By Zaria Gorvett – guest post

There’s no evidence that any of the current Covid-19 vaccines can completely stop people from being infected – and this has implications for our prospects of achieving herd immunity.

It was 17 June 2009. An 11-year-old boy returned to the US from the UK – and inadvertently brought something with him. Later that week, while attending a religious education programme in Sullivan County, New York, he developed a mysterious swelling of his salivary glands. He had mumps, a respiratory infection spread by contact with droplets in the air.

Meanwhile, the religious course continued. The 400 children in attendance spent hours each day engaging in prolonged face-to-face contact – specifically, a kind of Orthodox Jewish education involving facing a study partner, a chavrusa, across a narrow table, while analysing and debating text from the Talmud. By the time the programme ended, 22 others had been infected, along with three adults.

As the students went back to their homes, the virus spread to Brooklyn and Rockland County, then on to Ocean County and Orange County. In all, the outbreak lasted a year, and at least 3,502 people developed the disease.

When scientists analysed what had happened, they suggested that the chavrusa style of learning might have allowed for “particularly efficient transmission of mumps virus”. What might seem most surprising in this case is that the accidental super-spreader had received a full course of the MMR (measles, mumps and rubella) vaccine. It’s likely that he did have some immunity – like the other vaccinated children, he developed relatively mild symptoms with no complications – but he was still able to carry the virus and transmit it to others.

In fact, most vaccines don’t fully protect against infection, even if they can block symptoms from appearing. As a result, vaccinated people can unknowingly carry and spread pathogens. Occasionally, they can even start epidemics.


There are two main types of immunity you can achieve with vaccines. One is so-called “effective” immunity, which can prevent a pathogen from causing serious disease, but can’t stop it from entering the body or making more copies of itself. The other is “sterilising immunity”, which can thwart infections entirely, and even prevent asymptomatic cases. The latter is the aspiration of all vaccine research, but surprisingly rarely achieved.

Take meningitis as an example. For the kind caused by the bacteria Neisseria meningitidis, there are many vaccines available for the tens of different strains. The three given in the US – MCV4, MPSV4 and MenB – can together prevent 85-90% of disease cases. However, several have been shown to still allow people to “carry” the bacteria involved.

They can hide out in the nose or the back of the throat, from where they are able to infect others via sneezing, coughing, kissing, or sharing cigarettes or utensils. In one study of university students in the United Kingdom, the vaccine had no effect on the proportion of people harbouring the pathogen four weeks later.

“Two meningitis vaccines can have two very different effects on whether you can spread the disease,” says Keith Neal, professor emeritus of epidemiology at the University of Nottingham. “But only a minority of those people who get the germ go down with meningitis [in well-vaccinated communities] because they have immunity to it.”

It’s also possible to be infected with pertussis, hepatitis B, mumps, and (often, but not always) influenza, regardless of whether you have been vaccinated – though all these immunisations are highly effective at preventing people from developing serious symptoms or needing to be hospitalised.


While effective immunity is usually provided by a combination of white blood cells – such as B and T cells – along with antibodies, sterilising immunity is typically all about the latter. In particular, it relies on neutralising antibodies, which defend the body from pathogens by sticking to their outer surface and preventing them from interacting with their intended targets, such as the cells that line the nose, throat or lungs.

In the case of Covid-19, neutralising antibodies that recognise the virus bind to the spike protein on its surface, which it uses to enter cells. To achieve sterilising immunity, vaccines must stimulate enough of these antibodies to catch any virus particles entering the body and immediately disarm them.


“In a nutshell we don’t know, because they’re too new,” says Neal.

So far, the available Covid-19 vaccines have not been judged primarily on their ability to prevent transmission – though this is now being evaluated as a secondary endpoint for many of them. Instead, their efficacy was assessed by whether they could prevent symptoms from developing. “This means that we set our targets kind of pragmatically,” says Danny Altmann, professor of immunology at Imperial College London.

Israel had already vaccinated more than half of its citizens by the end of January, making it a useful place to study how the vaccines affect transmission (Credit: Getty Images)
Israel had already vaccinated more than half of its citizens by the end of January, making it a useful place to study how the vaccines affect transmission (Credit: Getty Images)

Scientists already know that the antibodies people develop after natural infections with Covid-19 don’t always prevent them from being reinfected. One study of British healthcare workers found that 17% of those who had antibodies already when the study began – presumably from a first infection – caught it a second time. Around 66% of these cases were asymptomatic, but it’s thought that you don’t need to have symptoms to be at risk of passing the virus on to others.

“For a virus like this, I almost think that’s asking too much of a vaccine,” says Altmann. “It’s really, really hard to do.”

Happily, this isn’t quite the end of the story.

There are some early hints that certain vaccines might be able to reduce transmission, even if they can’t eliminate it entirely. One way it might do this is by reducing the number of viral particles in people’s bodies. “It is quite likely that if the vaccines are making people less ill, they are producing less virus, and therefore will be less infectious, but that’s just a theory,” says Neal.

Sterilising immunity is also notoriously tricky to prove.

Since most clinical trials didn’t check whether the vaccines were preventing transmission, scientists are currently looking to see whether they are having an impact on infection rates in places where they have already been widely distributed. In the UK, you might expect that outbreaks in care homes – where vaccination efforts are being prioritised – would become less frequent, if the vaccines were having an effect.

But this is problematic. “There are two factors,” says Neal. “We’ve got lockdowns and a vaccine. So, it’s actually quite difficult to separate them out. Is it the vaccine? Is it the lockdown, or more likely a combination of both?”

Here’s what we know so far about the current vaccines’ ability to halt transmission. (But first – to avoid confusion, information about their ability to prevent symptoms or protect people from disease has not been included.)


Back in July last year, a study testing the efficacy of this vaccine in rhesus macaques – which have similar lung physiology to humans – provided some promising results. It found that while the monkeys were protected from serious illness, it did not prevent them from becoming infected with Covid-19 in the first place. Vaccinated monkeys were as likely to become infected as the unvaccinated ones, though they did have fewer viral particles in their lungs than the unvaccinated group.

The authors noted that their results suggested that the vaccine might not prevent the transmission of the virus, “however, it could significantly reduce illness”.

Fast-forward to the phase III trials in humans, and the picture becomes a little more complicated. Unusually, the Oxford-AstraZeneca vaccine didn’t just involve injecting the participants with two doses of either the new vaccine or a placebo – in this case, the meningitis vaccine – and then following up to see if they had developed any symptoms several weeks later. This trial also involved the additional step of asking them to complete a nose and throat swab each week, to test for asymptomatic infections.

According to these results, published in January 2021, the vaccine was 59% effective at preventing infections in those who received a half dose, followed by a standard dose – a group that also happened to be younger than the average for the study overall. However, among those who received two full doses, that figure dropped to just 4%. The research did not look at whether the vaccine had any impact on the number of viral particles in the patients’ lungs.

The authors explained that while the reduction in the number of infections – and therefore the potential for transmission – in the half-dose group was promising, further data was needed to confirm the findings.

The latest development is a new paper published in pre-print on 1 February, which revealed the results of a further month of studying the trial participants. The researchers found that the vaccine cut the number of cases with detectable virus by 67% after a single standard dose, and wrote that this shows “the potential for a substantial reduction in transmission”.


There isn’t yet any conclusive evidence that the Pfizer-BioNTech vaccine can prevent people from being infected with the coronavirus – and therefore halt its spread. But there are some early signs that it might.

In early January, the chief executive of Pfizer, Albert Bourla, said animal studies found that it provided significant protection from transferring the virus, though this hasn’t been proven in humans.

Then a small Israeli survey found that, out of 102 medical staff who had received two doses of the vaccine, only two had developed “low” amounts of antibodies. The other 98% had more antibodies than people who had been infected with Covid-19. The results were released via a press release, which quotes the head of the study speculating that these powerful immune responses were likely to prevent people from becoming carriers or spreading the disease.

However, there are a number of reasons to be cautious about interpreting these results, such as the small sample size and the fact that the research was not published in a peer-reviewed journal.

More recently, the Israeli Ministry of Health (MoH) looked at the health records of a million people in the country, and found that – a week after being fully vaccinated – just 317 people out of 715,425 tested positive for the coronavirus.

Again, this was not a clinical trial – there was no unvaccinated control group, and the effect could be down to something else, such as the impact of a lockdown imposed in December. But the infection rate was considerably lower than elsewhere (0.04%, while it’s estimated that 1.87% of people in England had the virus in the week ending 23 January).

A study by the nation’s domestic healthcare provider – Maccabi Healthcare Services – found similarly encouraging results. Out of 163,000 people given a full course of the vaccine, just 31 were infected, compared to 6,500 infections in an equivalent group of unvaccinated people.


Though the Moderna trial did not look specifically at whether the vaccine can prevent transmission, participants were checked for Covid-19 infection before they received their first and second doses – meaning it was possible to compare the rates of infection in these groups. In all, 14 people tested positive after having one shot, verses 38 who had received a placebo.

This suggests that the vaccine might be able to prevent two-thirds of asymptomatic cases after one shot. However, there were limitations to this provisional research – the number of people who tested positive was small, so the estimate may not be entirely accurate. It was published in a briefing submitted to the FDA, and has not yet been peer-reviewed.


The vaccine hasn’t yet been approved for use anywhere in the world – and like the others, it has not yet been comprehensively shown to prevent infections or transmission in humans.

But back in November, some early results got scientists excited.

The company revealed that it prevented the virus spreading entirely during studies in rhesus macaques, when they were given a high enough dose. These results put it in an exclusive club of vaccines that are able to prevent asymptomatic transmission completely in other primates – seen as a promising sign, because they have similar respiratory physiology to humans.

Now scientists are waiting to find out if the vaccine can achieve sterilising immunity in vaccinated humans, too.


Unfortunately, the ability of the vaccines to prevent transmission won’t just have an effect on how long social distancing rules need to be followed – it will also have an impact on herd immunity.

“If the vaccines don’t completely stop transmission, it will increase the amount of people we need to vaccinate to truly cross the herd immunity thresholds and drive down cases to somewhere near zero,” says Michael Head, a senior research fellow in global health at the University of Southampton. He explains that it’s not yet clear what the herd immunity threshold is, because it hasn’t been reached either through natural infection or through vaccination.

Herd immunity is the indirect protection from an infectious disease that populations acquire when enough people are immune. The threshold needed to achieve it depends on many different factors, such as the reproduction number of the virus, or “R” – the number of further people infected by each carrier – which itself varies widely. Some factors that affect the latter include where in the world you live, the variant involved, and the conditions on the ground, such as lockdowns.

This means that, even when scientists do know more, there will be no set threshold for herd immunity that works everywhere – but it’s possible to estimate roughly what it might be.

For example, one calculation suggests that for a vaccine that totally eliminates transmission, 60-72% of the population would need to have it, in order to accomplish complete herd immunity. But if the vaccine’s effectiveness were 80%, between 75 and 90% of people need to have it.

This is potentially higher than the vaccination ambitions of many countries. The UK is aiming to immunise every adult by September, which equates to around 51m out 67.5m people – 75% of the population in total. That’s assuming that every adult in the country is willing to be vaccinated, and healthy enough to be eligible.

However, most scientists aren’t expecting to eliminate the virus entirely. For the moment, the goal is to reduce its transmission as much as possible. “Even if you vaccinate, you’ve still got a fairly large number of susceptible people there,” says Head. “So, we will still see outbreaks happen. I think they would be fairly localised, but they would still cause concern and cause a burden of disease”.

Some scientists argue that the emphasis on preventing transmission is a red herring, because once enough people have been vaccinated, it doesn’t matter if they are still able to spread the virus – everyone will have immunity.

However, it may prove crucial for those who are unable to be vaccinated, for example because they are pregnant, too young, or too unwell.

Until we have an answer, perhaps we should all keep in mind the story of the 11-year-old boy with mumps – and act as though we haven’t been vaccinated, even if we have.

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There were multiple St. Valentines (including decapitated ones), but it was a medieval poet who first established the holiday’s romantic tradition.

On February 14, when we share chocolates, special dinners, or doily cards with our loved ones, we do it in the name of Saint Valentine. But who was this saint of romance?
Search the internet, and you can find plenty of stories about him—or them. One Saint Valentine was supposedly a Roman priest who performed secret weddings against the wishes of the authorities in the third century. Imprisoned in the home of a noble, he healed his captor’s blind daughter, causing the whole household to convert to Christianity and sealing his fate. Before being tortured and decapitated on February 14, he sent the girl a note signed “Your Valentine.”

Some accounts say another saint named Valentine during the same period was the Bishop of Terni, also credited with secret weddings and martyrdom via beheading on February 14.
Unfortunately for anyone hoping for a tidy, romantic backstory to the holiday, scholars who have studied its origins say there’s very little basis for these accounts. In fact, Valentine’s Day only became associated with love in the late Middle Ages, thanks to the English poet Geoffrey Chaucer.

“The two stories that everybody talks about, the bishop and the priest, they’re so similar that it makes me suspicious,” says Bruce Forbes, a professor of religious studies at Morningside College in Iowa.

Saint Valentine, who according to some sources is actually two distinct historical characters who were said to have healed a child while imprisoned and executed by decapitation.

Multiple Martyred Saint Valentines
Valentine was a popular name in ancient Rome, and there are at least 50 stories of different saints by that name. But Forbes said the earliest surviving accounts of the two February 14 Valentines, written starting in the 500s, have a whole lot in common. Both were said to have healed a child while imprisoned, leading to a household-wide religious conversion, and they were executed on the same day of the year and buried along the same highway.
The historical evidence is so sketchy that it’s not clear whether the story started with one saint who then became two or if biographers of one man borrowed details from the other—or if either ever existed at all.

Perhaps more disappointing for the romantics among us, the early accounts of the two Valentines are typical martyrdom stories, stressing the saints’ miracles and gruesome deaths but containing not a word about romance.

“They’re both mythical to begin with, and the connection with love is even more mythical,” says Henry Kelly, a scholar of medieval and renaissance literature and history at UCLA.

Tracing Valentine’s Day to Lupercalia
Saint Valentine’s Day has also been associated with a Christian effort to replace the older holiday of Lupercalia, which Romans celebrated on February 15. Some modern stories paint Lupercalia as a particularly sexy holiday, when women wrote their names on clay tablets which men then drew from a jar, pairing up random couples.

But, again, early accounts don’t support this. The closest parallel between Lupercalia and modern Valentine’s Day traditions seems to be that the Roman festival involved two nearly naked young men slapping everyone around them with pieces of goat skin. According to the ancient writer Plutarch, some young married women believed that being hit with the skins promoted conception and easy childbirth.

Whatever minor romantic connotations might have been part of Lupercalia, they didn’t translate to the new Christian holiday.

“It just drives me crazy that the Roman story keeps circulating and circulating,” Forbes says. “The bottom line for me is until Chaucer we have no evidence of people doing something special and romantic on February 14.”

A Chaucer Poem Links Romance to Valentine
So how did Chaucer create the Valentine’s Day we know today? In the 1370s or 1380s, he wrote a poem called *”Parliament of Fowls” that contains this line: “For this was on Saint Valentine’s Day, when every bird comes there to choose his mate.”

This was a moment in Europe when a particular set of romantic ideas took shape. Chaucer and other writers of his time celebrated romance between knights and noble ladies who could never marry—often because she was married already—creating tropes of yearning and tragic obstacles that still drive our romantic comedies today.

By the 1400s, nobles inspired by Chaucer had begun writing poems known as “valentines” to their love interests. It was only at this point that stories began to appear linking Saint Valentine to romance.

But there’s one final twist in the myth of Saint Valentine. When Chaucer wrote of the day when every bird chooses a mate, Kelly argues that he was thinking not of February 14, but of May 3, a day celebrating one of the many other Saint Valentines. After all, England is still awfully cold in mid-February.

In Kelly’s view, Chaucer was looking for a way to celebrate King Richard II’s betrothal to Anne of Bohemia on that day and found that was the feast day for Valentine of Genoa. (He could have chosen the Feast of the Holy Cross, but that wouldn’t have sounded as nice in the poem.) But, since his contemporaries were more familiar with the Feb. 14 Saint Valentine’s Day, that was the date that became attached to the new holiday of romance.
In some ways, that may be a good thing.

“February is the worst month in cold climates,” Kelly says. “It’s great to have something to look forward to.”


*The Parlement of Foules (modernized: Parliament of Fowls), also called the Parlement of Briddes (Parliament of Birds) or the Assemble of Foules (Assembly of Fowls), is a poem by Geoffrey Chaucer (1343?–1400) made up of approximately 700 lines. The poem is in the form of a dream vision in rhyme royal stanza and contains one of the earliest references to the idea that St. Valentine’s Day is a special day for lovers.

No, You Didn’t Win A Free MacBook Pro.

Who is keeping the scammers in business?

Danell teNyenhuis Black

I have won multiple MacBook Pros, iPad Airs, and iPhone 12’s in the past month. I don’t have an exact count because I immediately deleted the texts. I didn’t click for more details, and I didn’t provide any information.

Don’t get me wrong, I love my Apple gadgets, and I would never decline a free one. But I believe the adage that nothing in life is free except for prizes at a baby or bridal shower. Those are definitely free, and I am a fierce competitor when it comes to shower games!

Seriously though, I can’t believe that anyone believes they actually won an expensive gadget through a random text.

According to the FBI’s Internet Crime Complaint Center (IC3), in 2019, there were 467,361 complaints involving 3.5 billion in losses for these types of scams, along with other internet-based crimes.

Who clicks on these links? Judging by the above statistics, people click on the link, and many of them lose money in a scam. Reader’s Digest discussed the various types of text scams known as “smishing.”

I tried looking for stories of people admitting they clicked on the link. I found it article after article warning you to NOT click on the link. I was going to keep searching, but I got bored.

If you are someone who might believe you can win something through a random text, STOP CLICKING THE LINKS!! You are the reason I am inundated with spam texts. Repeat after me, “Nothing is free.” You’re welcome.


Kitchen utensils used in baking on Swan Island

BY Claire Lower

Traditionally, a “pinch” simply meant the amount you could literally pinch between your forefinger and thumb, which usually falls somewhere between 1/16 and 1/8 of a teaspoon. A smidgen is half a pinch (1/32 of a teaspoon), and a dash is a liquid measurement that translates to to 1/8 of a teaspoon. These terms are handy to know, but don’t fret if you have tiny measuring spoons; these units are most commonly used for seasoning, so it’s very unlikely you’ll ruin anything by playing a little fast and loose with these amounts.




Pizza has a long history. Flatbreads with toppings were consumed by the ancient Egyptians, Romans and Greeks. (The latter ate a version with herbs and oil, similar to today’s focaccia.) But the modern birthplace of pizza is southwestern Italy’s Campania region, home to the city of Naples.

Founded around 600 B.C. as a Greek settlement, Naples in the 1700s and early 1800s was a thriving waterfront city. Technically an independent kingdom, it was notorious for its throngs of working poor, or lazzaroni. “The closer you got to the bay, the more dense their population, and much of their living was done outdoors, sometimes in homes that were little more than a room,” says Carol Helstosky, author of Pizza: A Global History and associate professor of history at the University of Denver.

These Neapolitans required inexpensive food that could be consumed quickly. Pizza—flatbreads with various toppings, eaten for any meal and sold by street vendors or informal restaurants—met this need. “Judgmental Italian authors often called their eating habits ‘disgusting,’” Helstosky notes. These early pizzas consumed by Naples’ poor featured the tasty garnishes beloved today, such as tomatoes, cheese, oil, anchovies and garlic.


Italy unified in 1861, and King Umberto I and Queen Margherita visited Naples in 1889. Legend has it that the traveling pair became bored with their steady diet of French haute cuisine and asked for an assortment of pizzas from the city’s Pizzeria Brandi, the successor to Da Pietro pizzeria, founded in 1760. The variety the queen enjoyed most was called pizza mozzarella, a pie topped with the soft white cheese, red tomatoes and green basil. (Perhaps it was no coincidence that her favorite pie featured the colors of the Italian flag.) From then on, the story goes, that particular topping combination was dubbed pizza Margherita.

Queen Margherita’s blessing could have been the start of an Italy-wide pizza craze. But pizza would remain little known in Italy beyond Naples’ borders until the 1940s.

An ocean away, though, immigrants to the United States from Naples were replicating their trusty, crusty pizzas in New York and other American cities, including Trenton, New Haven, Boston, Chicago and St. Louis. The Neapolitans were coming for factory jobs, as did millions of Europeans in the late 19th and early 20th centuries; they weren’t seeking to make a culinary statement. But relatively quickly, the flavors and aromas of pizza began to intrigue non-Neapolitans and non-Italians.

One of the first documented United States pizzerias was G. (for Gennaro) Lombardi’s on Spring Street in Manhattan, licensed to sell pizza in 1905. (Prior to that, the dish was homemade or purveyed by unlicensed vendors.) Lombardi’s, still in operation today though no longer at its 1905 location, “has the same oven as it did originally,” notes food critic John Mariani, author of How Italian Food Conquered the World.

Debates over the finest slice in town can be heated, as any pizza fan knows. But Mariani credited three East Coast pizzerias with continuing to churn out pies in the century-old tradition: Totonno’s (Coney Island, Brooklyn, opened 1924); Mario’s (Arthur Avenue, the Bronx, opened 1919); and Pepe’s (New Haven, opened 1925).

As Italian-Americans, and their food, migrated from city to suburb, east to west, especially after World War II, pizza’s popularity in the United States boomed. No longer seen as an “ethnic” treat, it was increasingly identified as a fast, fun food. Regional, decidedly non-Neapolitan variations emerged, eventually including California-gourmet pizzas topped with anything from barbecued chicken to smoked salmon.

Postwar pizza finally reached Italy and beyond. “Like blue jeans and rock and roll, the rest of the world, including the Italians, picked up on pizza just because it was American,” explains Mariani.

Today international outposts of American chains like Domino’s and Pizza Hut thrive in about 60 different countries. Reflecting local tastes, global pizza toppings can run the gamut from Gouda cheese in Curaçao to hardboiled eggs in Brazil.