In addition to SARS-CoV-2 (COVID-19), six human coronaviruses (hCoVs) are known: four seasonal coronaviruses (hCoV-229E, -NL63, -HKU1, and -OC43) which cause mild upper respiratory diseases, and the two most recently discovered viruses, SARS-CoV-1 and MERS-CoV, which cause severe diseases.
Protection from Previous Exposure to Other Coronaviruses
At the start of the COVID-19 pandemic some people speculated if previous exposure to the Coronaviruses that cause the common cold might provide some protection against COVID-19.
In theory if the genetic makeup of the cold causing Coronaviruses is similar enough to COVID-19 then the body might be primed to fight COVID-19.
However, for this to be the case:-
- the viruses would need to share some common genetic features,
- you would need to have been infected by one of the other Coronaviruses,
- you would need to still have antibodies or a T cell response.
Previous research reported in 2015 which was undertaken by Keith Grehan from the University of Kent’s Viral Pseudotype Unit has suggested that it may be possible to create a universal Coronavirus vaccine by targeting the S2 region of the spike protein.
The research raised the possibility that the S2 region is a vaccine target that could be common to most, or all, of the betacoronaviruses.
“If we can confirm that humans do produce antibodies against the S2 region, there is a real possibility that a vaccine could work against all of the betacoronaviruses, including the OC43 virus, which causes colds,” Keith concluded.
Conversely, this raises the possibility that previous infection with OC43 may produce antibodies against the S2 region of the spike protein that may cross-react with COVID-19.
Pre-Existing Coronavirus Antibodies May Help
In November 2020 researchers at the Francis Crick Institute and University College London have found that some antibodies, created by the immune system during infection with common cold coronaviruses, can also target SARS-CoV-2 and may confer a degree of protection against the new viral strain. Crick Institute Article
In their paper, published in Science, the scientists found that some people, notably children, have antibodies reactive to SARS-CoV-2 in their blood, despite not ever having being infected with the virus. These antibodies are likely the result of exposure to other coronaviruses, which cause a common cold and which have structural similarities with SARS-CoV-2.
The spike of COVID-19 is made of two parts or subunits, performing different jobs. The S1 subunit allows the virus to latch onto cells and is relatively diverse among coronaviruses, whereas the S2 subunit lets the virus into cells and is more similar among these viruses. The work shows that the S2 subunit is sufficiently similar between common cold coronaviruses and SARS-CoV-2 for some antibodies to work against both.
It was previously thought that only antibodies to the S1 could block infection, but there is now good evidence that some antibodies to S2 can be just as effective.
hCoV Cross-Reactive T Cell Memory
There is now also evidence that pre-existing T cell immunity to common cold coronaviruses can prime the response to SARS-CoV-2 (COVID-19). Targets of T Cell Responses to SARS-CoV-2
In blood samples from healthy control donors (collected between 2015 and 2018) substantial cross-reactive coronavirus T cell memory was detected, suggesting cross-reactive T cell recognition between seasonal cold coronaviruses and SARS-CoV-2. All healthy donors were IgG seropositive to HCoV-OC43 and NL63 RBD, to varying degrees.
SARS-CoV-2-reactive CD4+ T cells were detected in ∼40%-60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2.