I am no medical expert, am just curious how vaccines work in general, especially in preventing severe illness and deaths. I have read articles, seen videos on youtube, and seen how efficacy is calculated, basically, 50% vax and 50% placebo, calculate the infected percentage to get the efficacy. I have also seen how vaccines are supposed to work, mRNA or not...basically your body will respond to a pathogen, be it spike protein or inactivated virus, etc... by creating Antibodies to neutralize future infections by the real thing. Antibodies attach to the "crown" spikes of the virus to prevent it from replicating and causing harm to the cells/body.

That said, there are recent articles or posts saying that CDC mentioned something about the equal viral load on vaccinated + unvaccinated. And that explains the efficacy of "Transmission" especially with the Delta variant, to be about 20% efficacy now against delta, specifically for Pfizer, specifically against "Transmission"

My questions are,

  1. If the viral load is the same, does that mean that the antibodies are not working in the vaccinated, preventing the virus from replicating
  2. If antibodies are not working, what else is there in the vaccine that is still helping to prevent severe illnesses and deaths?
  3. Why is death efficacy still at 90+%, I understand how it is calculated, but what is the theory behind why it prevents death in the vaccinated when 1) is proven true? I would have thought efficacy would include everything, transmission, severe illnesses, and deaths, as either the antibodies work or they, don't.

Thank you

  • I'm not familiar with the phrase "death efficacy", could you expand on it, perhaps give a reference specific to the claim as although it may have meaning, it's not clear what meaning it possesses. Oct 15 at 10:48
  • @ARogueAnt.: I'm sure (from the context) the OP means vaccine efficacy (VE) against death as the outcome, although the way they've contracted this is indeed highly unusual and confusing.
    – Fizz
    Oct 18 at 8:29

"Equal viral load" can be rather misleading because it refers to peak measure at one point in time and in one spot (in "the nose", more precisely by nasopharyngeal probe.) There are a couple of counterpoints to this:

  1. At least, in monkey [models] of re-infections with SARS-CoV-2, there's differential response in the nose and in the lungs after acquired immunity, with much less replication being observed in the lungs (where it could give severe disease) as opposed to the nose, where some replication was still noted after re-challenge:

After rechallenge, viral RNA was higher in NS [nasal swab] compared with BAL [bronchoalveolar lavage] but exhibited dose dependence and rapid decline, and median peak viral loads in NS were still >1.7 log10 compared with after the primary challenge (P = 0.0011, two-sided Mann-Whitney test; Fig. 5D).

enter image description here

(The groups 1-3 in the diagram are simply different challenge doses.)

Alas I don't know of similar studies in humans.

  1. Equal peak viral loads isn't necessarily just as infectious (to others) if the peak lasts less time, which seems to be the case with the vaccinated group, even in the case of breakthrough infection:

It's likely that people who have been vaccinated clear the infectious virus from the body faster. A previous study from Singapore had found that although levels of the virus were initially the same in those infected with the delta variant regardless of vaccine status, by day seven, levels of the virus dropped quickly in those who were vaccinated, which may reduce the ability to spread illness.

The relevant graph from this latter study:

enter image description here

  1. This situation is not really unique to Covid-19 vaccines.

There is precedent (for example, dengue [11], influenza [12–14], pertussis [15], pneumococcal bacteremia [16], rotavirus [17], and varicella [18]) that many vaccines confer greater efficacy against severe disease than milder disease.

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