A coronavirus vaccine candidate developed by the University of Cambridge could begin clinical trials in the UK in the autumn.
A £1.9 million funding boost from Innovate UK, the government’s innovation agency, has provided support for a collaboration between Cambridge spin-out company DIOSynVax, the University of Cambridge and the University Hospital Southampton NHS Foundation Trust.
The funding of £1.9 million will allow the team to take the vaccine candidate to clinical trial at the University Hospital Southampton NHS Foundation Trust and could begin as early as autumn this year.
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This comes after the director of the Oxford Vaccine Group said it was “just possible” that the Oxford vaccine candidate could finish clinical trials and have data to put before regulators before the end of this year.
However, on Saturday England’s chief medical officer, Professor Chris Whitty, said a vaccine for coronavirus may not be ready until next winter.
How does the Cambridge vaccine work?
Coronaviruses, like the virus that causes COVID-19, SARS-CoV-2, use spike proteins on their surface to attach to and invade cells in the body.
One vaccine strategy is to block this attachment, but not all immune responses against the virus and spike protein are protective. Antibodies to the wrong part of the spike protein have been implicated in triggering hyper-inflammatory immune responses causing life-threatening COVID-19 disease, experts say.
Additionally, COVID-19 is mutating and changes in the spike protein during the pandemic have already been observed.
The research team at Cambridge have used banks of genetic sequences of all known coronaviruses, including those from bats, the natural hosts of many relatives of human coronaviruses, to develop their vaccine candidate, called DIOS-CoVax2.
They have developed libraries of computer-generated antigen structures that can train the immune system to target key regions of the virus and system to make good anti-viral responses.
These immune responses include neutralising antibodies, which block virus infection, and T-cells, which remove virus-infected cells.
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Researchers say this “laser-specific” computer-generated approach is able to help avoid the adverse hyper-inflammatory responses that can be triggered by recognition of the wrong parts on the virus’s surface.
Professor Jonathan Heeney, head of the Laboratory of Viral Zoonotics at the University of Cambridge, and founder of DIOSynVax, said: “Our approach involves 3D computer modelling of the SARS-CoV-2 virus’s structure.
“It uses information on the virus itself as well as its relatives – SARS, MERS and other coronaviruses carried by animals that threaten to ‘spill over’ to humans again to cause future human epidemics.
“We’re looking for chinks in its armour, crucial pieces of the virus that we can use to construct the vaccine to direct the immune response in the right direction.
“Ultimately we aim to make a vaccine that will not only protect from SARS-CoV-2, but also other related coronaviruses that may spill over from animals to humans,” said Prof Heeney.
“Our strategy includes targeting those domains of the virus’s structure that are absolutely critical for docking with a cell, while avoiding the parts that could make things worse.
“What we end up with is a mimic, a synthetic part of the virus minus those non-essential elements that could trigger a bad immune response.”
What makes the vaccine different to other candidates?
While most vaccines use RNA or adenoviruses to deliver their antigens, DIOSynVax’s is based around DNA.
Once an antigen – a toxin or other foreign substance which induces an immune response in the body – is identified, the key piece of genetic code that the virus uses to produce the essential parts of its structure is inserted into a DNA parcel known as a vector.
The body’s immune cells take up the vector, decode the DIOS-vaccine antigen and use the information to programme the rest of the immune system to produce antibodies against it, researchers say.
How do viruses jump from animals to humans?
Every animal species hosts unique viruses that have specifically adapted to infect it. Over time, some of these have jumped to humans – these are known as ‘zoonotic’ viruses.
As our populations grow, we move into wilder areas, which brings us into more frequent contact with animals we don’t normally have contact with. Viruses can jump from animals to humans in the same way that they can pass between humans, through close contact with body fluids like mucus, blood, faeces or urine.
Because every virus has evolved to target a particular species, it’s rare for a virus to be able to jump to another species. When this does happen, it’s by chance, and it usually requires a large amount of contact with the virus.
Initially, the virus is usually not well-suited to the new host and doesn’t spread easily. Over time, however, it can evolve in the new host to produce variants that are better adapted.
When viruses jump to a new host, a process called zoonosis, they often cause more severe disease. This is because viruses and their initial hosts have evolved together, and so the species has had time to build up resistance. A new host species, on the other hand, might not have evolved the ability to tackle the virus. For example, when we come into contact with bats and their viruses, we may develop rabies or Ebola virus disease, while the bats themselves are less affected.
It’s likely that bats were the original source of three recently emerged coronaviruses: SARS-CoV (2003), MERS-CoV (2012) and SARS-CoV-2, the cause of the 2019-20 coronavirus outbreak. All of these jumped from bats to humans via an intermediate animal; in the case of SARS-CoV-2, this may have been pangolins, but more research is needed.