don't get covid. redux.
2022-Jan-30, Sunday 02:42 pm![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
mellowtiggerI issued my first warning against sars-cov-2 infection about 2 years ago. I've repeatedly said, "Don't get covid." My concern since then has not waned. Instead, we now have 2 more years of data on this novel infection, and I can organize my alarms into 4 broad categories.
1) immunosuppression: This is not the flu.
I remember from the HIV epidemic this difference between CD4 and CD8 T cells in the immune system: CD4 acts like a kind of early warning system (even for cancer), and CD8 responds to that warning call (even for cancer). HIV infects and eliminates CD4 cells. Without an early warning system, the human body no longer effectively combats incoming infections, which is why people with AIDS succumbed to a wide variety of opportunistic diseases. Effective HIV drugs work to boost CD4 counts.
SARS-CoV-2 is doing something similar. It's not killing the CD4 cells outright, but it is triggering them to specialize so that they no longer react to a wide variety of potential invaders. The papers call this process a loss of naive T cells. Same result as AIDS, though, it means that human bodies are losing an important "scout" to identify new problems. The metaphor I use at the moment to interpret these studies is that our CD4 cells develop a strong "prejudice" against a single particular strain of coronavirus. Preoccupied in this way, they fail to respond properly to other problems or even other strains of coronavirus. With this immunosuppression effect, humans become more susceptible to additional infections, and this modification persists for a long time after primary infection. This change holds additional significance for people who are already infected with HIV. I maintain that covid-19 will join other diseases in causing lifelong illness. There is no infected herd immunity to be achieved here. Like HIV, that beneficial effect won't happen with this virus, because the immune response is itself damaged by the infection.
2) broad systemic damage: There is no mild infection.
Even asymptomatic people have strong underlying viral load. Even mildly symptomatic people have myelin damage in the brain. Regardless of severity, the heart appears to sustain damage, and a sizable portion of all infected people will develop Long Covid. Some people develop autoimmune problems. Anyone who had severe primary infection and required hospitalization is still at 5x increased risk of later death from a variety of causes. This review politely calls some of the later risks "post-acute pulmonary manifestations" and "post-acute thromboembolic events". In other words, the disease doesn't end when the symptoms disappear from your initial infection.
3) airborn: Keep your distance.
You don't need to see the person who infects you. You share air space with everyone in the same building. It was suspected already 1.5 years ago, but same-building infection is happening again. Close contact is not required. The 6-foot rule is insufficient protection. Isolate as much as possible. Mask properly. Think happy thoughts for the many "essential workers" who have kept everything functioning for the last 2 years, so the rest of humanity can keep its distance. Don't foolishly waste that benefit you have been given.
4) permanent infection: Don't get covid.
My original proposal was that people who get infected will stay infected, because infected heart cells can be replaced at only 1% per year. My proposal appears closer to being confirmed. This report has a lot to say about the heart, including, "One study of 39 postmortem hearts detected SARS-CoV-2 by qRT-PCR in 24 (61.5%) cases, with 16 hearts exhibiting a high viral load (>1000 genomic copies per µg of total RNA)." Additionally, multiple studies are raising the possibility of long term infection in the brain and other systems, "for up to 230 days following symptom onset".
This is not the flu. There is no mild infection. Keep your distance. Don't get covid.
1) immunosuppression: This is not the flu.
I remember from the HIV epidemic this difference between CD4 and CD8 T cells in the immune system: CD4 acts like a kind of early warning system (even for cancer), and CD8 responds to that warning call (even for cancer). HIV infects and eliminates CD4 cells. Without an early warning system, the human body no longer effectively combats incoming infections, which is why people with AIDS succumbed to a wide variety of opportunistic diseases. Effective HIV drugs work to boost CD4 counts.
SARS-CoV-2 is doing something similar. It's not killing the CD4 cells outright, but it is triggering them to specialize so that they no longer react to a wide variety of potential invaders. The papers call this process a loss of naive T cells. Same result as AIDS, though, it means that human bodies are losing an important "scout" to identify new problems. The metaphor I use at the moment to interpret these studies is that our CD4 cells develop a strong "prejudice" against a single particular strain of coronavirus. Preoccupied in this way, they fail to respond properly to other problems or even other strains of coronavirus. With this immunosuppression effect, humans become more susceptible to additional infections, and this modification persists for a long time after primary infection. This change holds additional significance for people who are already infected with HIV. I maintain that covid-19 will join other diseases in causing lifelong illness. There is no infected herd immunity to be achieved here. Like HIV, that beneficial effect won't happen with this virus, because the immune response is itself damaged by the infection.
2) broad systemic damage: There is no mild infection.
Even asymptomatic people have strong underlying viral load. Even mildly symptomatic people have myelin damage in the brain. Regardless of severity, the heart appears to sustain damage, and a sizable portion of all infected people will develop Long Covid. Some people develop autoimmune problems. Anyone who had severe primary infection and required hospitalization is still at 5x increased risk of later death from a variety of causes. This review politely calls some of the later risks "post-acute pulmonary manifestations" and "post-acute thromboembolic events". In other words, the disease doesn't end when the symptoms disappear from your initial infection.
3) airborn: Keep your distance.
You don't need to see the person who infects you. You share air space with everyone in the same building. It was suspected already 1.5 years ago, but same-building infection is happening again. Close contact is not required. The 6-foot rule is insufficient protection. Isolate as much as possible. Mask properly. Think happy thoughts for the many "essential workers" who have kept everything functioning for the last 2 years, so the rest of humanity can keep its distance. Don't foolishly waste that benefit you have been given.
4) permanent infection: Don't get covid.
My original proposal was that people who get infected will stay infected, because infected heart cells can be replaced at only 1% per year. My proposal appears closer to being confirmed. This report has a lot to say about the heart, including, "One study of 39 postmortem hearts detected SARS-CoV-2 by qRT-PCR in 24 (61.5%) cases, with 16 hearts exhibiting a high viral load (>1000 genomic copies per µg of total RNA)." Additionally, multiple studies are raising the possibility of long term infection in the brain and other systems, "for up to 230 days following symptom onset".
This is not the flu. There is no mild infection. Keep your distance. Don't get covid.
no subject
Date: 2022-Jan-31, Monday 12:40 am (UTC)Another way to think of the naive T cell loss, which happens normally during aging, is that covid-19 simply ages the immune system prematurely. These papers are well beyond my knowledge level, so I admit to needing metaphors to understand some of the details they convey.
P.P.S. 2022 Feb 03 Thursday 11:00 am
Permanent infection is now officially being presented as a possible explanation for what's happening. See "Fig. 1: Putative mechanisms and diagnostic strategies for patients with post-COVID-19 syndromes." They specifically mention "Other ACE2-expressing organ systems" for viral persistence, which is what I've been harping about for 2 years.
https://www.nature.com/articles/s41590-021-01104-y
P.P.P.S. 2022 Feb 17 Thursday 1:30pm
5) paracrine senescence by viral syncytia
It seems that we finally know why autoimmune problems are a thing that happens in #LongCovid, and it's bad. An infected cell can glom onto nearby cells, using them as defense against the immune system, while slowly infecting them and producing more virus over time.
"COVID does not have to leave a cell to enter the next one… This means your immune system either has to wait to fight it until it bursts or they have to train our T cells to fight our own cells to get access to COVID and we don’t want that to happen… And even after you develop a T cell reaction to the virus, you still have to wait for the viral syncytia to burst and allow your Immune System to fight it or else we end up, possibly, training our T cells to fight our own cells… Which could lead to all kinds of complex inflammatory issues just like the ones we are seeing or, worse, using up or killing our naive T cells which we appear to have a limited supply of and are directly connected to aging."
- https://donford.substack.com/p/riskoflongcovid
P.P.P.P.S. 2022 Feb 26 Saturday 1:30pm
This video is an excellent overview of some T-cell biology. The presentation is the first 45 minutes. (You can ignore the following discussion for the next 45 minutes.) He makes a good argument in favor of nasal spray vaccination as our best hope. I look forward to getting that kind of booster vaccination as often as necessary.