This publish continues from my earlier publish, which discusses the scientific variations between COVID-19 and the seasonal flu. These two ailments progress so in another way as a result of the viruses that trigger them, SARS-CoV-2 and Influenza, respectively, have little or no in frequent. Right here I focus on the positive molecular particulars of those two viruses and the way they assault us.
1. The Virus Particles
Viral particles are available in all kinds of shapes, sizes, and compositions. Whereas this could sound like an esoteric element, the composition of viral particles is what determines how a virus finds and enters its most well-liked host cell. Viruses are known as obligate intracellular parasites, as a result of they can not do virtually something on their very own. They should enter a bunch cell and hijack it. They then reprogram that host cell to grow to be a manufacturing facility for making extra viruses, ultimately spilling them out to assault extra cells.
Viral particles of SARS-CoV-2 (L) and H1N1 influenza A (R).
Each influenza and SARS-CoV-2 particles include a lipid envelope, which is an outer protecting fabricated from fats molecules taken from the beforehand contaminated host cell, the one which produced the virus. Because of this handwashing is a key protection towards each viruses—cleaning soap dissolves the fatty envelope and destroys the viral particles.
Embedded within the lipid envelopes are so-called “spike proteins.” For influenza, this spike protein is named hemagglutinin (HA), whereas the SARS-CoV-2 spike protein is named glycoprotein S (gS). HA and gS are completely unrelated and in contrast to one another. As a result of the spike proteins are what discover and persist with the host cells, this explains why influenza and SARS-CoV-2 infect completely totally different cells.
2. Host Cells
The HA spike protein of influenza sticks to sialic acid, which pokes out from the floor of the cells that line the throat, nasal passages, and bigger airways of the lungs. These are the goal cells of influenza, which helps clarify why this an infection ends in heavy mucus manufacturing. The gS spike protein of SARS-CoV-2, however, sticks to the ACE2 protein which is discovered on cells very deep within the lungs. Completely totally different spike proteins means completely totally different goal cells.
Drawing of the lungs (L) and close-up of alveolar air sacs (R)
Actually, the principle goal cells of SARS-CoV2 are the alveolar cells, which type the very finish of the airways, the microscopic sacs of air surrounded by blood vessels the place gasoline alternate takes place. In different phrases, SARS-CoV-2 viruses infect the precise cells the place oxygen is absorbed by the lungs. Because of this extreme instances of COVID contain dangerously low blood oxygen ranges. Regardless of how a lot air they inhale, these sufferers can not take in sufficient oxygen as a result of the cells through which this occurs are ravaged by the an infection. Regular air solely comprises about 20 % oxygen, so giving sufferers 50 % and even 100% oxygen often helps.
(UPDATE: A brand new research discovered that ACE2 receptors are additionally discovered within the nasal passages and, whereas this isn’t the principle reason behind morbidity and mortality, it’s seemingly the route of first entry for the virus, serving to clarify why this bug is so contagious.)
3. Receptor Proteins
As talked about above, influenza viruses bind to sialic acid, which is discovered on the internal surfaces of the big areas all through the respiratory system. Influenza binds there, enters the cells, and begins the an infection. The receptor protein that SARS-CoV-2 binds to, nevertheless, is named ACE2 and it is a way more attention-grabbing story. Actually, COVID-19’s path to an infection by way of ACE2 may clarify a number of of the peculiar issues about this sickness.
ACE2 stands for angiotensin changing enzyme 2 and, because the title implies, it’s a essential protein for sustaining our blood quantity and our blood stress. It’s positioned within the tiniest air sacs in our lungs as a result of that is the place it could actually make intensive contact with the bloodstream by way of the thousands and thousands of tiny vessels that encompass these air sacs. We all know that people with hypertension and different cardiovascular ailments are at elevated danger of creating and dying from COVID-19 and the ACE2 receptor could also be partially accountable.
As well as, there’s information that sufferers on ACE2-inhibitors (a blood stress remedy) have higher outcomes than these with hypertension which are not on ACE2-inhibitors, not solely additional implicating this receptor within the severity of COVID-19 illness, but in addition opening up a possible avenue for therapy. ACE2-inhibitors are among the many many medicine being examined as COVID-19 therapies.
ACE2 may also clarify two of the demographic patterns of COVID-19. This illness appears to contaminate youngsters solely very not often, not like influenza, which sickens youngsters mercilessly. That is believed to be as a result of the lung cells of youngsters have a lot much less ACE2 on them than adults’ do. The SARS-CoV-2 virus merely doesn’t persist with youngsters’s cells.
Additional, males are at better danger than girl, by an element of two, of each contracting and dying from COVID-19. As soon as once more, the expression of ACE2 could clarify this, as it’s identified to be expressed extra in males. Hypertension can be extra frequent in males than in ladies. ACE2 could be the key issue connecting all these variables.
4. Genetic Materials
SARS-CoV-2 is within the Coronavirus household and the viruses that trigger the seasonal flu are Influenza viruses. Whereas each use RNA as a substitute of DNA for his or her genetic materials, SARS-CoV-2 has a single piece of +RNA (or “sense RNA”) which appears very very like our personal pure mRNA and may be learn by our cells as such. This genome encodes 14 proteins and may be very massive by viral requirements.
The genomes of SARS-CoV-2 (L) and Influenza A (R)
The genome of influenza viruses, however, consists of a number of small items of RNA, which is itself very uncommon amongst viruses. Their tiny genome encodes simply 8 proteins, however, much more surprisingly, it’s fabricated from “-RNA” (or “anti-sense RNA”), which can’t be learn by the cell in its unique type.
Whereas this may occasionally seem to be an arcane distinction, it exhibits that the 2 viruses are solely very distantly associated. They’re in the identical phylum (the way in which that people and nice white sharks are), however their ancestors diverged tens or tons of of thousands and thousands of years in the past. Additionally, the totally different sorts of genomes means they hijack our cells in several methods.
5. SARS-CoV-2 is a “Novel” Coronavirus
With occasional exceptions, the strains of influenza that flow into globally every year, inflicting the seasonal flu that sickens thousands and thousands, are variations of earlier strains which have additionally circulated. They don’t seem to be wholly new to us, simply mutated just a little bit. This implies that the antibodies we have now from getting the flu (or a vaccine) in earlier years are sometimes partially efficient in future years. They gained’t fully inhibit the brand new pressure, however they may weakly persist with it, like a weight dragging it down, and this reduces the severity of the an infection, slowing its progress whereas our immune system scrambles to generate particularantibodies. This interprets right into a shorter, much less extreme sickness.
SARS-CoV-2 just lately jumped from bats to people, making it a “novel” virus. It isn’t merely a variation of one thing our physique has seen earlier than. (Regardless of the same title, it’s NOT a mutant of SARS-CoV-1, which prompted the SARS outbreak of 2002.) So far as our immune system is anxious, SARS-CoV-2 is totally new and not one of the antibodies in our arsenal acknowledge it.
Due to this fact, the an infection has a giant head begin, unfettered by any antibodies. By the point we start to make antibodies to struggle it, it has already established itself all through our lungs (and different tissues, it appears). As soon as an an infection is entrenched in our personal cells, it’s a lot more durable to clear as a result of we will’t merely kill all of the virus-producing alveolar cells as a result of then our lungs gained’t work in any respect. Actually, that’s a part of why COVID-19 is so lethal. Each the virus itself and our immune system crew as much as assault the very cells that carry out a essential position in our our bodies—getting oxygen from the air.
The flu is often brought on by novel viruses as properly, just lately jumped from another species. You’ve most likely heard of swine flu, chook flu, and so forth. That’s exactly why these had been lethal pandemics and not simply the common seasonal flu. They weren’t simply slight tweaks of viruses that we’ve been constructing antibodies for over the course of our lives. (Facet word—in case you get the flu vaccine yearly, you seemingly construct up cumulative immunity that may shield you in future years.)
It’s tempting to need to reduce the terrifying menace that COVID-19 poses, however COVID-19 and the flu are very totally different diseases as a result of they’re brought on by very totally different viruses. The continued comparisons aren’t simply unhelpful, they’re a part of wild conspiracy theories and a large misinformation marketing campaign that public well being officers at the moment are calling the infodemic.
Please be a part of the answer, slightly than the issue, by sharing articles primarily based on actual science with out political agenda. And please keep residence as a lot as attainable. When you should exit, put on a masks, maintain your distance from others, and wash your arms totally earlier than and after. By slowing the unfold of this illness, we may give our scientists and healthcare suppliers the time they should develop therapies which are urgently wanted for probably the most susceptible amongst us.