There aren’t a lot of silver linings to the pandemic.
One of them, from my eyes, is learning the speed at which the scientific community can progress when highly focused on a problem. Remarkably, we invented, tested, began manufacturing and distributing multiple very safe and effective coronavirus vaccines in under 12 months. It is wildly impressive that we did this. Yay, science!
But that speed also means that my articles from recent weeks need a bit of an update, because we’re learning so much so fast. In particular, I’ve written about three topics that I wanted to share the latest info about:
• How quickly will vaccine manufacturing ramp up and when can you get one?
• What impact will the new coronavirus variants have on the pandemic?
• How much can you still spread COVID-19 even if you’ve been vaccinated?
Let’s dive in.
To recap, I created some models to help identify when the general public in Utah may get the vaccine and I was able to narrow it down to somewhere between early April to mid-June depending on how optimistic we wanted to get.
On this front, I have mostly good news to report.
First, we’ve been able to distribute more of the coronavirus vaccine more quickly than I expected. In particular, Utah being able to get back unused vaccine from a few pharmacies added thousands of extra doses I didn’t account for, and some second doses that we were holding back earlier in the pandemic went in arms instead.
The result is that we are vaccinating more people sooner. Last week, we were able to use 100,000 doses, whereas my earlier models didn’t have that happening until next week. Instead, next week, Utah is slated to receive about 108,000 doses from the federal government.
Getting shots in 100,000 arms so soon does mean that those people will need second doses more quickly than expected, so expanding availability will be key.
And in this arena, the news is a little more wishy-washy. The good news is that Moderna announced it would deliver 100 million doses by the end of March and 100 million more by the end of May to the federal government, matching Pfizer’s accelerated timeline. These companies are exceeding their delivery contracts, which means they should meet the pace of my most optimistic model and Gov. Spencer Cox’s optimistic projections.
On the other hand, the Johnson and Johnson vaccine will only have a few million vaccines manufactured and ready to go when the federal government gives the company the go ahead, which should happen in the next couple of weeks. That authorization is a bit delayed; the company would need to pump out a few million vaccines per week in order to meet Cox’s announced projections of 33,000 J&J doses per week to Utahns by the end of February. My “average” model, which projected 50% of that number, might be more accurate with regards to this vaccine.
Still, with the overall good news, we’ve been able to open up vaccine availability to more groups, sooner. Cox even announced Thursday that appointments would be immediately available for those between 65 and 69, about 10 days before they were originally slated to open March 1. On that date, any adult of any age with a qualifying preexisting condition will be able to be vaccinated.
Who gets the vaccine next?
Utahns with certain severe and chronic health conditions, will be eligible to receive the COVID-19 vaccine on March 1. Here is a list of those qualifying health conditions, according to the Utah Department of Health:
• Solid organ transplant recipients.
• Certain cancers.
• People who are immunocompromised (have a weakened immune system) from blood, bone marrow or organ transplants; HIV; use of corticosteroids long-term, or use of other immune-weakening medicines long-term.
• Severe kidney disease or dialysis, or with stage 4 or 5 chronic kidney disease.
• Uncontrolled diabetes.
• Severe obesity (body mass index over 40).
• Chronic liver disease, including chronic hepatitis B or C.
• Chronic heart disease (not including hypertension).
• Severe chronic respiratory disease (other than asthma).
• Neurologic conditions that impair respiratory function, including Down syndrome, multiple sclerosis, Parkinson’s disease, cerebral palsy, quadriplegia or hemiplegia.
• Stroke and dementia (Alzheimer’s, vascular, frontotemporal).
• Asplenia, including splenectomy or a spleen dysfunction, including sickle cell disease.
After that? Well, that hasn’t been announced. Utah leaders could open it up to 55+, but I wouldn’t be surprised to see the governor just open the doors to everyone. Either way, we’re talking about realistic vaccine availability to the general public quite soon. I might bet on April for the first general public appointments, with everyone being able to schedule one in May.
Of course, we want to know if the vaccines will actually work on the new variants spreading among us. My original article focused on the variant that started in the United Kingdom labeled B.1.1.7, but now we’re getting a greater understanding of all of the ways the coronavirus has mutated.
These variants, all mutating in different people in different places, have developed some of the same changes to the coronavirus structure. Those changes — and the epidemiological record confirms this — mean that the virus benefits from mutating in these specific ways. In other words, these variants spread more quickly than what we’ll call “coronavirus classic” in a mostly unvaccinated population.
There are two families of variants you should know about.
• The B.1.1.7 variant is the U.K. variant. It is now spreading in the U.S. in a major way, doubling cases every 10 days and is definitely spreading in Utah. U.S. evidence shows it’s between 35% and 45% more likely to be spread than standard coronavirus. U.K. evidence also showed it’s likely to have a higher risk of death than the regular virus.
The good B.1.1.7 news is that the vaccines still seem to work well against it. Effectiveness might be impacted by just a few percentage points.
• The B.1.351 variant started in South Africa, and is pretty similar to the P.1 variant, which was discovered in Brazil. This group is more worrisome because studies showed that the Oxford/AstraZeneca vaccine didn’t work as well against them. In fact, South Africa stopped vaccinating people while it figured out what was going on. So far, we’ve seen B.1.351 and P.1 in a combined 12 U.S. states, but not in Utah — yet.
But as we know, the Oxford vaccine is less effective than the two mRNA vaccines we have in the U.S. One study compared how the Moderna and Pfizer vaccines performed against the two variants in a lab.
In the middle of each graph is a common form of coronavirus classic, while the left and right show how many antibodies were generated when the two vaccines were used against the two variants. As you can see, the U.K. variant antibodies saw a small decrease, but the South African antibodies decreased much more significantly.
Still, even these decreased antibody amounts will be more helpful than nothing. Notice the scale in the charts — antibody creation is being cut significantly, but not knocked out entirely. T-cells should still be created, too. In other words, the vaccines we have right now still will provide some good protection against this variant.
The other cool thing about the mRNA vaccine technology is that it should be easily editable. If we want to create a version of the Pfizer or Moderna vaccines that specifically target this, or any other coronavirus variant, we can just change the mRNA used while keeping the rest of the recipe the same. That wouldn’t impact the safety of the vaccine at all, so we could skip some of the lengthy trial periods.
In the coming weeks, we’ll get a better idea if we need to do that. Studies are ongoing for the U.S. vaccines against the South African variant in more human subjects. If it’s still around 90% effective, we probably won’t have to change much. If it’s around 50%, it’s time to develop a new recipe, and might mean booster shots for the new variants would be required — similar to how we get a yearly flu shot.
Vaccines and transmissibility
Because the vaccines were tested for their effectiveness in tamping down disease in an individual, we didn’t really know how much they would prevent the coronavirus from being spread from person to person. That meant we had to do some guessing with preliminary data.
But now, we’re getting more evidence that transmission is significantly down among the vaccinated. What’s going on in Israel is perhaps the best example: over half of the population has been vaccinated with the Pfizer vaccine, and that country is starting to see real decreases in transmission.
Those vaccinated are in a great spot. Of the 416,900 people that Maccabi Healthcare Services in Israel had vaccinated, only 254 picked up COVID-19 after the second dose. All 254 cases were mild, too.
But it appears that those hundreds of thousands of healthy people aren’t spreading the virus as much, either. Cases dropped 41% in a six-week period, even among the non-vaccinated.
Even better, a new study this week looked at how Israelis were impacted after just the first dose, not having yet received the second. And in the 12-28 day period after getting the first dose, even those who were infected had significantly less viral load in their respiratory system, about four times less. That means they’re going to be less effective at spreading the virus.
Between this and the preliminary data that showed a 63% reduction in asymptomatic infections in Moderna’s vaccine, we have a pretty good idea now: The U.S. vaccines definitely reduce transmissibility. It’s probably not 100%, as they appear to reduce severe disease, probably not 95%, as they appear to reduce mild disease, but very likely in the 60-90% range.
So to sum all of this up: We are getting people vaccinated quicker than originally planned, those vaccines appear to work against the variants or can be easily adjusted, and when you get vaccinated you are less likely to get someone else sick.
This definitely counts as progress.
Andy Larsen is a data columnist. He is also one of The Salt Lake Tribune’s Utah Jazz beat writers. You can reach him at firstname.lastname@example.org.