Fewer kids may be carrying coronavirus without symptoms than believed, study says

(HealthDay)—Are infected-but-healthy children major “silent spreaders” of the new coronavirus? New research out of northern Italy, once a COVID-19 hotspot, suggests they might not be.

Rigorous COVID-19 testing of children and adults admitted to a hospital in Milan for reasons other than coronavirus found that just over 1% of kids tested positive for SARS-CoV-2, compared to more than 9% of adults.

That suggests a very low rate of asymptomatic infection among children, and does “not support the hypothesis that children are at higher risk of carrying SARS-CoV-2 asymptomatically than adults,” the researchers reported in the Sept. 14 online edition of JAMA Pediatrics.

One U.S. expert in infectious disease found the report encouraging.

“Since the start of the pandemic it has been very difficult to determine what the actual role of children in the spread of the virus is,” said Dr. Amesh Adalja, senior scholar at the Center for Health Security at Johns Hopkins University, in Baltimore.

“It is becoming clear that they do not amplify this virus the way they do influenza when it comes to community spread,” Adalja said.

In the new study, physicians led by Dr. Carlo Agostoni, of the Ca’Granda Foundation Maggiore Polyclinic Hospital in Milan, conducted two sets of nasal swab tests, up to two days apart, on 214 newly admitted patients.

Eighty-three of these new admissions were children and 131 were adults. All were admitted to the hospital in March and April, at the height of northern Italy’s COVID-19 outbreak. However, all of the patients were admitted for reasons unconnected to COVID-19, and none had shown any symptoms of the illness.

So how many were secretly carrying the virus nonetheless? Based on the swab tests, only 1.2% of the pediatric patients turned up positive for infection, compared to 9.2% of adults.

The low rate of carriage among kids in a city with a burgeoning number of COVID-19 cases suggests “that [children’s] role as facilitators of the spreading of SARS-CoV-2 infection could be reconsidered,” the study authors wrote.

Still, the researchers stressed that this is a small sample from just one hospital, so the findings shouldn’t be considered definitive.

And of course community outbreaks of COVID-19 tied to asymptomatic but infected children are happening in the United States. On Friday, researchers from the U.S. Centers for Disease Control and Prevention issued a report on a cluster of cases originating from two Salt Lake City day care facilities. The report found that 12 youngsters infected with coronavirus (only three showed any symptoms) enrolled at two day care centers easily passed SARS-CoV-2 to at least 12 family members, one of whom ended up hospitalized.

So as millions of children head back to school, uncertainty as to their role in the spread of COVID-19 continues, Adalja said.

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Could magnesium pills be the secret to staying strong in later life?

Could magnesium pills be the secret to staying strong in later life? Research suggests links between physical strength and the levels of the mineral in muscle tissue

Preparing for her 14th marathon later this year, 77-year-old Sylvia Jennings offers some words of reassurance: ‘As long as you can get your shoes on and get out of the door, I think you’re OK.’

She first took up running age 59, and believes her remarkable athletic performance in older age is linked to a mineral many of us apparently lack.

There’s no doubt that Sylvia, who has four children and nine grandchildren, takes keeping fit more seriously than most.

Around 16 per cent of over-65s are getting less than the recommended minimum daily intake of 270mg for women and 300mg for men, according to an analysis of data from Public Health England’s ongoing National Diet and Nutrition Survey [File photo]

‘I have kept up my exercise routine during lockdown by running about ten to 12 miles a week, but I’ll have to get it up to 16 or 18 ahead of the marathon,’ she says.

‘On Mondays and Fridays, I used to swim 20 lengths, but since the lockdown I’ve been going out cycling. I used to go to a weekly yoga class, and now I do it online.’

And the retired florist, who lives in Bexley, Kent, with her husband Fred, 77, a retired police officer, thinks her muscle power and stamina may be helped by the daily magnesium supplements she started taking ten years ago.

‘I read about the benefits and decided to try it,’ she says. ‘I just felt it might keep my bones and muscles going a bit longer.

‘I’ve not had tests to see if I have a deficiency, but I thought it was likely I was lacking it in my diet.’

Research suggests there may be something in her thinking.

A recently published study from the University of East Anglia, involving 441 people, found a direct link between physical strength in older people and the amount of magnesium present in their muscle tissue.

The mineral, known to regulate muscle function, is found in beans, nuts, seeds, leafy green vegetables, fish, meat and dairy. One sign of a deficiency is frequent cramps.

Yet, as with many other nutrients, our magnesium intake has declined due to our increasing reliance on processed foods, as well as falling levels of nutrients in soil.

Around 16 per cent of over-65s are getting less than the recommended minimum daily intake of 270mg for women and 300mg for men, according to an analysis of data from Public Health England’s ongoing National Diet and Nutrition Survey.

‘Decades of intensive farming have depleted soil nutrient levels, making it harder to maintain healthy levels of magnesium,’ says Robert Pickard, an emeritus professor of neurobiology at Cardiff University, who led the study. ‘It is definitely a worrying trend.’

The discovery of a link between muscle power in older people and the magnesium content of their muscle tissue was made with a scanning technique — magnetic resonance spectroscopy (MRS) — used to detect magnesium molecules. 

A team of researchers from the University of East Anglia in Norwich, and experts from the National Institute on Aging, in the U.S., investigated muscle strength in the 441 people, aged 24 to 98, who are volunteers in a long-term study of the effects of ageing, set up by the U.S. government.

The scientists asked volunteers to perform a variety of physical tests over a three-day period and the results, published in the journal Frontiers In Physiology, showed muscle power was directly linked to the presence of magnesium in muscle tissue.

‘No one has ever done a large-scale study of this kind,’ said Dr Donnie Cameron, the lead researcher from the University of East Anglia.

‘We showed that there’s as strong a relationship between magnesium and muscle strength in men as there is in women, but women are more at risk of muscle weakness and mobility issues in old age because they have worse rates of magnesium deficiency.

The discovery of a link between muscle power in older people and the magnesium content of their muscle tissue was made with a scanning technique — magnetic resonance spectroscopy (MRS) — used to detect magnesium molecules [File photo]

‘This is a new finding. We originally thought this deficiency might be related to the menopause because women tend to lose more magnesium at menopause, but we also looked at younger women and they have lower magnesium levels than men of the same age.

‘We are going to have to do more research to tease out the reasons for this. It could be to do with the interaction between magnesium and sex hormones.’

Another four-year analysis, also by the University of East Anglia, using data from 500,000 people aged 40 to 69 involved in the UK Biobank study of ageing, has shown that those who had the highest magnesium intakes had significantly bigger and stronger muscles than those with the least.

The fact is, everyone’s muscles gradually shrink and lose power, says Ailsa Welch, a professor of nutritional epidemiology at the University of East Anglia.

‘And, while we have incomplete information on this, it is likely that people who eat more magnesium have better muscle mass and power as they age.’

She thinks that extra magnesium may eventually be shown to help halt muscle loss.

‘It may well be worth giving [older people] supplements,’ she adds, ‘but we haven’t got there with the evidence yet.’

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Genetic mutations may be linked to infertility, early menopause

A new study from Washington University School of Medicine in St. Louis identifies a specific gene’s previously unknown role in fertility. When the gene is missing in fruit flies, roundworms, zebrafish and mice, the animals are infertile or lose their fertility unusually early but appear otherwise healthy. Analyzing genetic data in people, the researchers found an association between mutations in this gene and early menopause.

The study appears Aug. 28 in the journal Science Advances.

The human gene—called nuclear envelope membrane protein 1 (NEMP1)—is not widely studied. In animals, mutations in the equivalent gene had been linked to impaired eye development in frogs.

The researchers who made the new discovery were not trying to study fertility at all. Rather, they were using genetic techniques to find genes involved with eye development in the early embryos of fruit flies.

“We blocked some gene expression in fruit flies but found that their eyes were fine,” said senior author Helen McNeill, Ph.D., the Larry J. Shapiro and Carol-Ann Uetake-Shapiro Professor and a BJC Investigator at the School of Medicine. “So, we started trying to figure out what other problems these animals might have. They appeared healthy, but to our surprise, it turned out they were completely sterile. We found they had substantially defective reproductive organs.”

Though it varied a bit by species, males and females both had fertility problems when missing this gene. And in females, the researchers found that the envelope that contains the egg’s nucleus—the vital compartment that holds half of an organism’s chromosomes—looked like a floppy balloon.

“This gene is expressed throughout the body, but we didn’t see this floppy balloon structure in the nuclei of any other cells,” said McNeill, also a professor of developmental biology. “That was a hint we’d stumbled across a gene that has a specific role in fertility. We saw the impact first in flies, but we knew the proteins are shared across species. With a group of wonderful collaborators, we also knocked this gene out in worms, zebrafish and mice. It’s so exciting to see that this protein that is present in many cells throughout the body has such a specific role in fertility. It’s not a huge leap to suspect it has a role in people as well.”

To study this floppy balloon-like nuclear envelope, the researchers used a technique called atomic force microscopy to poke a needle into the cells, first penetrating the outer membrane and then the nucleus’s membrane. The amount of force required to penetrate the membranes gives scientists a measure of their stiffness. While the outer membrane was of normal stiffness, the nucleus’s membrane was much softer.

“It’s interesting to ask whether stiffness of the nuclear envelope of the egg is also important for fertility in people,” McNeill said. “We know there are variants in this gene associated with early menopause. And when we studied this defect in mice, we see that their ovaries have lost the pool of egg cells that they’re born with, which determines fertility over the lifespan. So, this finding provides a potential explanation for why women with mutations in this gene might have early menopause. When you lose your stock of eggs, you go into menopause.”

McNeill and her colleagues suspect that the nuclear envelope has to find a balance between being pliant enough to allow the chromosomes to align as they should for reproductive purposes but stiff enough to protect them from the ovary’s stressful environment. With age, ovaries develop strands of collagen with potential to create mechanical stress not present in embryonic ovaries.

“If you have a softer nucleus, maybe it can’t handle that environment,” McNeill said. “This could be the cue that triggers the death of eggs. We don’t know yet, but we’re planning studies to address this question.”

Over the course of these studies, McNeill said they found only one other problem with the mice missing this specific gene: They were anemic, meaning they lacked red blood cells.

“Normal adult red blood cells lack a nucleus,” McNeill said. “There’s a stage when the nuclear envelope has to condense and get expelled from the young red blood cell as it develops in the bone marrow. The red blood cells in these mice aren’t doing this properly and die at this stage. With a floppy nuclear envelope, we think young red blood cells are not surviving in another mechanically stressful situation.”

The researchers would like to investigate whether women with fertility problems have mutations in NEMP1. To help establish whether such a link is causal, they have developed human embryonic stem cells that, using CRISPR gene-editing technology, were given specific mutations in NEMP1 listed in genetic databases as associated with infertility.

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Vascular development may be at risk in autism

A Canadian collaboration led by Dr. Baptiste Lacoste has undertaken the first ever in-depth study of vasculature in the autistic brain. The product of four years of work, a paper published today in Nature Neuroscience lays out several lines of novel evidence that strongly implicate defects in endothelial cells—the lining of blood vessels—in autism.

Dr. Lacoste, a scientist at The Ottawa Hospital and an assistant professor in the University of Ottawa’s Faculty of Medicine and Brain and Mind Research institute, heads a lab that specializes in neurovascular interactions in health and disease. In collaboration with researchers at McGill University, Laval University, and the National Research Council of Canada, Dr. Lacoste’s team used a mouse model with one of the most common genetic mutations found in autism spectrum disorder—16p11.2 deletion, or “16p” for short.

The team, in which Dr. Lacoste’s graduate student Julie Ouellette and research associate Dr. Xavier Toussay played prominent roles, also used cells derived from the tissue of human autistic adults who carry the 16p mutation.

Nerves and blood vessels not in synch

“If you imagine you have a luxury car—a Ferrari—and it’s beautiful, sitting in your garage. But if you don’t put gas in the tank, the car won’t drive,” says Dr. Lacoste. “It’s exactly the same with the brain. It’s the most complex organ, but if you don’t have blood supply, the brain just doesn’t work properly.”

Normally, when brain cells light up, blood rushes to the active brain region, a phenomenon called ‘neurovascular coupling’. But when neurons of mice with the 16p deletion are stimulated, this study found that vascular responses in those brain regions were delayed and weaker.

This disconnect—or ‘neurovascular uncoupling’—was shown to originate in the blood vessels themselves: Arteries isolated from these mice and kept alive in a medium also showed a weak and sluggish response to chemicals that induce dilation of blood vessels. The team further isolated the source of the deficit in the endothelium, as opposed to the other cell types, such as muscle cells, that surround blood vessels.

Difficulties in development

Dr. Lacoste’s work further shows that problems with blood vessels begin very early in life for those who carry the 16p deletion. In a petri dish, both human-derived and mouse endothelial cells with the mutation were unable to sprout the extensions that normally connect blood vessels to each other, allowing the vascular network to expand and grow. Endothelial cells in the brains of newborn autistic mice had the same problem.

By adolescence, the mice still showed reduced vascular density in their brains. Interestingly, in contrast to the problems in the circulatory system, the researchers found that the neurons in the brains of these young mice appeared to be surprisingly well organized.

As the mice grew, other cells in the brain compensated for their dysfunctional endothelial cells, so that by adulthood they had developed a full network of blood vessels. However, as the researchers’ previous experiments showed, these blood vessels remained dysfunctional in adult mice.

“It’s a bit like if a plumber comes to your house and does a bad job installing the pipes,” says Dr. Lacoste. “You will have trouble getting the right water pressure in your sink from then on.”

Blood vessels and autistic behavior

When a person or mouse carries a 16p mutation, that genetic difference is replicated in every cell in their body. This makes it harder to pin down the cause of systemic developmental differences.

To address this difficulty, Dr. Lacoste’s team generated mice that only expressed the mutation in their endothelial cells—so-called “conditional mutants”. These mice showed similar deficits in their vascular development as whole-body mutants.

Remarkably, although every other cell in their brain and body was genetically normal, these conditional mutants displayed some behavioral signs of autism: hyperactivity, stereotypic movements, and motor learning impairment.

This indicated that the problems in the blood vessels contributed to neuronal dysfunction, which in turn led to the outward signs and symptoms of autism.

Further avenues of inquiry

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Here's When a Sore Throat Might Be a Symptom of the Coronavirus

Since news of COVID-19, which was first detected in December 2019 in Wuhan, China, exploded onto the scene, there has been one thing that remains constant: Each day we learn more and more about the virus.

That includes its potential symptoms, which often seem run-of-the-mill. Take a sore throat—you might be tempted to shrug off this symptom, but even as one of the less commonly known ones (the most prevalent are fever, dry cough, tiredness, and shortness of breath), it may still indicate infection.

In fact, the World Health Organization notes that 13.9 percent of COVID-19 patients have presented with sore throats.

“Some patients that have experienced sore throat during COVID-19 have reported that it feels like a super dry throat,” says Leo Nissola, M.D., a scientist and investigator at the COVID-19 National Convalescence Plasma Project as well as advisor at COVIDActNow. “And the medical reports show redness in the throat, without bacterial infection, like strep, for example.”

Is a Sore Throat a Symptom of COVID-19?

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That’s a tricky question.

There are numerous causes for inflammation of the inner lining of the throat, including allergies, upper respiratory infections (both viral and bacterial), acid reflux, and even throat cancer.

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Not to mention this: “There is still so much we don’t know about COVID-19 and what we do know has been evolving over time,” says Inna Husain, M.D., an assistant professor in otolaryngology at Rush University Medical Center in Chicago.

“At this time, all upper respiratory illnesses are COVID-19 until proven otherwise.” What’s more, an April review in the European Archives of Oto-Rhino-Laryngology revealed that ear, nose, and throat symptoms may precede the development of severe cases of COVID-19.

That said, “there is nothing intrinsically different between a sore throat brought on by COVID-19 and one brought on by any other upper respiratory infections,” says Michael Lerner, M.D., a Yale Medicine laryngologist and assistant professor of otolaryngology at Yale School of Medicine.

What, Exactly, Does a “Sore Throat” Mean?

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On a basic level, you will experience some sort of discomfort in your throat. More specifically, you’ll feel pain when swallowing that can be achy, sharp, or even create a burning sensation.

A sore throat may also be accompanied by a runny nose, nasal congestion, cough, or fever. Other symptoms, according to Alexandra Kreps, M.D., an internist at Tru Whole Care, include “changes in your voice, swollen lymph nodes in your neck or jaw area, and when looking at your tonsils in a mirror they may be red and irritated or could have white patches or pus if severely infected.”

However, Dr. Nissola, says “it is more likely to be a COVID-related sore throat if there are more symptoms, such as fever and malaise.”

A good rule of thumb: “If your sore throat is also accompanied with fever or cough, be suspicious. If your sore throat comes after an episode of heartburn likely its related to reflux. If it is accompanied by sino-nasal congestion, runny nose, and sneezing, it may be allergies,” says Dr. Husain.

What Should You Do If You Have a Sore Throat?

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How you treat your sore throat symptoms should really consider the root cause.

Generally, though, Dr. Husain recommends hydration (drinking water or tea), steam inhalation, and lozenges containing lubricants such as honey. Pain relievers such as Tylenol can also help with discomfort.

Adds Dr. Lerner: If sore throat is from excessive coughing, you can address it though cough suppressants. For nasal congestion, which causes mouth breathing and dryness, try humidification or hydration through nasal saline or irrigation. “Patients that have COVID-19, should be cautious of nasal spread and do this in a safe way, so as not to expose others to aerosols and droplets that may occur from these types of treatments,” he says.

If sore throat is due to allergies, on the other hand, pretreatment with antihistamine prior to allergy season or known allergen exposure— in other wards take an allergy pill— can be helpful, says Dr. Husain.

Last, if the sore throat is caused by reflux, following an anti-reflux diet may lead to a favorable outcome. “I would encourage people to eliminate anything heavily acidic or citrus as this can irritate the lining of the throat. Hard foods such as crackers or chips can also be irritating,” says Dr. Husain, who notes that if a sore throat is present, avoiding coffee or alcohol as well as reducing smoking cigarettes, smoking marijuana, and avoiding vaping is recommended.

While none of these things will necessarily “cure” a sore throat, they can help with some of the discomfort associated with it.

Should You Get Tested for COVID-19 if You Have a Sore Throat?

“For people with nuisance, acute onset symptoms, or any other listed by the Centers for Disease Control as potentially a symptom for COVID, it is important to talk to your healthcare provider to help determine if testing is appropriate,” says Dr. Learner.

Overall, to help keep COVID-19 or any infection or illness at bay, wash your hands frequently, wear a mask and engage in social-distancing.

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Blood sample can be used to assess the severity and prognosis of frontotemporal lobar degeneration in the future

Biomarkers to support the diagnosis of frontotemporal lobar degeneration (FTLD) and to assess the severity and expected prognosis of the disease are needed. Neurofilament light chain (NfL) measured from a blood sample strongly correlates with the duration of the disease in FTLD patients and the rate of brain atrophy, according to a new study published by the University of Eastern Finland in the Annals of Clinical and Translational Neurology.

FTLD is the second most common cause of degenerative and progressive dementing diseases in the working-age population after Alzheimer’s disease. FTLD is divided into two subgroups based on the primary symptoms. Early symptoms of the most common form of FTLD, behavioral variant frontotemporal dementia (bvFTD), include changes in behavior, personality, and executive functions. In the second subgroup, primary progressive aphasia (PPA), the primary symptoms are linguistic, including naming problems and problems in speech production. FTLD patients often have also concomitant motor neuron disease (FTD-MND), and there is some overlap in the neuropathology and genetic alterations between these diseases. Several predisposing genetic mutations have been recognized for FTLD, of which the C9orf72 repeat expansion is exceptionally prevalent in Finnish patients.

NfL is an intracellular structural protein that maintains the shape of the nerve cells and the axons. Upon neuronal damage, NfL is released into the intercellular space, from where it eventually ends up in the blood. Indeed, elevated blood NfL levels are observed in a variety of neurodegenerative diseases and after brain trauma. Previously, NfL levels have been measured in cerebrospinal fluid, where it has a higher concentration than in the blood. However, new ultra-sensitive methods allow measuring NfL also in the blood, making blood NfL a minimally invasive biomarker for neurodegeneration.

The new study found that patients with high levels of blood NfL had a shorter duration of the disease and a faster rate of brain atrophy. High levels of blood NfL were detected particularly in the FTD-MND and PPA groups. Also, carriers of the C9orf72 repeat expansion had elevated blood NfL levels. These results provide valuable information on the course of the disease in FTLD patients showing different clinical symptoms or harboring diverse genetic backgrounds.

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We may be able to eliminate coronavirus, but we’ll probably never eradicate it. Here’s the difference

Compared to many other countries around the world, Australia and New Zealand have done an exceptional job controlling COVID-19.

As of May 7, there were 794 active cases of COVID-19 in Australia. Only 62 were in hospital.

The situation in New Zealand is similar, with 136 active cases, only two of whom are in hospital.

If we continue on this path, could we eliminate COVID-19 from Australia and New Zealand?

Control –> elimination –> eradication

In order to answer this question, we first to need to understand what elimination means in the context of disease, and how it differs from control and eradication.

Disease control is when we see a reduction in disease incidence and prevalence (new cases and current cases) as a result of public health measures. The reduction does not mean to zero cases, but rather to an acceptable level.

Unfortunately, there’s no consensus on what is acceptable. It can differ from disease to disease and from jurisdiction to jurisdiction.

As an example, there were only 81 cases of measles reported in Australia in 2017. Measles is considered under control in Australia.

Conversely, measles is not regarded as controlled in New Zealand, where there was an outbreak in 2019. From January 1, 2019, to February 21, 2020, New Zealand recorded 2,194 measles cases.

For disease elimination, there must be zero new cases of the disease in a defined geographic area. There is no defined time period this needs to be sustained for—it usually depends on the incubation period of the disease (the time between being exposed to the virus and the onset of symptoms).

For example, the South Australian government is looking for 28 days of no new coronavirus cases (twice the incubation period of COVID-19) before they will consider it eliminated.

Even when a disease has been eliminated, we continue intervention measures such as border controls and surveillance testing to ensure it doesn’t come back.

For example, in Australia, we have successfully eliminated rubella (German measles). But we maintain an immunization schedule and disease surveillance program.

Finally, disease eradication is when there is zero incidence worldwide of a disease following deliberate efforts to get rid of it. In this scenario, we no longer need intervention measures.

Only two infectious diseases have been declared eradicated by the World Health Organisation – smallpox in 1980 and rinderpest (a disease in cattle caused by the paramyxovirus) in 2011.

Polio is close to eradication with only 539 cases reported worldwide in 2019.

Guinea worm disease is also close with a total of just 19 human cases from January to June 2019 across two African countries.

What stage are we at with COVID-19?

In Australia and New Zealand we currently have COVID-19 under control.

Importantly, in Australia, the effective reproduction number (Reff) is close to zero. Estimates of Reff come from mathematical modelling, which has not been published for New Zealand, but the Reff is likely to be close to zero in New Zealand too.

The Reff is the average number of people each infected person infects. So a Reff of 2 means on average, each person with COVID-19 infects two others.

If the Reff is greater than 1 the epidemic continues; if the Reff is equal to 1 it becomes endemic (that is, it grumbles along on a permanent basis); and if the Reff is lower than 1, the epidemic dies out.

So we could be on the way to elimination.

In both Australia and New Zealand we have found almost all of the imported cases, quarantined them, and undertaken contact tracing. Based on extensive community testing, there also appear to be very few community-acquired cases.

The next step in both countries will be sentinel surveillance, where random testing is carried out in selected groups. Hopefully in time these results will be able to show us COVID-19 has been eliminated.

It’s unlikely COVID-19 will ever be eradicated

To be eradicated, a disease needs to be both preventable and treatable. At the moment, we neither have anything to prevent COVID-19 (such as a vaccine) nor any proven treatments (such as antivirals).

Even if a vaccine does become available, SARS-CoV-2 (the virus that causes COVID-19) easily mutates. So we would be in a situation like we are with influenza, where we need annual vaccinations targeting the circulating strains.

The other factor making COVID-19 very difficult if not impossible to eradicate is the fact many infected people have few or no symptoms, and people could still be infectious even with no symptoms. This makes case detection very difficult.

At least with smallpox, it was easy to see whether someone was infected, as their body was covered in pustules (fluid-containing swellings).

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