We don't have evidence that any vaccine prevents asymptomatic spread from occurring, mostly because tracking people as carriers without any symptoms has rarely ever been done.
mRNA is used to make protein for every protein in your body. No, it's not 1:1, it varies due to a couple different factors but mRNA can be used again and again as a template for protein synthesis, 10-1000X. These vaccine RNA's are somewhat stablized to prolong half life so they are likely to achieve the upper bound.
Antigen detection tests are looking for Nucleoprotein, not the Spike. This is because in each virus particle there are ~75 Spike trimers but on the order of 400-1000 NP proteins, so a lower detection limit can be achieved with NP. Currently these limits are on the order of ~50-100 virus particles/swab which is close to 2 orders of magnitude above rtPCR. But the Ag detection is still ~80% compared to rtPCR and prone to miss low levels of RNA- that some would argue are likely non-infectious anyway.
The Nature lit I was reading yesterday had somewhat disturbing sidenote reports of long term presence of Antigen in the intestinal biopsies.
https://www.nature.com/articles/s41586-021-03207-w
Evolution of antibody immunity to SARS-CoV-2
NP is a weird protein that can phase seperate and form droplets with RNA, but these proteins really shouldn't persist months later without some continued replication.Quote:
SARS-CoV-2 antigen persistence
Antibody evolution occurs by somatic mutation and selection in germinal centers wherein antigen can be retained in the form of immune
complexes on the surface of follicular dendritic cells for prolonged
periods of time. Residual protein in tissues represents another potential
source of antigen. SARS-CoV-2 replicates in ACE2-expressing cells in
the lungs, nasopharynx and small intestine22–25, and viral RNA has been
detected in stool samples even after the virus is cleared from the nasopharynx26–28. To determine whether there might be antigen persistence
in the intestine after resolution of clinical illness, we obtained biopsies
from the upper and lower gastrointestinal (GI) tract of 14 individuals,
an average of 4 months (range 2.8-5.7 months) after initial SARS-CoV-2
diagnosis (Supplementary Table 7). Immunostaining was performed to
determine whether viral protein was also detectable in upper and lower
GI tract, with de-identified biopsies from individuals pre-dating the
pandemic (n=10) serving as controls. ACE2 and SARS-CoV-2 N protein
was detected in intestinal enterocytes in 5 of 14 individuals (Fig. 5a–d,
Extended data Fig. 9a-h and 10a-b, and Supplementary Table 7) but not
in historic control samples (Extended data Fig. 9i-l). When detected,
immunostaining was sporadic, patchy, exclusive to the intestinal epithelium and not associated with inflammatory infiltrates (Extended
data Fig. 9a-h and 10a-b). Clinically approved nasopharyngeal swab
PCR assays were negative in all 14 individuals at the time of biopsy.
However, biopsy samples from 3 of the 14 participants produced PCR
amplicons that were sequence verified as SARS-CoV-2 (Methods and
Supplementary Table 7). In addition, viral RNA was detected by in situ
hybridization in biopsy samples from the two participants that were
tested (Extended data Fig. 10c-d) but not in historic control samples
(Extended data Fig. 10e).