HCoV-OC43 (one of human coronaviruses causing common cold) can generate cross-reactive antibodies against SARS.
Immunity to HCoV-OC43 appears to wane appreciably within one year.
Here’s the paper which mentions both of these facts. (The actual paper is not important, I expect these facts to be well-known to coronavirus researchers, if the paper itself is not terribly mistaken and if I haven’t misread anything.)
Even if cross-immunity is mild, won’t it make sense to intentionally infect people with HCoV-OC43? Downside seems quite small compared to the number of deaths, and intuitively it seems that “mild cross-immunity” = “less severe SARS-CoV-2 cases”, which is extremely valuable.
I notice I’m confused, since these facts should be well-known to pretty much everyone who’s working on the vaccine. What’s the explanation for why it’s not a good idea?
Possible explanations, but I’m probably missing something:
Vaccines which cause the actual illness are considered unethical. (Probably not? I don’t expect humanity to be that stupid.)
Mass-producing HCoV-OC43 virus is too hard for some reason. (Possible? I don’t know much about vaccine production, and I’m clueless about whether it’s even possible to mass-produce and store a “live” virus; but this seems solvable through organized infection parties, etc.)
Researchers or medical organizations don’t want to rely on expected utility. Related hypothesis: time and productivity wasted by infecting many people with HCoV-OC43 is too valuable, and infecting everyone with HCoV-OC43 at the same time would hurt economy too much. (I don’t believe this, but I haven’t really tried to estimate this. If the alternative would be “wait for the real vaccine which is just around the corner”, then yes, let’s wait, but if the alternative is waiting for 12-18 months, then it doesn’t feel right.)
Maybe I don’t understand what “mild immunity” means and it’s not that valuable of a perk to intentionally cause it? (But the same paper I quoted talks about HCoV-OC43 importance for predicting future SARS-CoV-2 outbreaks.)
Maybe being infected with HCoV-OC43 is too risky because getting two viruses at the same time is dangerous? Or because it would confuse the situation and complicate diagnoses of the real SARS-CoV-2? (Maybe… If everyone is sick with common cold then it would help SARS-CoV-2 to spread since everyone would be sneezing and coughing. But it also seems like a question of good timing and at least worth considering.)
There’s speculation that having acquired immunity to similar viruses leads to worse outcomes with COVID-19, and that’s why children don’t have many symptoms. This is still highly speculative, I won’t be surprised if it turns out to be something totally different, but it would make me nervous about this plan.
Okay, SARS-CoV-2 is pretty different from SARS-2003 (“~76% amino acid identity in the spike protein”), this might be the reason it won’t work. OTOH, I don’t know how different HCoV-OC43 is from both SARS strains.
Similar to the thing Elizabeth mentioned, I’m concerned about the possibility of antibody-dependent enhancement wherein an imperfect antibody match actually worsens the course of the infection.
I’ve tried to look into this. My results weren’t conclusive, but I think it’s a very real possibility for this virus, and fairly likely to slow vaccine development due to the added testing it neccessitates.
One thing I’m not sure about: how hard is it to get your hands on HCoV-OC43? With high confidence and in quantities suitable for pretty much guaranteeing to give someone a cold / some immunity? (Do excessive quantities lead to a more severe cold?)
This does really seem like something someone should be working on. Probably someone is, somewhere...
EDIT: Here is one paper on the consequences of HCoV-OC43 infection:
Among other things: “Recent studies have suggested [that human coronaviruses] can cause severe lower respiratory tract illnesses in children.” and “In our population, HCoV-OC43 infections generally caused upper respiratory tract infection, but can be associated with lower respiratory tract infection especially in those coinfected with other respiratory viruses.”
EDIT 3: I would really love for someone who knows things to take a look at this paper actually, and help interpret it. It is only studying children, and notes that “HCoV-OC43 infections tend to occur before 2 years of age” (does that mean adults can’t get it? or they aren’t exposed to it much? Does exposing them to it generate a useful immune response?), and also that, among the children selected for the study, children with HCoV-OC43 had better outcomes than controls (but I have no idea how to normalize this for statistical issues; the subjects were children who tested positive for HCoV-OC43, whereas the controls were children who were tested for respiratory viruses but were negative for HCoV-OC43.)
Two facts:
HCoV-OC43 (one of human coronaviruses causing common cold) can generate cross-reactive antibodies against SARS.
Immunity to HCoV-OC43 appears to wane appreciably within one year.
Here’s the paper which mentions both of these facts. (The actual paper is not important, I expect these facts to be well-known to coronavirus researchers, if the paper itself is not terribly mistaken and if I haven’t misread anything.)
Even if cross-immunity is mild, won’t it make sense to intentionally infect people with HCoV-OC43? Downside seems quite small compared to the number of deaths, and intuitively it seems that “mild cross-immunity” = “less severe SARS-CoV-2 cases”, which is extremely valuable.
I notice I’m confused, since these facts should be well-known to pretty much everyone who’s working on the vaccine. What’s the explanation for why it’s not a good idea?
Possible explanations, but I’m probably missing something:
Vaccines which cause the actual illness are considered unethical. (Probably not? I don’t expect humanity to be that stupid.)
Mass-producing HCoV-OC43 virus is too hard for some reason. (Possible? I don’t know much about vaccine production, and I’m clueless about whether it’s even possible to mass-produce and store a “live” virus; but this seems solvable through organized infection parties, etc.)
Researchers or medical organizations don’t want to rely on expected utility. Related hypothesis: time and productivity wasted by infecting many people with HCoV-OC43 is too valuable, and infecting everyone with HCoV-OC43 at the same time would hurt economy too much. (I don’t believe this, but I haven’t really tried to estimate this. If the alternative would be “wait for the real vaccine which is just around the corner”, then yes, let’s wait, but if the alternative is waiting for 12-18 months, then it doesn’t feel right.)
Maybe I don’t understand what “mild immunity” means and it’s not that valuable of a perk to intentionally cause it? (But the same paper I quoted talks about HCoV-OC43 importance for predicting future SARS-CoV-2 outbreaks.)
Maybe being infected with HCoV-OC43 is too risky because getting two viruses at the same time is dangerous? Or because it would confuse the situation and complicate diagnoses of the real SARS-CoV-2? (Maybe… If everyone is sick with common cold then it would help SARS-CoV-2 to spread since everyone would be sneezing and coughing. But it also seems like a question of good timing and at least worth considering.)
So, what am I missing here?
There’s speculation that having acquired immunity to similar viruses leads to worse outcomes with COVID-19, and that’s why children don’t have many symptoms. This is still highly speculative, I won’t be surprised if it turns out to be something totally different, but it would make me nervous about this plan.
Okay, SARS-CoV-2 is pretty different from SARS-2003 (“~76% amino acid identity in the spike protein”), this might be the reason it won’t work. OTOH, I don’t know how different HCoV-OC43 is from both SARS strains.
Similar to the thing Elizabeth mentioned, I’m concerned about the possibility of antibody-dependent enhancement wherein an imperfect antibody match actually worsens the course of the infection.
I’ve tried to look into this. My results weren’t conclusive, but I think it’s a very real possibility for this virus, and fairly likely to slow vaccine development due to the added testing it neccessitates.
I opened a question on it here.
I would also like to know the answer to this.
One thing I’m not sure about: how hard is it to get your hands on HCoV-OC43? With high confidence and in quantities suitable for pretty much guaranteeing to give someone a cold / some immunity? (Do excessive quantities lead to a more severe cold?)
This does really seem like something someone should be working on. Probably someone is, somewhere...
EDIT: Here is one paper on the consequences of HCoV-OC43 infection:
https://www.ncbi.nlm.nih.gov/pubmed/23337903
Among other things: “Recent studies have suggested [that human coronaviruses] can cause severe lower respiratory tract illnesses in children.” and “In our population, HCoV-OC43 infections generally caused upper respiratory tract infection, but can be associated with lower respiratory tract infection especially in those coinfected with other respiratory viruses.”
So safety might be in question.
EDIT 2: Scihub link: https://sci-hub.tw/10.1097/INF.0b013e3182812787
EDIT 3: I would really love for someone who knows things to take a look at this paper actually, and help interpret it. It is only studying children, and notes that “HCoV-OC43 infections tend to occur before 2 years of age” (does that mean adults can’t get it? or they aren’t exposed to it much? Does exposing them to it generate a useful immune response?), and also that, among the children selected for the study, children with HCoV-OC43 had better outcomes than controls (but I have no idea how to normalize this for statistical issues; the subjects were children who tested positive for HCoV-OC43, whereas the controls were children who were tested for respiratory viruses but were negative for HCoV-OC43.)