Dangers of Variants Are Building for Rhode Islanders - Nick Landekic
Nick Landekic, Guest MINDSETTER™
Dangers of Variants Are Building for Rhode Islanders - Nick Landekic

The SARS-CoV-2 virus is a single-stranded RNA virus, in the same family as Ebola, influenza, measles, rabies, and hantavirus. Though SARS-CoV-2 might mutate comparatively slower than others in this nasty group, RNA viruses in general mutate quickly.
The backbone of the virus is its ‘nucleotide sequence’, as set of about 30,000 ‘letters’ of RNA, ribonucleic acid, that codes information for how the virus is assembled. The virus infects our cells, and reprograms and turns them into ‘zombies’ to make more copies of itself. When a viral particle, called a virion, infects a human cell, in about 10 hours the cell bursts open and releases about 1,000 new virion copies. In the process of making multiple copies of itself, errors can happen to the nucleotide information sequence. Changes in any of these ‘letters’ are a mutation. Mutations are random and most are of no consequence or can even be deleterious to the virus. It also usually takes multiple accumulated mutations to make a meaningful change in the virus’s behavior, such as making it more easily transmitted or resistant to vaccines.
GET THE LATEST BREAKING NEWS HERE -- SIGN UP FOR GOLOCAL FREE DAILY EBLASTThe process of evolution selects for mutations that help the virus survive. Mutations that make a strain more easily transmitted, or to evade treatments and vaccines, enhance its survival, become dominant, and cause more infections and deaths. Once that happens, a new mutation can spread fast.
Even though mutations that are helpful to the virus – and thus harmful to us – might only occasionally happen, the sheer numbers show the danger. There are so many virions reproducing that mutations can accumulate quickly.
It’s possible to study and measure the speed of viral mutations in the lab. It becomes harder to estimate and predict the rate and frequency of mutations happening in people, in part because there are far more mutations circulating than have been, or can be, identified. One study of 12,343 individual viral samples found 1,234 mutations. Another study of 3,067 viral samples found 782 variations. Yet another study of 4,521 viral lines found 3,169 unique point mutations, and a study of 10,022 viral lines found 5,775 variants .
The inescapable bottom line is, the more people that are infected with the virus, the more mutations we will get and the faster they will emerge, since our bodies are the incubators where mutations happen.
In the human body, there are over 100,000,000,000 – one hundred billion – of our cells that the coronavirus targets and can infect. Not just your nose and lungs, but your digestive tract, your heart, your brain, your blood vessels, even your bladder. This means that each person infected by the coronavirus can generate trillions of virions and potentially thousands to millions of mutations. Though most of these will be irrelevant, this process multiplied by hundreds of thousands of infected people, hour after hour, means that dangerous mutations can quickly emerge – and have.
Mutations are always happening, and an infected person is constantly spreading the virus. One milliliter of sputum, about 20 drops, perhaps in a sneeze, can contain 10,000,000 – ten million – virions. There could be a mutation found in each sneeze. Just by breathing an infected person can release up to 100,000 virions per minute, literally millions every hour.
The virus can stay airborne for at least three hours. It’s not known for sure, but it may be possible to become infected by inhaling just a hundred virions . It’s also been shown infection can spread in a restaurant from 20 feet away in just 5 minutes. With an infected person exhaling million of virions every hour – and more with sneezing – you might want to think about this the next time you consider eating indoors with strangers.
The virus wants to survive and spread, and mutations that help it do that push out other weaker strains. 5 prominent mutations have been identified so far that result in the virus spreading more easily. While these are often called the “U.K.” or “South Africa” variants, they are evolving independently. Similar mutations are appearing in multiple places at the same time. The names are simply where they were first identified.
Some parts of the virus are mutating faster than others, such as the region that codes for the spike protein. This is a particularly dangerous part of the virus, because the ‘spike’ is how the virus attaches to and infects our cells. Ominously, the rate of mutations may be accelerating.
Mutations have been found so far in Massachusetts, Connecticut, New York, and about half the states. Specialized testing procedures are needed to identify mutations; they cannot be recognized in a standard COVID test.
Despite some recent reduction in the numbers, Rhode Island for many months has consistently been in the bottom and among the poorest performing states by almost any measure. We currently have the third highest infection rate in the country, and for a time had the worst infection rate anywhere in the world. We are still at a Critical level of infection.
One out of every 500 Rhode Islanders have already died of COVID-19, the fourth highest per capita death rate in the country. Rhode Island is a dismal 45th in terms of vaccination progress.
Officially, more than one in ten Rhode Islanders have already been infected. The actual number is no doubt much higher. The easier we make it for infection to spread, the harder hit we will be with new mutations.
Even if a mutation does not cause more severe illness and is “only” more easily spread, more infections means more deaths. The rules of contagion dictate that a 50% increase in transmissibility results in an 8-fold increase in deaths.
In addition to being more easily spread, some of the mutations are also becoming resistant to antibody drug treatments - and vaccines. Evolutionary pressures select for viral mutations that can evade our immune system – and drugs and vaccines. If the structure of the spike protein is affected in a mutation, vaccines and drugs can work less well against it since the spike protein is generally what they target. Many studies are documenting this emerging resistance.
Another consequence of the new mutations is that it’s possible to get re-infected after having been already ill with an earlier strain. Whatever immunity a person might have had from being infected, may not provide protection against new mutations.
Wherever new mutations have been found, they have quickly become dominant and death rates have risen sharply. In the U.K. and South Africa, two countries that were among the first to be hit with new, more easily transmitted mutations, deaths skyrocketed after periods of relative control.
More infected people equals more mutations. An infected person can be contagious for 10-20 days. 200,000 infected Rhode Islanders, contagious for 10 days each, would collectively spew out about 300 trillion - 300,000,000,000,000 - virions just by breathing. Even more with sneezing. This is why our lives depend on wearing good masks, to protect both those around us, and ourselves.
The virus has already mutated, and will continue to do so. The high infection rate in Rhode Island means we could be a breeding ground, a petri plate for new mutations. If we want to avoid the fate of places like the U.K. and South Africa – and the devastating deaths that come with it - the only solution is to bring down the infection rate, as Dr. Michael Fine has repeatedly and eloquently warned. If we don’t have the self-discipline for the kinds of containment measures that have worked in many other countries, then we all need to get vaccinated as soon as possible, much faster than has been happening so far in Rhode Island.
Otherwise, if Rhode Island isn’t careful, we may well be next. The next deadly mutation to emerge might be called the “Rhode Island strain”.
Nick Landekic a retired scientist and biotechnology executive with over 35 years of experience in the pharmaceutical industry.
