IFR, transmission), flu is not a very informative prior for vaccines without some major adjustments.
To be considered effective, the flu vaccine has to protect against symptomatic disease by *any* flu strain, whether it is in the vaccine or not. There are usually at least 4 circulating flu strains and sometimes the vaccine doesn't match one or more strains. That's a big ask...
Read 11 tweets
27 Oct
Brief explanation of the difference between methods of the ICL/REACT study and the many longitudinal studies I have cited before. These studies below, including ours, followed individuals over time to quantify antibody levels and decay
The ICL work is a yes/no population study to check the frequency of people with antibodies. For these types of tests, a strict cutoff is used to minimize the number of false positives (telling someone they have antibodies when they don't). This comes at a cost of telling...
some people they don't have antibodies when they do. Lesser of two evils. But for this reason, seroprevalence studies aren't ideal for quantifying the duration
of antibody production. Consider the graph below of a stereotypical antibody response, with range of outcomes in gray Image
Read 5 tweets
31 Aug
I've been reading the discussion on re-infection events, with some now arguing that this is not rare. This is being interpreted at the extremes that protective immunity is not possible. In this thread, I am going to argue that re-infections are rare based on data so far.
First, let's look at our toolbox on how re-infections can be measured w/o sequencing everyone. This Herculean paper on common coronas medrxiv.org/content/10.110… uses Ab responses as surrogates for re-infection. You will see that in the top row, there are periodic spikes in Abs... Image
This means that a person has been productively infected by a same or similar virus, and the immune system revs up again with new Abs. Keep in mind that these data are for common cold-causing coronaviruses, not SARS-CoV-2. However, we now have a dozen+ reports on serology...
Read 9 tweets

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