Connor Bamford is a research fellow in virology at Queen’s University Belfast. He is particularly interested in changes to spike proteins occurring on COVID-19 variants. Especially the UK one, which he says is ‘more concerning than other, harmless changes to the virus’. That’s because battles rage between spike proteins and vaccines at this point.
We Need to Understand How the Spike Protein Works
Viruses are unable to survive on their own, unlike many bacterial or fungal pathogens. They need to enter ‘host’ cells to replicate, after hijacking their biochemical machinery to build new virus particles. Human body cells have negatively-charged fatty outer coatings to protect their enzymes, proteins and DNA against these invasions.
Attacking viruses have fatty, positively-charged enveloping membranes and the two repel each other. Viruses therefore need to lock the two membranes together with a ‘spike’ glycoprotein bridge. Three spike proteins combine forces, Connor Bamford explains. One binds to the target cell, one fuses with the membrane, and the third penetrates the host cell.
The Ongoing Battle Between Spike Proteins and Vaccines
Pfizer, Moderna and BioNTech vaccines use safe versions of virus spike proteins to train immune systems to make antibodies. However, as viruses mutate, their biochemical properties change too, and this can knock on to their spike proteins.
Most COVID variants are harmless from this perspective. But some cause viruses to become more infectious. This can be when antibodies no longer bind on attacking spike proteins, or the spike protein becomes ‘stickier’, explains Connor Bamford.
This is how mutated spike proteins made the UK and South African coronaviruses deadlier. We may be confronting a never-ending story of battles raging between spike proteins and vaccines. Vaccines are not drop your guard cards. We are learning they may be our paroles, just for now.
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Preview Image: How Virus Gets into Cells