- Nature study shows immunity to SARS coronavirus can last up to 17 years
- Study was conducted among dozens of resolvers (patients who recovered)
- It shows long-lasting memory T-cells that react to the SARS-CoV-1 Nucleocapsid Protein (SARS-CoV NP)
- The same T cells were found to be 'cross reactive' to the SARS-CoV-2 NP
DUBAI: How long does immunity to SARS coronavirus last? Seventeen (17) years, a study shows.
The key to this long-term immunity are memory “killer” T-cells. The cells were found to react to the Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Protein (SARS-CoV NP), according to a study published in Nature.
Memory T-cells are the main agents of long-term immunity. Until now, not much is known about the presence of pre-existing memory T cells in humans with potential to recognise (and neutralise) SARS-CoV-2.
Long-lasting memory T cells
The research team, headed by Nina Le Bert of the Duke-NUS Medical School in Singapore, investigated SARS-CoV-1 recovered patients on the island-state. Their paper had been published in the peer-reviewed journal on July 15, 2020.
The team was surprised by what they discovered: 17 years after the first SARS coronavirus (SARS-CoV-1) pandemic emerged (in 2003), they found evidence that immunity is still present in people who were infected and had recovered.
SARS infected 8,000 people and killed nearly 877, before it fizzled out. The study had a rather small number of convalescents – it had 37 subjects — all patients with history of the original SARS in 2003.
However, they did find 23 people who were confirmed SARS survivors still possessing long-lasting memory T cells "reactive” to SARS-NP (nucleocapside protein) more than 200 months after the initial infection.
The long-lasting memory T-cells specific to SARS may also hold the key to immunity to SARS-CoV-2, the virus that causes COVID-19, the researchers stated.
It is a commonly used lab test to detect antibodies in the blood, via solid-phase capture technique using individual peptide-coated plates.
A smaller study on antibodies against MERS-CoV conducted by a team in Jordan, published in 2016 in Medscape, also showed the dominant role of antibodies among people who recovered from MERS-CoV.
The observed persistence of these antibodies contributes to the understanding of individual immune responses to coronavirus-related infections, including that which trigger the "common cold".
Four of them are endemically transmitted and cause the common cold (OC43, HKU1, 229E and NL63). SARS-CoV (or also known as SARS-CoV-1) and MERS-CoV have caused limited epidemics of severe pneumonia. All of them trigger antibody and T cell responses in infected patients: however, antibody levels appear to wane faster than T cells.
Antibodies vs memory T-cells
Scientists focussed on antibodies and memory T-cell.
What they found: While SARS-CoV-1-specific antibodies dropped below the detection limit within 3 years, SARS-CoV-1 specific memory T cells have been detected even 11 years after SARS infection.
The team also studied these T cells in individuals with no history of SARS or COVID-19 or of contact with SARS-CoV-2 infected cases (which they referred to as "unexpose").
It's only recently that SARS-CoV-2-specific T cells in recovered patients have seen studieed. Their potential protective role has been inferred from studies in SARS and MERS patients.
To study SARS-CoV-2 specific T cells associated with viral clearance (neutralising the virus), the team collected blood from 36 individuals after recovery from COVID-19 (mild to severe).
Then, they studied the T cell response against selected structural (nucleocapsid protein-NP) and non-structural proteins (NSP7 and NSP13 of ORF1) of the large SARS-CoV-2 proteome (whole assembly of proteins expressed by the virus).
They figured out: There were organised 82 overlapping peptides covering the entire NP into small peptide pools (of 7-8 peptides).
The demonstration that COVID-19 and SARS recovered patients can mount T cell responses against shared viral determinants implies that SARS-CoV-1 infection can induce T cells able to cross-react against SARS-CoV-2, they theorised.
Previously, the research team had demonstrated that patients who recovered from SARS-CoV-1 harbour T cells specific for epitopes within different SARS-CoV-1 proteins -- which had persisted for 11 years after infection.
Now, on the 17th year after the SARS epidemic, the team once again collected blood samples and tested if the same patients ("resolvers") still harbourr cells reactive against SARS-CoV-1.
Moreover, the team also checked whether these have cross-reactive potential against SARS-CoV-2 peptides.
Response to peptides
To their surprise, the team found that 17 years after infection, indeed the T cell responses (as measured by what the they called as "IFN-γ" responses) to SARS-CoV-1 "peptides" were still present.
Subsequently, they also tested if SARS-CoV-2 NP peptides — 94% identical to the SARS-CoV-1 peptides — induce IFN-γ responses from the same T cells of SARS resolvers. Once again, they found that T cells from all 23 individuals tested reacted to SARS-CoV-2 NP peptides.
"A clear and robust expansion of NP-reactive cells was detected in 7 out of 8 individuals tested," the researchers wrote. "SARS-CoV-2 NP-specific T cells are part of the T cell repertoire of individuals with a history of SARS-CoV-1 infection and are able to robustly expand after encounter with SARS-CoV-2 NP peptides," they added.
"These findings demonstrate that virus-specific T cells induced by betacoronanvirus infection are long-lasting, supporting the notion that COVID19 patients will develop long-term T cell immunity," the researchers stated
Why are T cells (NSP7/13-specific) detected and often dominant in SARS-CoV-1/2 "unexposed" donors while representing a minor population in SARS-Cov-1/2 recovered individuals?
The cause is "unclear", say the researchers.
The could only hypothesise: "This finding suggests that other presently unknown coronaviruses, possibly of animal origin, might induce cross-reactive SARS-CoV-2 T cells in the general population."
Why is SARS-CoV-2 more “efficient” in spreading, compared to SARS/MERS/Ebola, even if they’re from the same virus (coronavirus) family?
First, no two viruses are the same.
However, they also said that "understanding the distribution, frequency and protective capacity of pre-existing structural or non-structural SARS-CoV-2 cross-reactive T cells could be hold the key to explain some of the differences in infection rates or pathology observed during the current COVID-19 pandemic".
Did the past "common cold" cause by other coronavirus strains trigger the T-cell reaction against SARS-CoV-2 pepetides?
Members of the scientific community speculate that given the study results, it is possible that common cold coronaviruses (of which 4 had been identified) may potentially stimulate an immune response — that in effect help lessen or attenuate the 'pathogenicity' (ability to cause disease) or viral infectivity — to SARS-CoV-2.
They posit that this (common cold caused by other strains of coronavirus) could be the origin of the pre-existing T-cell immunity in people who have never had SARS, MERS, or COVID19.
Safer route to immunity?
Scientists hypethesise that introducing coronavirus "common cold" virus might be a faster and possibly safer route to immunity to SARS-CoV-2 than the development of vaccines (many of which are under development).
The study, however, stopped short of concluding that that they have reached the point where the "common cold" coronaviruses have achieved some success in suppressing SARS-CoV-2.