A new study published in Science Advances says that SARS-COV-2 offers increased protection against common cold.
COVID-infected people who have high levels of anti-SARS-CoV-2 antibodies also have increased antibodies against the common cold.
Coronavirus infection gives protection against seasonal human coronaviruses (HCoVs). It’s unclear if SARS-CoV-2 infection increases pre-existing HCoV-specific antibodies or elicits cross-reactive β-CoV antibodies that target conserved epitopes.
A study published in Science Advances compares the spike epitopes of β-HCoV targeted by preexisting serum antibodies to the epitopes targeted by antibodies evoked by SARS-CoV-2 infection using electron microscopy-based polyclonal epitope mapping (EMPEM) methods.
HCoVs are responsible for one-third of all common cold infections. In the human population, two HCoVs, 229E and NL63, and two βHCoVs, OC43 and HKU1, are endemic. By the age of 15, the majority of the population has contracted HCoV. The infection rate and prevalence, on the other hand, vary with geographical area.
Most people have antibodies to HCoVs since the population has been exposed to them. The antibodies attack the virus’s spike protein and nucleocapsid protein. However, antibody levels decline with time, and reinfections can occur within a year.
The highly pathogenic Middle East respiratory disease (MERS) CoV, SARS-CoV, and SARS-CoV-2 are also among the β-CoVs. The extreme toxicity and transmissibility of SARS-CoV-2 has resulted in the COVID-19 pandemic.
The spike protein attaches to the host cells’ angiotensin-converting enzyme 2 (ACE2) receptor. Cellular entrance is mediated by this binding. As a result, the spike protein determines the host range and cell types infected (cell tropism). It’s also a primary target for neutralizing antibodies, making it an important antigen for vaccine research.
The SARS-CoV-2 spike is similar to the SARS spike by 69.2 percent and the OC43 spike by 27.2 percent. Its spike bears no resemblance to that of other β-CoVs. Nonetheless, preexisting immunity to HCoVs is linked to COVID-19 illness outcomes. This could be due to an increase in anti-HCoV-spike-specific antibodies following infection with SARS-CoV-2. It’s also possible that SARS-CoV-2 infection causes antibodies to cross-react with the HCoV spike.
Individuals infected with SARS-CoV-2 who have high anti-SARS-CoV-2 antibody levels also have higher anti-β-HCoV antibody levels.
The researchers in this study created soluble protein domains of the HKU1, OC43, SARS, MERS, and SARS-CoV-2 spike proteins. Negative stain electron microscopy was used to examine these creations (ns-EM).
Blood samples were taken from eight donors before the COVID-19 pandemic and three donors after the pandemic who had SARS-CoV-2 infection. Anti-spike antibodies were detected in the serum using an enzyme-linked immunosorbent assay (ELISA).
Anti-OC43 spike antibodies were found in all eight pre-pandemic (PP) samples. Anti-HKU1 spike antibodies were found in all eight samples at extremely low levels. This could be due to the fact that OC43 is more widely used over the world than HKU1. Anti-SARS-CoV-2 spike antibodies were not found in any of the samples. Anti-SARS and anti-MERS spike antibodies were found in low quantities in one serum sample.
Anti-SARS-CoV-2 spike antibodies were found in abundance in all three SARS-CoV-2 convalescents (SC) sera. Anti-SARS, anti-MERS, anti-OC43, and anti-HKU1 spike antibodies were also present. As a result, SARS-CoV-2 infection can result in cross-reactive antibodies to the β-CoV spike proteins.
The researchers next tested whether PP and SC sera killed the OC43 virus as well as the SARS and SARS-CoV-2 pseudoviruses. None of the PP sera neutralized the SARS or SARS-CoV-2 pseudovirus, as expected. The OC43 virus, as well as the SARS and SARS-CoV-2 pseudoviruses, were neutralized by the SC sera.
Using ns-EMPEM, the researchers identified the epitopes targeted by anti-spike antibodies in PP serum. Antibody-spike complexes were studied structurally. This analysis only employed a subset of the antibodies, not the whole antibody.
The researchers used three PP sera to undertake high-resolution cryo-EMPEM investigations with OC43 spike.
The researchers also looked into the nature of anti-spike antibodies after infection with SARS-CoV-2. ns-EMPEM was used to screen the three SC sera for anti-SARS-CoV-2 spike.
Anti-SARS-CoV-2 spike residues that are similar or identical to at least three of the four other -CoVs were mapped structurally, and numerous conserved patches in the S2 subunit of the spike protein that can elicit cross-reactive antibodies were discovered. As a result, cross-reactivity across β-CoVs is a target for the S2 subunit.
Anti-OC43 spike antibodies were found in the PP and SC serum. Two SC sera contained antibodies to NTD site 1, two SC sera contained antibodies to the interface, and one SC serum contained antibodies to the S2 subunit. The anti-S2 antibody-targeted helix 1014 to 1030, a highly conserved region of the spike protein throughout the -CoVs. Anti-SARS-CoV-2 antibodies were found in PP samples with high levels of anti-OC43 antibodies, but they did not correlate with protection against SARS-CoV-2 infection.
Anti-HKU1 spike antibodies were shown to be higher after a SARS-CoV-2 infection. The C-terminal domain (CTD) and/or the NTD and S2 domains were targeted by these antibodies.
Antibodies to the S1 subunit were found in both PP and SC sera, although antibodies to the S2 subunit were more prevalent in SC sera.
The study found that an infection with the SARS-CoV-2 virus leads to the production of antibodies that respond with the conserved β-CoV spike epitopes, while also increasing the levels of anti-spike antibodies against HCoV. COVID-19 pathogenesis is linked to this cross-boosting. Individuals who have been vaccinated or previously infected with SARS-CoV-2 may get immunity to seasonal HCoVs as a result of this cross-boosting.
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