In a paper published on The lancet researchers of University of Hong Kong used 50% plaque reduction neutralization test (PRNT) antibody titre data from 115 sera collected longitudinally from 90 to 386 days after onset of symptoms or first RT-PCR confirmation from 62 RTPCR confirmed SARS-CoV infected individuals, to estimate that PRNT antibody will remain detectable for around 1,717 days after symptom onset and that a threshold for 50% protection from re-infection will be maintained for around 990 days post-symptom onset, in symptomatic patients. PRNT titres in mildly symptomatic children wane faster than in adults.

The results indicate that sera collected from 201 to 386 days post infection have detectable PRNT50 and PRNT90 antibodies in 100% and 92.3%, respectively; and detectable by spike RBD ELISA assays in 92.6% of sera. The sVNT was positive in 100% of sera collected from day 90−150 post infection, dropped to 73.1% using the revised 30% inhibition cut-off but 96.2% positive using the previous cutoff of 20% inhibition, which we previously found tohave acceptable specificity.
In symptomatic COVID-19 patients, it is estimated that PRNT50 antibody would remain detectable for 1717 days post-infection, 1574 days for mild infections and 2709 days for severe infections. However, because the slope of decline was not significant for symptomatic patients, these may be under-estimates. The finding that 97.5% of individuals remain positive in spike RBD ELISA assays for over 200 days has implications for sero-epidemiology and suggest that waning of antibody is unlikely to be a major issue for spike RBD ELISA, sVNT or PRNT assays.
These findings of a slow decay of neutralizing antibody are in agreement with data from recent studies suggesting the presence of spike RBD specific bone marrow specific plasma cells late in convalescence which are known to be those responsible for long lasted antibody responses. RBD-specific memory B cells remain unchanged or even increased over the first six to eight months. After a new infection, short-lived plasmablasts are an early source of antibodies. But these
cells recede soon after a virus is cleared from the body and memory B cells patrol the blood for reinfection, while plasma cells resident in bone marrow continue to secrete lower levels of antibodies for decades. Furthermore, even if protection from re-infection may wane beyond two years after infection, immune memory for both B and T cell compartments are likely to remain and will lead to rapid increase in neutralizing antibody upon re-infection, thus conferring even longer protection from severe disease. SARS-CoV-2-specific CD4+ T cells and CD8+ T cells declined with a half-life of 3 to 5 months respectively and these are also likely to contribute to modulation of disease severity.

These findings suggest that neutralizing antibody mediated protection from re-infection against the original strains of SARS-CoV-2 is likely to remain for 700 days or more after symptomatic COVID-19 infection but variants of concern may lead to an erosion, but not abrogation, of this protection.

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