The antibodies that the human body creates after being infected with a virus can be very powerful. Typically, a virus enters the body by way of a call and uses it as a factory to create duplicates of itself, which in turn spread and infect new cells.
The antibodies work by binding to the virus and this can block it from attaching to and entering the cells in the human body in the first place. But in case the virus does not need to exit the cell in order to spread to the neighbouring cells, can the antibodies be effective against it is the question.
Scientists recently asked this question for SARS-CoV-2, which causes Covid-19. This highly infectious coronavirus can change human cells, making them fuse with two or more nearby cells. These super-cells, with large merged cell bodies, are excellent viral factories.
The super-cells, known as syncytia, share multiple nuclei, the part of the cell that contains the genetic material, and abundant cytoplasm, the jelly-like substance that surrounds the nucleus.
Having more of these components in one giant cell helps the virus replicate more efficiently. And by fusing cells, SARS-CoV-2 increases its resources without being exposed to the neutralising antibodies that slosh around outside our cells.
The study by Alex Sigal and colleagues tested two coronavirus variants (alpha and beta) for their ability to transmit from cell to cell and investigated whether this mode of transmission was sensitive to antibody neutralisation. The alpha variant (first identified in the UK) is sensitive to antibodies, and the beta variant (first identified in South Africa) is less sensitive to these antibodies.
The Sigal study, which is yet to be published in a scientific journal, revealed that cell-to-cell transmission with both variants successfully evaded antibody neutralisation. This shows that when the virus takes hold, it will be more difficult to eliminate in cells that can fuse with each other.
Viruses have coexisted with humans and animals for millennia, so they have evolved tricks to avoid being recognised by our immune system. Such an immune evasion strategy is the direct transmission from cell to cell, which doesn’t always require cell fusion.
It is also possible for viruses to travel to their next host cells by exploiting tight associations between neighbouring cells that shield them from antibodies. It is reasonable to assume that antibodies are most effective at preventing entry into the host cell and less effective in parts of the body where the infection is already established.
Luckily, our immune system has also evolved alongside viruses, and we have learned to build defences that work in many ways.
T cells are white blood cells that, following vaccination or infection, are trained to recognise and kill infected cells. They don’t rely on recognising free-floating virus, so cell-to-cell transmission does not reduce their ability to seek and destroy viral factories. Like cells capable of producing antibodies, T cells can remember a previous infection and act rapidly when the same virus comes along again.