Central Kenya is on the UK Red list and is in lock-down again, one year to the day since it was first locked down. This time, serious Covid-19 infections are on the rise and total deaths have passed 2000, a figure thankfully still low compared to many other countries. Most air travel has ceased and Corona (Swahili abhors words that end in consonants, so I will use that term for Covid-19/ SARS-CoV-2) has ruined Easter plans for many.
Angela Merkel, of whom I am usually a great fan, annoyed me the other day by linking the latest German lock-down to the arrival of the British (or did she say Englisch?) variant. Since when do viruses have nationalities or passports? Every day we hear of Brazilian, Indian, South African variants, which makes people panic, politicizes the pandemic and has led to Sinophobia, already ramped up by The Donald. Yet of one thing we can be sure: by the time a new variant has been identified, it will already have spread to hundreds or thousands of others, and is probably already in other countries.
Last week I was asked by a UK history student, currently locked down in Kenya, to explain the difference between viral immunology and molecular epidemiology, phrases he had read in a newspaper. He asked why he had to be blinded by science, to which I replied that it was time he was enlightened by science. It reminded me of an argument we had at University years ago when an art student scoffed at a physics graduate who had not heard of James Joyce. Why is it that the ‘reasonably educated’ are expected to have heard of Dante, Donne, Durer and Michelangelo but not Dalton, Bohr, Heisenberg, Planck, Crick or Edwin Hubble? If I wanted to start an argument, I could suggest that the latter group’s contribution to modern life is far greater than the former’s. Is the gap between the scientist and the ‘ordinary’ person widening?
So I told him the next time he thought he was alone, he should contemplate the fact that his body is a mere biome, providing a home for hordes of ‘living’ creatures (I write 'living' in quotation marks because viruses cannot really be called alive). These include an estimated 380 trillion (or 380,000,000 million) viruses, which have set up home in his body and are doing no harm at all. No, it’s the recent immigrants that are the problem. Many of humanity’s nastiest diseases originated in animals, including both influenza and smallpox viruses, which together killed around 320 million people in the 20th Century alone. Jared Diamond in Guns, Germs and Steel has a chapter entitled ‘The lethal gift of livestock’, which I would retitle ‘The lethal risk of proximity to animals’ because having pets and eating wild animals is no less dangerous than milking cows.
How do viruses hop from one species to another? Transmission of an animal virus might start with a human acting as an accidental host. The person may get unwell but is unable to pass the virus on to another person (e.g. Foot and Mouth in humans). Later in its evolution, a virus may go back and forth between animal and humans; this is called a zoonosis (e.g. brucellosis). Eventually, an animal virus (e.g. rinderpest) may mutate sufficiently as to cause a new disease in humans (measles).
Epidemic diseases have four characteristics. First, they thrive as 'crowd diseases' spreading quickly in densely populated areas from infected persons to healthy people, so that most of a population is exposed. Second, they are acute illnesses; so we either die or recover completely. Third, those who do recover develop antibodies, or are vaccinated, often resulting in lifelong immunity. Finally, viral epidemics may die out, unless the virus is super labile (like influenza). Bacterial spores such as anthrax can persist and hide in the soil for centuries but a virus cannot. If it persists in the body, it may eventually merge with a host’s DNA and live happily ever after.
Coronaviruses have been around for at least 8000 years and the arrival on the scene of a new virus infecting humans is no surprise either. These viruses are small (26-32,000 bases compared to 3 billion bases in the modestly-sized human genome). They comprise a single strand of RNA, as distinct from the more stable, mostly double-stranded DNA viruses like smallpox. Corona is transmitted faster than DNA viruses and it mutates faster, but nothing like the high rate of mutation seen in other RNA viruses like influenza or HIV. The first coronaviruses were identified in humans in 1962. SARS-CoV-1 appeared in 2003, then MERS, both of which were much more pathogenic than ‘our’ new Corona (SARS-CoV-2). In 2013, a coronavirus (RaTG13) was identified from the Chinese horseshoe bat (Rhinolophus affinus). A very similar virus was then recovered from a Malayan pangolin, 98% similar to the 2020 ‘Corona’, so it is almost certain that the edible pangolin served as the intermediary host between the bat and the first human to be infected.
Ignorance is mother to conspiracy theories and I will continue to believe the official Chinese line. I went to Wuhan a few years ago. It's one of the most polluted cities I have ever visited but it hosts one of the most prestigious virology institutes in the world. The most likely scenario goes like this: a blood sample from a sick patient was sent to the institute and identified as a new Covid virus. The officials probably kept quiet, hoping it was an accidental host infection, but it was too late: other humans were already infected. But this hardly suggests anything sinister. I think the Chinese were just keeping their fingers crossed and hoping for the best.
Corona in humans is a wonderful example of evolution in action. It is much easier to demonstrate evolution in a virus than trying to show how humans evolved from the first fish which crawled out of the sea hundreds of millions of years ago. A virus cannot replicate on its own so it inserts its genetic material in the host’s cells, co-opting proteins to create viral replicates, until new viral particles burst out in their millions. As the virus replicates, its genes will undergo random 'copying errors' called genetic mutations (substitution of one nucleotide base with another). Over time, these mutations can lead to alterations in the viral surface proteins, or antigens. Mutations on key sites on the Corona genome (e.g. K417N or 501 etc.) lead to ‘variants’ which are only noticed when they have characteristics that make life harder for the hosts (us). Most mutations are harmless, while a few are deleterious to the virus. From the virus’ point of view, mutations are useful if it increases its chances of perpetuity, such as adapting itself to a new host species. New variants of Covid are just better adapted (e.g. faster at transmission or cleverer at evading the host’s antibodies and immune system) but not necessarily more pathogenic because it is not in the interest of a virus to kill its host quickly. A coronavirus with a small genome of 30,000 base pairs still has lots of opportunities to mutate.
Stage one in viral evolution is where it has mutated well enough to jump from one species to another. Stage two is where the new host species is able to infect another of the same species. The virus may have a negative effect (illness) on the new host but if it kills the host within a few hours of infection, it has to find a new host quickly. With Ebola, just touching a victim is enough to transmit the virus. If it kills its host before the host can infect others, the virus will also disappear. At 20-50 nanometres coronaviruses are small (a nanometre being one thousand millionth of a metre) so high numbers will ensure efficient transmission. One millilitre (ml.) of nasopharyngeal fluid in a patient contains between 8-10 million copies of the coronavirus, plenty of scope for a mutation. Meanwhile there is an endless battle going on between the host and the virus: antibodies lock onto the outer surface proteins of a virus and prevent it from entering host cells, so a mutation in the virus can trick the antibody. A virus that appears different from other viruses that have infected the host has an advantage: the host has no pre-existing immunity (antibodies) to that virus. Many viral adaptations involve changes to the virus’ outer surface. This is evolution in action and it takes only hours or days.
Fortunately, most of us have been lucky with Corona. Up to 80% of cases are asymptomatic and the death rate among symptomatic patients is low, about 2 percent and falling, giving an overall death rate of 4 per thousand. Compare that to Ebola, another RNA virus which has a mortality rate of at least 50%. Epidemics have destroyed civilizations, as illustrated by the European conquest and depopulation of the New World. As humans become increasingly urban and travel faster and wider, the chances of more deadly viral epidemics increase.
Novel RNA, DNA and protein-based vaccines may save the day for most of us this time. I read that films such as Cassandra Crossing, Contagion and Outbreak have become hugely popular recently. They remain fictional but if we do not learn from what is historically a minor epidemic, we may be in for a nastier shock next time.