That's not what it said at all. Let's read the Results --- which once again shows that there is no "natural herd immunity" because antibodies do not last in many people naturally infected. And also outlines T-Cell response (not immunity) that one of the tests covered (out of the entire series of tests). Your attempt to take one sentence out of context does not change the reality.
Once again the paper is about antibody immunity - read the title so you understand this.
So, you can stop posting all of your misinformation regarding long term immunity and herd immunity. Also, please stop all of the scaremongering regarding covid-19 variants.
Like I said, the Lancet is just toilet paper.
Dynamics of SARS-CoV-2 neutralising antibody responses and duration of immunity: a longitudinal study
Results
We approached 517 patients for participation in the study, of whom 288 consented for outpatient follow-up and collection of serial blood samples. 164 patients were followed up and had adequate blood samples collected for analysis, with a total of 546 serum samples collected (
appendix pp 7–12) during treatment in hospital and post-discharge, up to 180 days post-symptom onset. The breakdown of the number of samples at each timepoint was as follows: 64 samples at 14 days post-symptom onset, 39 samples at 21 days post-symptom onset, 127 samples at 28 days post-symptom onset, 30 samples at 60 days post-symptom onset, 158 samples at 90 days post-symptom onset, and 128 samples at 180 days post-symptom onset. 42 (26%) of 164 patients were women, and the median age was 44 years (IQR 34·5–56; range 21–74). 72 (44%) of 164 patients had at least one comorbidity, 47 (29%) had hypertension, and 27 (16%) had diabetes. 34 (21%) of 164 patients were asymptomatic at presentation. No patients had a documented history of previous SARS infection.
Based on the slope of the regression line and whether the samples crossed the significance threshold of 30% inhibition (
figure 1A), we identified five distinctive patterns of neutralising antibody dynamics as follows: negative, individuals who did not, at our intervals of sampling, develop neutralising antibodies at the 30% inhibition level (19 [12%] of 164 patients); rapid waning, individuals who had varying levels of neutralising antibodies early on (around 20 days post-symptom onset), but seroreverted in less than 180 days (44 [27%] of 164 patients); slow waning, individuals who remained neutralising antibody-positive at 180 days post-symptom onset (46 [28%] of 164 patients); persistent, although with varying peak neutralising antibody levels, these individuals had minimal neutralising antibody decay (52 [32%] of 164 patients); and delayed response, a small group that showed an unexpected increase of neutralising antibodies during late convalescence (≥90 days post-symptom onset; three [2%] of 164 patients). These classifications of samples could be determined using a decision tree to evaluate the neutralising antibody levels at 28 days post-symptom onset, 90 days post-symptom onset, and 180 days post-symptom onset (
appendix p 4).
To better characterise the distinguishing features of each group, we applied a linear regression analysis to illustrate the slopes of change for each group (
figure 1B). For groups 2, 3, and 4, although they all showed a general trend of waning, the speed of waning (ie, the slope of change) was very different, which resulted in very different neutralising antibody levels at 180 days post-symptom onset, with the rapid waning group showing almost all samples at less than 20% inhibition, the slow waning group at 40% inhibition or above, and the persistent group at 80% inhibition or above.
The fifth group, the delayed response group, showed an unusual increase of neutralising antibodies during the convalescent period. The mechanism and significance of this finding is unclear. Two [67%] of three patients in this group had pneumonia in hospital, but none required oxygen and one was treated with remdesivir. Since hospital discharge, two (67%) patients in the delayed response group did not report any febrile illness or acute respiratory infection, and one (33%) patient reported three episodes of asthma exacerbation. None of the patients in the delayed response group reported exposure to known patients with COVID-19 or migrant workers, who comprised most patients with COVID-19 in Singapore. As the sample number is very small (three patients), these individuals were excluded from further analysis in the current study and will be followed up in future studies if we encounter more samples in this category.
IgG maturation (ie, increase in avidity) may play a part in our observations. All samples were subjected to avidity testing and the data revealed three important findings (
figure 1C). First, levels of receptor binding domain (RBD)-binding IgG antibody avidity correlated with the levels and waning rates of neutralising antibody across all patient groups. Second, for the negative, rapid waning, and slow waning groups, there was a corresponding biphasic kinetics for avidity change, with more rapid rise in the first phase (from days 15–30 post-symptom onset) than the second phase (from days 31–180 post-symptom onset). Third, for the persistent group, avidity reached a high level very early (15–30 days post-symptom onset) and showed a less obvious biphasic change.
To investigate if cytokine levels correlated with antibody waning patterns in patients with COVID-19, we profiled concentrations of cytokines and chemokines in the plasma at 30 days post-symptom onset and 180 days post-symptom onset (
appendix p 5). At the late convalescent timepoint of 180 days post-symptom onset, higher levels of pro-inflammatory cytokines (IFN-γ, IL-12p70, and IL-17A), pro-inflammatory chemokine (IP-10), and growth factors (human growth factor) were observed in the persistent group compared with all other groups. This result contrasted with patients in the negative group, with lower concentrations of pro-inflammatory IFN-γ, IL-12p70, and IL-17A at 180 days post-symptom onset compared with all other groups. There was no difference in IL-6 levels across the different groups (data not shown).
For a subset of 23 samples randomly selected from each group at day 180, we tested T cells that were reactive to peptides of S, M, NP, ORF3a, and ORF7/8 proteins to investigate if there was a correlation between T-cell immunity and different antibody kinetics. We made two observations (
appendix p 6). First, all patients in each group maintained substantial specific T-cells at 180 days post-symptom onset and the T-cell response was multi-specific, with most donors having T-cells reactive to NP, M, and S. Second, there was no clear difference in T-cell immunity between the groups, consistent with previous findings.
6
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We found significant differences in terms of age, presence of comorbidities, baseline symptoms, investigations, and clinical outcomes when comparing all four groups against each other and in the persistent antibody group compared with the other three groups with waning or absent antibodies (
table 1). We observed a distinct stepwise progression from the negative group to the persistent group, whereby patients with persistent antibodies were older and had more comorbidities, including hypertension and diabetes mellitus.
