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I've read that SARS-Cov-2 has several variants, e.g.:
When does one decide to refer to a virus as a new variant?
- I looked at /questions/tagged/variant?tab=Votes
- The question What determines when a virus becomes a “new strain”? addresses strain. Is strain the same as variant?
We use them as synonyms. However, variant is, in my view, more colloquial than scientific. Strains are in the literature often defined by their distinct genome compared to other strains of the same species (might be one base-pair substitution or more). In microbiology, including viruses, we often think of a strain as the proliferation of a single distinct DNA/RNA molecule.
A new way of rapidly counting and identifying viruses
A Lancaster University professor has introduced a new concept for rapidly analysing for the presence of a virus from colds to coronaviruses.
Based on analysing chemical elements the methodology, which has been adapted from an analytical technique used to identify metallic nanoparticles, is able to detect the presence of viruses within just 20 seconds.
Although the tests would need to be performed in a lab, it could be used to quickly identify whether people admitted to hospitals have been infected by a virus -- enabling clinicians to decide treatments and also whether to admit patients into isolation wards.
The proposed technique, called 'Single virus inductively coupled plasma mass spectroscopy' (SV ICP-MS) analysis, can be used to quickly determine families of viruses. However, although the concept can identify that someone has a type of coronavirus for example, it would not be able to determine the type of coronavirus, or variants. Additional tests would still be required to find out the specific virus someone was infected with.
While SV ICP-MS is not an alternative for tests developed to specifically identify types of Covid-2 infections, it could be used to discriminate if viruses from one family, such as coronaviruses, are present or not. If a virus is found to be present, more specific testing would be needed.
The concept, developed by Professor Claude Degueldre, from Lancaster University's Department of Engineering, uses diluted samples of fluids, such as nasal mucus or saliva, from patients. A plasma torch is used to atomise and ionise the virus particles. Measurements of intensities for selected masses of the elements from the viruses provide rapid results to show the presence of a virus or not. This process works on DNA and RNA virus types within seconds.
Complementary analysis such as existing sequencing techniques can be tested to complete the identification, though they can take up to two days.
Another key benefit is the ability to test a large number of samples quickly.
Professor Degueldre said: "What we are proposing here is not a new Covid test but is a new concept to rapidly find out if there are viruses present. This would be useful if people are ill but it is not known if they have a virus or another health condition that is making them sick. This concept would inform the clinical team whether or not there is a virus to inform early treatment actions and other measures such as the need for isolation. More detailed tests would still be required to discover the exact viral infection, but results from these take longer.
"Another application for the concept is to test water samples from sewage systems or down flow in rivers. The results would enable public health experts to identify areas of cities that have viral outbreaks."
The concept is still at an early stage and further research and experiments are needed to further develop the process.
How They Are Being Rigorously Studied for Safety
Viral vector vaccines are safe and effective.
Viral vector vaccines for COVID-19 are being held to the same rigorous safety and effectiveness standards [332 KB, 24 pages] external icon as all other types of vaccines in the United States. The only COVID-19 vaccines the U.S. Food and Drug Administration (FDA) will make available for use in the United States (by approval or emergency use authorization) are those that meet these standards.
Why do scientists track variants?
Tracking different strains helps scientists figure out if certain mutations alter the way a virus functions, Dr. Adalja says. Some viral mutations may impact the best form of treatment, he points out, which would be vital information for a deadly illness like COVID-19.
In the case of SARS-CoV-2, scientists are monitoring its variants in an effort to understand how genetic changes to the virus might impact its infectiousness (and thus, its spread), the severity in illness it causes, the best form of treatment, and the effectiveness of available vaccines, Dr. Russo says.
For example, this is why you need to get the flu shot every year. Scientists develop the vaccine depending on which strains are most widely circulating for that particular flu season.
Should I choose one type of vaccine over another?
Although the overall efficacy of the Moderna and Pfizer vaccines is higher than the Johnson & Johnson vaccine, you should not wait until you have your choice of vaccine – which is likely a long way off anyway. The Johnson & Johnson vaccine is nearly as good as the mRNA-based vaccines at preventing serious disease, and that’s what really matters.
The Johnson & Johnson vaccine and other viral-vector vaccines like the one from AstraZeneca are particularly important for the global vaccination effort. From a public health perspective, it’s important to have multiple COVID-19 vaccines, and the Johnson & Johnson vaccine is a very welcome addition to the vaccine arsenal. It doesn’t require a freezer, making it much easier to ship and store. It’s a one-shot vaccine, making logistics much easier compared with organizing two doses per person.
As many people as possible need to be vaccinated as quickly as possible to limit the development of new coronavirus variants. Johnson & Johnson is expected to ship out nearly four million doses as soon as the FDA grants emergency use authorization. Having a third authorized vaccine in the U.S. will be a big step towards meeting vaccination demand and stopping this pandemic.
Editor’s note: Johnson & Johnson is a funder of the PBS NewsHour.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Left: Vials of Johnson & Johnson's Janssen COVID-19 vaccine candidate are seen during the Phase 3 emsemble trial in an undated photograph. Photo courtesy Johnson & Johnson/Handout via Reuters
Is there any link between the Oxford vaccine trials—carried out in Brazil and South Africa—and the new variants?
Pollard doesn’t think so. He told The BMJ, “The number of people in the vaccine trials is so small that it’s unlikely that our efforts would put any pressure on the virus to drive it to select new variants. Most trials only have a few hundred people vaccinated in cities of hundreds of thousands or millions of people. I don’t think vaccination has anything to do with new variants today.”
He explained, however, that the variants may be arising in Brazil and South Africa because of high transmission (as many as 40-50% of people being infected) in populations living in crowded conditions. Pollard said, “In those settings, variants of the virus that emerge that are able to spread despite existing post-infection immunity will be selected. If that’s the case, it doesn’t necessarily mean that we’re going to find ourselves in a position where vaccines don’t work against hospitalisation or severe disease, but it may be more difficult to prevent milder disease and transmission. We need to monitor the situation carefully and work out the process that would be needed to make an adjusted vaccine, should the need arise.”
Vaccination Against the New Variants: Real-World Data
We’re definitely not out of the pandemic woods yet, and neither is this blog – so let’s talk some more about antibodies today, in the hopes that we’re getting closer to the time when I (and all of us) can ignore immunology for a while.
But we’re not ignoring it today! There’s a lot of news, a lot of worry, and a lot of speculation about the variant forms of the coronavirus and what that means for the vaccination programs that are underway around the world. The short answer, fortunately, is that the antibody protection you get from the current vaccines still looks solid.
How can I say that, with so much evidence that the antibodies have decreased affinity towards the variant strain proteins? Here’s a new preprint that makes this clear. It shows neutralizing antibody activity in pseudovirus assays against the British (B.1.1.7) and South African (B.1.351) variants, with data versus a panel of monoclonal antibodies, versus convalescent plasma from coronavirus patients, and versus plasma from people who have received the vaccines.
First, the monoclonals. Checking B.1.1.7 against 12 different monoclonals showed that ten of these were equally effective, and two others showed only a small decrease in potency. The B.1.351 variant, though, was tougher. Five of the monoclonals had their activity very significantly impaired, and that includes the Lilly and Regeneron ones that are being used in the clinic right now. B.1.351 seems to evade the Lilly monoclonal outright, although the two-antibody Regeneron cocktail still seems effective as that mixture. This means that anyone using monoclonal antibody therapy with the currently available agents (and those in development as well, also tested in this work) is going to have to keep a close eye out for B.1.351 infections and related strains.
Mapping these activity changes versus single mutations showed that two residues that are trouble are the E484K and K417N mutations. That topic is taken up in more detail in this new paper. It looks at a complete mutational map of the Spike protein’s receptor-binding domain (RBD) and compares the activities of the Lilly and Regeneron antibodies. They picked up on both of the mutations above in the reported variant strains, as well as flagging Y453F, which has shown up in some of the mink-driven variants in Europe. They have also identified some mutations that escape one or the other monoclonal that have not shown up in the wild yet. Mapping all these onto the RBD structure is instructive – there are certainly some patterns that can be rationalized, but as the authors note, there are still mutations in the key RBD binding areas that don’t affect either antibody, and there are also mutations with very noticeable effects that aren’t in direct contact with either antibody at all.
But so far we’re just talking about monoclonals. If you are infected by such a coronavirus, or if you receive any of the current vaccines, you will absolutely not be generating a monoclonal response yourself. No, the whole point of our immune systems is that they come at the problem from a whole set of different directions at once. And in the antibody part of that response, you will make a very long list of different ones, which will in turn be gradually refined and adapted over time. So let’s look at that preprint discussed above and see what happens against convalescent plasma and plasma from vaccinated patients.
Checking plasma from 20 patients who recovered from the coronavirus earlier this year, the authors found that four of them had no loss of potency against either B.1.17 or B.1.351. 16 of the plasma samples showed a drop in potency against B.1.351, and 11 samples showed a drop against B.1.1.7. Those activity drops were 2.7 to 3.8 fold in the latter case, and 11 to 33-fold against the former (more on these numbers in just a moment). Most of that B.1.351 drop seems to be attributable to the E484K mutation. Here’s another preprint that’s just come out looking at convalescent plasma response to the B.1.351 variant and another closely related one, this time using live virus instead of pseudovirus constructs. They also find that the IC50 values are worse in the six patients they examined (more on this below!)
Now to the vaccinated-patient plasma samples, because that’s what a lot of people are really wondering about: how well does being vaccinated with the current agents provide you with protection against the new variants? The authors studied serum from 12 patients that had been given both doses of the Moderna vaccine and 10 patients who had had both doses of the Pfizer/BioNTech one. The activity drop against the B.1.1.7 variant was only about 2-fold in both groups, whereas the overall activity drop against the B.1.351 variant was 6.5-fold in Pfizer vaccinnees and 8.6-fold in Moderna ones.
OK, real-world time. First, those numbers tell us that being vaccinated provides a person with more protection than being infected with the coronavirus itself. That was already thought to be the case for the more common coronavirus forms out there, but it’s good to see that it carries over to these two new variants as well. You will get substantially better protection from being vaccinated, and you don’t have to take your chances with the unpredictable and potentially deadly course of an actual coronavirus infection, either. Now that we have vaccines, the idea of letting the virus just run through a population to achieve immunity by that route looks more obscene than ever. And make no mistake, it has always been an obscene idea as far as I’m concerned. These data also make a case that people who have already been infected naturally and recovered could benefit from being vaccinated, although from a public health standpoint they could be much further back in the line than people who have not yet been exposed.
What about those activity drops, especially the larger ones against the B.1.351 variant? Does that still leave room for protection? Here’s the good news: it very much does. Here’s a graph from the paper I’ve been discussing for most of this post (via Eric Topol on Twitter, who is a solid source for info on this sort of thing), showing activity against the two new variants versus the good ol’ D614G variant that everyone was worked up about a few months ago:
As pointed out by virologist Roberto Burioni this morning on Twitter, it’s important to pay attention to the Y axis on these – it’s a log scale. The bottom of the graph is not a flat-zero no activity line the bottom is still a hundredfold dilution of the serum from the patients. You have to do that in order to get an assay window to see the differences – straight serum from vaccinated patients should still hammer these viral strains right down. As Burioni says, “There is a decrease, but from extremely high levels. I think these data are very good“. And I agree. It would be very interesting indeed to see this experiment run with plasma from people who have only had the first shot of each of these vaccines, though, wouldn’t it?
The thing we have to watch for, then, are much larger decreases than the sixfold, 11-fold, 30-fold levels. The preprint from the South African team mentioned above is worth considering in that light. It’s a small sample (six patients) of plasma from people who recovered from “first wave” coronavirus, looking at how such antibodies deal with B.1.351 types. Of the six, the activities are 5.7-fold lower, 9.6-fold, 38.1-fold, 53.2-fold, 204-fold, and one that was a complete knockout. Those last two are of concern, for sure, especially the KO. Now, you’d want to see a larger patient sample, to know how common those big drops are. And you’d especially want to see this experiment run versus vaccinated patient plasma, as shown above, which should be better across the board. Update: in response to some questions, yes – one thing the South African data may be telling us is that there will be people who have been through a round of infection who will be more vulnerable to re-infection with one of the new variants. Antibody titers are not the whole story, of course, and there’s always the antibody clonal maturation over time that’s helping out. But I wouldn’t want to take that risk myself, and we shouldn’t take the risk of having these variants spread so much that we find out.
What the data are telling us right now is that it definitely looks like vaccination can still handle the variant forms of the coronavirus that we are seeing – but that we also have to be on our guard, because there is no law that says that this protection can’t be breached. Taking public health measures to decrease the spread of the new variants is critical, as is getting as many people vaccinated as quickly as possible. If we mess either of those up, we are asking for serious trouble.
But there’s even a potential way out of that trouble, although you’d hate to have that emergency and to break that particular glass. As Moderna has said, variant mRNAs can be turned out quickly to be formulated as a new vaccine. Putting one together with the E484K and K417N point mutations (and others) should be basically the same process as what’s been used to make the currently administered ones (both Moderna and Pfizer/BioNTech). You would take a hit in production, of course, because you’d have to stop the current forms and start up the new ones. And you would be taking a small-but-real risk that these might perform differently in adverse events (but this would still be similar to the way that we roll out different flu vaccines every year). So the mRNA technologies offer us a potential counterattack, which is good – but let’s try not to have to use it!
The H5N8 Bird Flu and Why We Should Pay AttentionThe Northern Pintail, a migratory duck. One of them carried the High Pathogenicity Avian Influenza Virus H5N8 to Japan (Photo: Kohei Ogasawara).
Before COVID, reports of a new bird flu trickling or even sweeping out of Asia didn&rsquot garner much attention. That&rsquos certainly changed. So when two members of the China Novel Coronavirus Investigating and Research Team, who co-authored the first warning of what was to come in February 2020 in The New England Journal of Medicine, sound a new alarm, maybe we should listen.
In a short Insights Perspective published in Science, &ldquoEmerging H5N8 avian influenza viruses,&rdquo Weifeng Shi and George Gao make the case for concern that a bird flu now in more than 46 countries across Europe, Asia, and Africa has jumped to humans. Only seven poultry farm workers in Russia were reported to have gotten sick, while trying to contain an outbreak among their feathered charges. But there must have been a time, in the fall of 2019, when COVID, too, had sickened only a few people.
An avian influenza virus would need to pass easily from person-to-person to seed a pandemic in people, like SARS-CoV-2 does. That&rsquos unlikely, but as we&rsquove learned, not impossible.
An influenza virus has a more complex surface than the spike triplets of SARS-CoV-2. &ldquoH,&rdquo &ldquoN,&rdquo and numbers are shorthand to describe the surfaces of varieties of the more common A strain of influenza.
A flu virus is festooned with two types of glycoproteins (proteins with attached sugars). One type, hemagglutinin (HA), comes in 16 varieties and many subtypes within those varieties (&ldquoclades&rdquo and &ldquosubclades&rdquo in the lexicon). The other, a neuraminidase (NA), has nine types. The HAs look like spikes the NAs resemble lollipops.
The 1918 Spanish flu and the swine flu of 2009 were H1N1. Bird flus are H5. Thousands of influenza epidemics that have wiped out bird populations have been documented since 1878.
Flu viruses reinvent themselves frequently, through point mutations that alter an individual RNA base (&ldquodrift&rdquo), as well as through larger-scale, fast recombination events that swap gene segments (&ldquoshifts&rdquo). SARS-CoV-2, in contrast, begets new variants with combinations of point mutations and small deletions, such as two RNA bases.
New viral variants are concerning because they can alter transmissibility, pathogenicity, and the host&rsquos immune response. We modify vaccines to keep up with the natural mutation of viruses.
To cover multiple bases, flu vaccines consist of two types of influenza A and one type of influenza B. Conventional flu vaccines focus on a part of the hemagglutinin that the immune system recognizes as a stimulus to churn out antibodies. Efforts to create a more universal flu vaccine have been in the works since the 1930s. Candidates target the shared parts that don&rsquot change, such as the stalks that support the hemagglutinins.
Shi and Gao present a family tree of the H5 flu virus currently sweeping large swaths of the planet and deduce where it came from. Researchers glimpse viral evolution by comparing genome sequences, limited of course by what we notice.
The current &ldquohighly pathogenic avian influenza virus&rdquo &ndash HPAIV in the lingo &ndash began with an H5N1 variant striking chickens in Scotland in 1959. A strain of H5N1 that killed geese in Guangdong, China in 1996 joined and has taken off, diversifying, especially since 2010.
By 2013, the virus had mutated itself into H5N8 in Zhejiang, China, and then appeared in Russia and several other European countries. It reached Canada by the end of 2014, thanks to birds migrating along the Bering Strait that August. Then H5N8 emerged anew in Russia, Mongolia, Europe, India, and China. Meanwhile, H5 flu viruses paired with N2, N3, N6, and N9 also appeared in various places.
Tracking the trajectory of flu among migratory birds in Japan reveals how fast the situation can change.
In October 2020, researchers from Hokkaido University reported in the journal Viruses evidence of H5N8 in droppings in a lake from migratory birds. By late March 2021, more than 30 new outbreaks among domestic poultry and wild fowl had been reported in Japan, traced to migratory birds from Europe.
Sick birds flying from Europe to Japan was unusual for two reasons: new flus usually come from East Asia, and it all happened in just a few months. Plus, the European H5N8 variant is a bit different. A few of the single-RNA-base mutations alter the encoded amino acids in ways that make the virus bind more tenaciously to the sialic acid receptors on cells of the human lower airways. That might explain why, so far, the variant viruses don&rsquot pass from person to person &ndash buried deep in the lungs, they&rsquore less likely to spew out in a cough or sneeze. But the infected person suffers severe respiratory distress.
Taken together, it&rsquos clear that new bird flu viruses are all over the place, flown from here and there, perhaps mixing themselves into dangerous new variants.
Even if we can&rsquot chart all the outbreaks, they appear to now be continuous and spreading, perhaps setting the stage for a pandemic should they meet and merge into a frightening confluence. And with a virus as inherently changeable as influenza, and as deadly as the H5N8 bird strains, could a new ability to pass person-to-person seed another pandemic? This time of flu?
That&rsquos what Shi and Gao fear: &ldquoThe zoonotic potential of AIVs warrants continuous, vigilant monitoring to avert further spillovers that could result in disastrous pandemics.&rdquo
&ldquoBecause of the long-distance migration of wild birds, the innate capacity for reassortment of avian influenza viruses, the increased human-type receptor binding capability, and the constant antigenic variation of HPAIVs, it is imperative that the global spread and potential risk of H5N8 avian influenza viruses to poultry farming, avian wildlife, and global public health are not ignored.&rdquo
&bull Rev up surveillance of the highly pathogenic flu viruses on poultry farms and in wild bird populations
&bull Learn more about the transmissibility, pathogenicity, and effect on the human immune response of one particular subtype of H5N8 (188.8.131.52b), and update vaccines
&bull Decrease small-scale family-based poultry farming and increase large-scale farming, and better manage live poultry markets
&bull Avoid wild birds, don&rsquot hunt or eat them, and maintain public health measures during flu season
Don&rsquot put away those COVID masks just yet! And get vaccinated, against COVID as well as flu.
Covid variants will be the next big challenge. Can vaccines protect us?
A ll viruses mutate. They do this to adapt and survive better in their specific host. The virus that causes Covid-19 is no different: it has moved from the animal realm, where it most likely originated in bats, to the human world. Since then, scientists have been locked in a battle between the spread of the virus and the ability to immunise against it. We now have the vaccines to protect us against Covid-19 – but what happens when this virus mutates further, as it likely will?
As lockdown restrictions ease, south London has already seen a cluster of new cases related to the South African variant. Over the next six months, dealing with emerging variants will be one of the major challenges that scientists face. Some vaccines show promising signs of coping with new variants – the mRNA vaccines manufactured by Pfizer and Moderna seem to offer some protection against the variants first identified in Kent and South Africa. Most virologists think that Covid-19 vaccines will protect against severe disease and death, even in people who have been infected by a mutated strain of the virus.
But there are still potential difficulties. Being vaccinated doesn’t necessarily prevent you from becoming asymptomatically infected with Covid-19 and passing the virus on. Moreover, some vaccines may offer little or no protection against people becoming infected by a Covid-19 variant and passing this on to others (but experts believe that vaccines, together with a host’s natural immune response, should still offer enough residual protection to prevent severe disease and death). For example, clinical trials and laboratory studies show the AstraZeneca vaccine is only about 10% effective at protecting against the South African variant, but scientists still think the jab will protect against serious disease from this variant. Another question is how long vaccine immunity lasts for, and whether people become more susceptible to different variants as their antibody levels drop over time.
Virologists are hoping that the vaccines will induce what we refer to as long-term anamnestic immunity. Essentially, this would mean that after being vaccinated, a person’s B cells and T cells would remember (possibly for life) the particular S proteins of the virus to which they have been exposed. Therefore, if the person encountered the virus again, their immune system could rapidly respond by producing activated B cells (which produce antibodies) and T cells (which kill virus-infected cells) to fight it.
The virus that causes Covid-19 can produce new variants in at least two different ways. Firstly, the virus can undergo recombination, which is what happens when different pieces of genes from different viruses infect the same cell and mix to produce new variants. Secondly, the virus can infect one immunocompromised patient for a long time, and then evolve within that patient to produce a new variant. This evolutionary process can lead to the emergence of a new variant that can evade the immune responses of its host, which may give it certain advantages when it spreads to other people.
So how can we combat new variants when they arise? Some of the first-generation Covid-19 vaccines, such as the mRNA ones, induce a wider range of protection than others. And there are already plans in place to update the Pfizer, Moderna and AstraZeneca vaccines to match the South African variant more closely. But it’s practically and economically difficult to continually update every Covid-19 vaccine each time a new variant appears. Although vaccine redesign has been made easier by the introduction of “vaccine platforms”, there is still a significant time lag involved with manufacturing new shots and administering them en masse to vulnerable populations.
One option is to treat Covid-19 as we do seasonal influenza. Every year, experts carefully select an updated flu jab based on what they think will become the dominant influenza strain. We could apply this principal to Covid vaccines to cover as many new variants as possible. This is the purpose of the World Health Organization’s network of laboratories in the USA, UK, China, Japan and Australia, which work together to identify emerging strains of the influenza virus.
A global Covid-19 surveillance network could operate in the same way. This would involve hospital diagnostic labs from around the world submitting clinical samples to labs that could then compare the different viral sequences from different hemispheres. A surveillance network would determine how many Covid vaccines would need to be designed, manufactured and distributed to target emerging variants. A new vaccine might be required annually or every few years, depending on how quickly variants emerge.
Of course there is always the possibility of a doomsday variant that escapes all existing vaccines and natural immunity. With influenza, this is a very familiar risk: experts call it a “pandemic” strain. In years to come, this may also be a risk for the virus that causes Covid-19. Only constant vigilance, monitoring and collaboration will help the world detect such a variant, and prevent a catastrophic pandemic from occurring again.
Julian Tang is a clinical virologist and honorary associate professor in the respiratory sciences department at the University of Leicester
SINGAPORE: As of May 3, the Ministry of Health (MOH) has found 29 COVID-19 local cases that were infected with variants of concern or interest.
These 29 local cases have viral variants that were first detected in the United Kingdom, South Africa, Brazil or India.
On Tuesday (May 4), MOH director of medical services Kenneth Mak said that seven cases in three local clusters have one of the variants first detected in India - the B16172. This includes the Tan Tock Seng Hospital cluster which had 40 cases as of Tuesday.
READ: 5 COVID-19 cases in Tan Tock Seng Hospital cluster have Indian variant of coronavirus
READ: Authorities studying possibility of airflow and ventilation issues at Tan Tock Seng Hospital ward
Education Minister Lawrence Wong, who co-chairs the COVID-19 task force, said that while there were unlinked cases of COVID-19 before, these did not develop into clusters.
"The new variant strains have higher attack rates, they are more infectious, they are causing larger clusters than before," he said. "Due to the new variants, (the cases) are more infectious and larger clusters are forming."
Here's what we know so far about the new variants:
VARIANTS DETECTED IN SINGAPORE
Mr Wong noted at the task force press conference on Tuesday that the global COVID-19 situation had worsened, with new variants and cases spreading from South Asia to Southeast Asia.
MOH has listed the COVID-19 variants detected in local or imported coronavirus cases in Singapore, and six different strains were also found among local cases.
Ten local cases have one of two sub-variants from India. Seven have been infected with the B16172 variant, while three were found with the B16171 variant.
Eight local cases have the B1351 variant that was first found in South Africa.
New COVID-19 variants: Do the UK and South Africa virus strains pose a danger to Singapore?
The B117 or UK variant, which had been flagged earlier, was detected in seven cases and there were three cases of the P1 Brazilian strain of SARS-CoV-2.
LOCAL CLUSTERS WITH VARIANTS
A number of COVID-19 clusters that have formed in Singapore are tied to the coronavirus variants.
"Of note, seven cases in three of our local clusters have the B16172 or Indian variant," said Assoc Prof Mak on Tuesday.
Five of these cases are part of the cluster at Tan Tock Seng Hospital, one case is the immigration officer deployed at Changi Airport Terminal One and a case in the third cluster is a cleaner at a community care facility at Tuas South.
Professor Mak added that these viruses had been found to be "phylogenetically distinct", suggesting that the clusters were not linked.
"We have not completed the phylogenetic testing of all cases that we have and we're likely to see more viral variants identified over time," he said.
He added that the presence of these viral variants of concern affirmed Singapore's strategy to vaccinate all healthcare workers and prioritise vaccination for older Singaporeans.
"Had we not done so, the Tan Tock Seng cluster would have been significantly larger at this time," he said. "And the likelihood of that cluster getting out of control that much greater."
WHAT IS THE B1617 VARIANT?
The COVID-19 virus is constantly mutating, but the the World Health Organization (WHO) has a "watchlist" of the variants that pose a risk to public health.
The viral variant B1617, which was first seen in India, has been classified as one of seven "variants of interest" by WHO. These are variants that are being monitored as they show mutations that have epidemiological implications, such as the transmissibility or severity of the disease.
Assistant Professor October Sessions from the Saw Swee Hock School of Public Health said that as the virus spreads, the likelihood of new variants appearing increases and these will co-circulate until one gains a fitness advantage over the others.
"The majority of these variants will be neutral - they will not change the behaviour of the virus," he said.
Variants of concern, as opposed to variants of interest, must have an impact on diagnostics, treatments or vaccines, be more contagious or cause more severe disease. The UK, South African and Brazilian variants have been listed as variants of concern by WHO.
"Though this work is in progress, these criteria have not been characterised for the majority of variants that are rapidly evolving in India."
READ: India government ignored warnings on COVID-19 virus variant, scientists say
READ: India COVID-19 variant: What we know so far
Scientists are still studying whether the variant is driving an unexpected explosion in cases in India. WHO said in its Apr 27 update that preliminary modelling suggests it has "a higher growth rate than other circulating variants in India, suggesting potential increased transmissibility".
"It is often hard to tease out whether increased spread is due to relaxation of societal measures, decreased compliance or the virus itself," said Professor of Medicine at NUS Yong Loo Lin School of Medicine Dale Fisher.
"I think most of us believe that all these variants of concern are more transmissible because they have quite quickly become dominant and there are shared mutations."
KEY MUTATIONS IN THE B1617 VARIANT
There are three sub-strains of the B1617 variant - B16171, B16172 and B16173, and they share some characteristic mutations.
The variant has been called the "Bengal strain" as it was first detected in that region in India. It has also been called a triple mutant - although the variant contains a total of 13 spike protein mutations, there are three which are of concern.
All three mutations have been detected in other globally circulating variants and experts say they have evolved independently as the virus adapts to better infect humans.
One of the mutations, E484Q, which is very similar to the E484K mutation found in the South African and Brazilian variants, has been called the "escape mutation". This is because it appears to partially "escape" immunity from prior infection or vaccines.
Another mutation, L452R, was associated with large outbreaks in California and is estimated to be 20 per cent more transmissible than earlier waves of the virus. A third mutation, P681R, is also thought to make the virus more infectious.
Professor Fisher said that the variants have an increased capacity to bind: "It is like a lock and a key where the virus spike protein is the key and the receptors on the host cell are the lock. The mutations have a better key shape so it takes less virus to cause disease."
This means that precautions such as safe distancing, masks and hand hygiene have to be "done very well", he said.
"The measures still work but the new viruses are better at infecting so (they) will take advantage of small breaches that you may have gotten away with when the virus was the earlier strains."
Asst Prof Sessions added there have now been many documented cases of people shedding the virus beyond the 14-day mark.
"In response to this and the increased presence of more highly transmissible strains currently circulating in nearby countries, the stay-home notice has now been increased to 21 days to prevent the escape of the viruses into the community," he said.
Some microorganisms are harmless and even helpful. A microorganism is only considered a pathogen if it causes disease. Harmless viruses, bacteria, fungi, protozoa, and parasites are simply called microorganisms.
Fungi. Fungi are important in nature. They help to break down dead organisms to make the nutrients accessible for new growth. The mushrooms that you eat are fungus, while bread is made with a fungus — yeast. One extremely helpful fungus — Penicillium notatum — helps us to make the antibiotic penicillin.
Protozoa. Some types of protozoa are useful to treat water or keep soil healthy.
Bacteria. Your gut contains helpful bacteria that keep you healthy and help you digest food. Having a healthy gut biome has even been linked to mental health and heart health. A balanced gut biome has also been linked to increased immune response, cancer prevention, and lower incidence of rheumatoid arthritis in early studies.
Viruses. Even viruses can be useful. Scientists now use viruses in gene therapy to treat certain conditions. They alter a virus so it is no longer harmful, and add whatever helpful DNA information will treat the condition. They then use the virus's natural ability to infect your cells and replicate to carry the helpful DNA into your body. This new DNA causes your cells to make a new protein, potentially helping a genetic condition. This treatment is still experimental but has been used in trials to treat cancer, heart disease, and more.
abpi: "Fungi," "Parasites," "Protozoa."
BMC Biology: "Q&A: What are pathogens, and what have they done to and for us?"
CDC: "COVID-19 and Animals," "Frequent Questions About Hand Hygiene," "Zoonotic Diseases."
diseases: "Viral Vectors in Gene Therapy."
Harvard Health Publishing: "Can gut bacteria improve your health?"
heart.org: "How bacteria in your gut interact with the mind and body."
MedlinePlus: "How does gene therapy work?"
Minnesota Department of Health: "5 Common Ways Germs are Spread," "Causes and Symptoms of Waterborne Illness."