By the end of February 2020, cases of coronavirus (Covid-19) in Italy were climbing with remarkable speed. Individuals were leaving the country’s north with no symptoms, unknowingly carrying the virus, and turning up in other places around the world. Sure enough, the first cases of Covid-19 that cannot be traced back to travellers from previously affected places have begun to appear in England. By 1 March, Scotland’s first case took the UK total to 36, and that figure has since increased to 85 at the time of writing.
Italy is seeing the numbers of those infected double every few days. Therefore it is probable that, within a week or two, UK cases will have risen to around 300 and that thousands of people will have been infected by mid-March.
Within weeks of its outbreak in December 2019, Chinese scientists made the genetic sequence of coronavirus (Sars-CoV-2) publicly available, enabling the search for a vaccine to begin in haste. There are different approaches to vaccine design. The polio virus, for example, was originally grown in bulk before being chemically “inactivated” and then injected into people. Small parts of the virus called antigens stimulate antibodies that then pounce if the real virus enters the body.
Mutated live viruses, such as measles, mumps, and rubella, that no longer cause diseases provoke even stronger immunological responses. These whole-virus preparations, however, take time and resources to produce. Individual antigens in isolation can train the immune system without having to come into contact with the virus itself. The hepatitis B and human papillomavirus (HPV) vaccines are of this sub-unit type.
A recent variation on this approach involves “plug and play”, in which raw pieces of DNA or RNA (Ribonucleic acid) are injected into the body and then start producing sub-units of viral protein that the immune system learns to fight.
One US company, Moderna, has an RNA vaccine ready to test on the key Sars-CoV-2 S protein. Inovio Pharmaceuticals is another firm advocating the DNA approach. But testing the safety and efficacy of these vaccines will take months, and we won’t have a vaccine before 2021.
Of the dozens of pre-existing anti-viral drugs that were used in China following the outbreak’s start, only one is still being trialled – a compound called remdesivir, which was originally invented to stop the Ebola virus between 2014 and 2016 (it didn’t work). This compound targets an enzyme that replicates the genetic material in coronavirus. Remdesivir entered phase III clinical trials at the end of February 2020.
Unfortunately, even if the drug does work, the task of manufacturing enough to treat the millions of people around the world who will need it is gargantuan.
Without a vaccine, and with coronavirus spread across every continent except Antarctica, the World Health Organisation says that public health officials are in “unchartered territory”.
What is to be done? It may sound trivial to emphasise hand hygiene, but the virus sits on surfaces and will transmit to our fingers and, all too easily from there, to our mouths and noses. Crowded places should be avoided. Schools should be closed, in spite of the problems this creates for working parents, and major gatherings should be cancelled (the UK government plans to introduce emergency legislation that will empower it to curtail public events and designate no-go areas).
The explosive spread of Covid-19 in South Korea (5,186 cases reported at the time of writing, the highest number outside of China) can be traced to members of a religious sect who contracted the virus through close proximity to an infected member before returning to their communities, triggering an epidemiological chain reaction.
Transmission of the virus is ultimately a matter of probability. The fewer opportunities we give it to reach us, the better our chances of avoiding infection (working from home is advisable). The likelihood is that most of us will ultimately become infected (reportedly around 60 per cent, with most suffering mild symptoms if anything at all).
The remarkable ability of the virus to spread arises from its ability to replicate in the upper respiratory tract (mouth and nose). The 2002-2003 Sars-CoV virus, although similar to Covid-19, only replicated deep in the lungs. The disease was more serious as a result, but it also meant that transmission did not occur before people were already sick and could be identified and isolated. Asymptomatic people wandering around spreading Covid-19 are central to its transmission, and also explain why the disease has caused more alarm across the world than Sars did in 2002-2003.
Several of my medical colleagues say they hope to get hit by coronavirus early, when there are beds available with oxygen and sufficient NHS staff to cope. On 1 March, Health Secretary Matt Hancock claimed that the NHS has around 50 beds currently suitable for ventilating isolated patients, and the ability to scale rapidly to 500 and then 5,000 beds before too long. But based on the estimated number of people likely to become infected, even Hancock’s optimistic aspiration of 5,000 beds will not be enough.
It is possible that the infection rate will not increase as fast as we fear. Rapid and widespread implementation of good public health practices will help. The fading of winter, with increased temperatures and ultraviolet light, might slow the virus’s spread (the genome is UV-sensitive and the virus’s ability to survive on surfaces diminishes as temperatures rise).
But unlike seasonal flu, it is clear from some of the places in which the disease is spreading, such as Singapore, that warmer weather does not prevent transmission and there is little evidence it will help.
The discovery of the cause of Covid-19 within days of the disease being recognised has enabled the development of several experimental vaccines. Historically, epidemiology has also shown how to curtail the spread of diseases.
Covid-19 will infect millions and deaths will occur in the UK. Science has offered potential solutions in record time. Political will is now needed to minimise the virus’s impact on mankind.
This article appears in the 04 Mar 2020 issue of the New Statesman, Inside No 10