On the menu today: unraveling those ominous claims that people can get reinfected with the coronavirus merely weeks or months after they think they’ve beaten it; the governor of Mississippi explains why he doesn’t think “herd immunity” is a realistic option, while some New York neighborhoods offer some eye-popping figures suggesting it may not be that far away; and the media praise the wrong Democratic governors.
What You Need to Know about Reinfection and Your Immune System
Yesterday brought two stories that seemed like just about the worst news we could get in this pandemic. First, the Guardian over in the U.K. reported on a study by King’s College London suggesting that after infection, coronavirus patients could lose their built-in immunity to reinfection fairly quickly:
Blood tests revealed that while 60 percent of people marshalled a “potent” antibody response at the height of their battle with the virus, only 17 percent retained the same potency three months later. Antibody levels fell as much as 23-fold over the period. In some cases, they became undetectable.
“People are producing a reasonable antibody response to the virus, but it’s waning over a short period of time and depending on how high your peak is, that determines how long the antibodies are staying around,” said Dr Katie Doores, lead author on the study at King’s College London.
Then, over in Vox, D. Clay Ackerly, an internal medicine and primary-care physician practicing in Washington, D.C., described a 50-year-old patient who tested positive, suffered the effects, tested negative twice, then tested positive again with more severe symptoms a second time, about six weeks later:
It is possible, but unlikely, that my patient had a single infection that lasted three months. Some Covid-19 patients (now dubbed “long haulers”) do appear to suffer persistent infections and symptoms.
I believe it is far more likely that my patient fully recovered from his first infection, then caught Covid-19 a second time after being exposed to a young adult family member with the virus. He was unable to get an antibody test after his first infection, so we do not know whether his immune system mounted an effective antibody response or not.
We’ve had these worries earlier this year. Back in early April, South Korean doctors initially believed they were seeing people get sick a second time from “reactivation” of the virus. The Korean CDC initially characterized these cases as “reactivation” of the virus, not reinfection, believing the body fights off the virus for a while, at a sufficient level to make the virus seem dormant, and then the immune system stops fighting it as effectively, causing a second flare-up.
But by the end of the month, the South Korean CDC concluded the patients tested positive a second time “because fragments of the virus remained in their bodies and showed up in test kits.” Apparently, the tests the South Koreans were using were “so sensitive that [they] can still pick up parts of the small amount of RNA from a cell even after the person has recovered from COVID-19.”
An earlier antibody test on Dr. Ackerly’s patient would have been particularly useful in unraveling this mystery. Maybe the patient’s body exhibited something similar to the original South Korean theory — his body fought off almost all of the virus but not quite all of it, enough to test negative. (We should also recognize that some small portion of tests will give inaccurate results. If the tests are 90 percent accurate, wouldn’t one patient out of 100 positive patients generate two false negatives in a row?) With the virus mostly but not entirely gone, the patient’s immune system “relaxes”. . . and eventually, the virus returns with a vengeance, worse the second time because the viruses that survived the first battle are a little tougher and the ones that are best adapted to fight the patient’s immune system.
Or maybe this patient’s immune system is just not that strong. As noted yesterday, a lot of how our body responds to pathogens is determined by our genes, and some human beings hit the jackpot and have immunity or near-immunity to some common health problems. (A small minority of humans are immune to mosquito bites.) In the eyes of the patient, the difference between “reinfection” and “reactivation” is probably moot; in either case, you get sick, you get better, you think you’re in the clear, and then you get sick again.
It is also theoretically possible that this patient encountered a mutated strain of the coronavirus that is too different from the first strain for his body to effectively fight it off. Before you start worrying about that, keep in mind that so far, the only significant mutation of SARS-CoV-2 that researchers have uncovered is one that makes it more contagious, not more deadly or too different for a patient’s immune system to recognize. (Some scientists think the virus might be getting less deadly, but the jury is still out on that, so to speak. A declining rate of death among the infected, like we’re seeing right now, might be because the virus is growing less virulent, but it’s difficult to differentiate that factor from the improvements in treatment and less vulnerable patients getting infected in the current waves.)
As Ed Cara notes, the body’s response to a viral infection utilizes both antibodies and T-cells, which you may have heard of in the context of cancer treatments. T-cells are produced in bone marrow but get their name because they develop in the thymus gland. T-cells are basically the special forces of your immune system and split into two groups. The first, CD8, acts as the Navy SEALS of your immune system: They take on infections, virus bacteria, and tumors and, God willing, take them all down. The second category of T-cells, CD4, are the support staff, performing a variety of duties . . . including the production of cytokines. (Readers who remember past articles about chloroquine and hydroxychloroquine recognize that term from the discussion of the dangers of “cytokine storms” and how that drug can prevent the immune system from overreacting at attacking healthy cells.) Our bodies’ production of T-cells slows after puberty and basically is gone by age 65, which is one reason why elderly people are more vulnerable to infection.
As this Wired article lays out, some new research suggests that bodies with not-so-great antibody levels can still have effective T-cell responses against this virus. The study found SARS-CoV-2-specific CD8 T-cells were found in about 70 percent of recovering patients and 100 percent of patients had CoV-2-specific CD4 T-cells. But also, “importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40 percent –60 percent of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.”
In other words, 40 to 60 percent of people who hadn’t caught the virus yet had T-cells that had been “in training” against regular non-SARS-CoV-2 coronaviruses and that were likely to be effective in fighting off SARS-CoV-2. (Suddenly, asymptomatic cases make a bit more sense. Those folks are probably lucky enough to have immune systems that are top-tier and never let the SARS-CoV-2 virus get enough traction to generate symptoms. Remember, coughs, sneezes, runny noses, and other symptoms of sickness are ways the body is trying to expel the invader.)
The body’s immunity against reinfection from other types of coronaviruses is pretty impressive. Keep in mind: Most of the common colds are coronaviruses; if our bodies couldn’t retain the ability to fight them off, we would keep catching the same cold over and over again throughout the winter. One study of seven Jordanians infected with MERS — Middle East Respiratory System — found that six had antibodies in their system nearly three years later. (That sample may seem small, but remember MERS only infected about 2,500 people total.)
Is Herd Immunity Still Far, Far Away . . . or a Closer Than Most People Think?
Last night, Mississippi governor Tate Reeves offered a clear and succinct series of tweets, laying out why he’s not putting too much hope in “herd immunity” taking effect in his state. He noted that just to reach the threshold of 40 percent infected, the number of infected in his state would have to increase from the roughly 37,000 known infections to about 1.2 million. Are there asymptomatic people walking around Mississippi, unaware they have the virus? Sure. Are there 100,000? Half a million? A million?
Reeves summarizes, “on our worst day of new cases, we had just over 1,000. It has typically been between 700-900 during this most aggressive time. To get to 40% infections, we’d need 3,187 new cases every day for a full year from today. We would need to TRIPLE our worst day — every day — for a year.”
With that said, it is reasonable to believe that certain neighborhoods and communities that were particularly hard hit in the early stages of this pandemic might have reached herd immunity, or something close to it. A of couple days ago, the New York Times reported, “At a clinic in Corona, a working-class neighborhood in Queens, more than 68 percent of people tested positive for antibodies to the new coronavirus. At another clinic in Jackson Heights, Queens, that number was 56 percent. But at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn, only 13 percent of people tested positive for antibodies.” The article cautiously notes that the people who come into the clinic to be tested may not be representative of the neighborhoods as a whole.
New York political leaders are particularly pleased with the declining number of deaths and new cases these days. Yes, this is what happens when the virus has burned through an area so thoroughly — the virus finds fewer and fewer people who don’t have the antibodies.
There are very few places in this country that (a) were not hit hard in the first wave, (b) are not getting hit hard now, and (c) are not relatively remote and sparsely populated.
ADDENDUM: In case you missed it yesterday, the problem is not merely that most national media institutions are biased in favor of Democratic governors over Republican ones. The problem is also that certain voices in our media are biased in favor of big-state, better-known Democratic governors over other Democratic governors.