Does catching the common hold reduce COVID-19 symptoms?
A phlebotomist takes blood through a finger prick during a Covid-19 antibody test -  AFP/File Angela WEISS, Alexey DRUZHININ  New research suggests a possible connection between catching the common cold and a later COVID-19 infection. The common cold virus is a type of coronavirus, belonging to the same family as the SARS-CoV-2 virus that causes the COVID-19 disease. These findings come from Stanford University School of Medicine where researchers have reviewed data patterns that suggest that people with COVID-19 may experience milder symptoms when specific immune cells remember previous encounters with seasonal coronaviruses. By seasonal coronaviruses, this is primarily the common cold. Such immune cells can mobilize faster against SARS-CoV-2. The researchers state that thus possibly suggests why children, who tend to contract more colds than adults, appear to be more resilient to infection by SARS-CoV-2. The immune cells are killer T cells, which are present in blood and lymph. This is based on an analysis of killer T cells taken from COVID-19 patients displaying the worst symptoms. The cells in these patients exhibit fewer signs of having had previous run-ins with common-cold-causing coronaviruses. When a killer T-cells receptor detects a peptide on a cells surface that is out of place (such as from a viral infection) the T-cell reproduces and produces cells with receptors designed to target the same peptide sequence. After the infection, some of the original T cells become memory T cells and exhibit continued sensitivity and they can be reactivated should the same (or similar) peptide be detected in the future. The reason there could be an affect from the SARS-CoV-2 virus is because the genetic sequence is relatively similar to common-cold-causing coronavirus strains. The scientists reached their conclusion by assessing blood samples taken from healthy donors before the COVID-19 pandemic began. The researchers then determined the numbers of T cells targeting each peptide represented in the panel. This showed that unexposed individuals killer T cells targeting SARS-CoV-2 peptides that were shared with other coronaviruses were more likely to have proliferated than killer T cells targeting peptides found only on SARS-CoV-2. The level of effectiveness from these memory cells depends upon the speed at which they detect a virus and at which they replicate. These effect was demonstrated through laboratory studies, using blood samples taken from patients and measuring cell counts. The study was funded by the U.S. National Institutes of Health. The paper is titled CD8+ T cells specific for conserved coronavirus epitopes correlate with milder disease in COVID-19 patients, and it is published in the journal Science Immunology.