Three major scientific controversies about coronavirus

It is unclear how well masks work.
People Image Studio/Shutterstock

Manal Mohammed, University of Westminster

Although political leaders have closed borders in response to COVID-19, scientists are collaborating like never before. But the coronavirus (SARS-COV-2) is novel – and we don’t yet have all the facts about it. As a result, we may have to change our approach as new scientific data comes in.

That doesn’t mean the science isn’t trustworthy – we will get the full picture over time. And there is already great research that can help inform political decisions. Here are three topics that scientists disagree on.

Face masks

The novel coronavirus spreads by droplets from coughs, sneezes and speaking. To halt the spread of the virus, face masks have become compulsory in many countries.

But there has been much debate among scientists over the effectiveness of face masks on reducing the spread of COVID-19. A report from a multidisciplinary group convened by the Royal Society has come out in favour of the public wearing face masks. These documents, which have not been peer reviewed, argue that face coverings can contribute to reducing the transmission of COVID-19 if widely used in situations where physical distancing is not possible.

One relatively small clinical study also showed that infected children who wore masks did not pass on the virus to family contacts.

But the science is complex. Face masks won’t stop the wearer from inhaling small airborne particles of coronavirus, which can cause infection. A recent study reported that wearing a mask may also give a false sense of security, meaning wearers may ignore other important infection control measures.

Research has also shown that when people wear masks, the exhaled air goes into the eyes. This generates an impulse to touch the eyes. And if your hands are contaminated, you may infect yourself. Indeed, WHO warns that masks can be counterproductive unless wearers avoid touching their face and adopt other management measures.

We also know that face masks can make us breathe more often and more deeply – potentiality spreading more contaminated air.

Many scientists therefore disagree with the Royal Society report, requesting more evidence on the efficacy of masks. Ideally, we need randomised controlled trials involving many people from an entire population to trace how masks affect infection numbers.

That said, other scientists argue that we should use face masks even though perfectly reliable evidence is lacking – to be on the safe side. Ultimately though, without a vaccine, the strongest weapons we have are basic preventive measures such as regular hand washing and social distancing.


Immunologists are working hard to determine what immunity to COVID-19 looks like. Much of the studies have focused on “neutralising antibodies”, produced by so-called B-cells, which bind to viral proteins and directly prevent infection.

Studies have found that levels of neutralising antibodies remain high for a few weeks after infection, but then typically begin to wane. A peer-reviewed study from China showed that infected people had steep declines in levels of antibodies within two to three months of infection. This has created doubt over whether people get long-term protection against subsequent exposure to the virus. If this study turns out to be accurate – the result needs to be backed up by other studies – it could have implications for whether it is possible to produce vaccines with long-lasting immunity.

3D illustration of T cells attacking a cancer cell.
T cells attacking a cancer cell.
Meletios Verras/Shutterstock

While many scientists believe antibodies are the key to immunity, others argue that other immune cells called T-cells – produced when the body encounters the molecules that combat viruses, known as antigens – are involved too. These can become programmed to fight the same or similar viruses in the future. And studies suggest that T-cells are at work in many patients fighting COVID-19. People never infected may also harbour protective T-cells because they’ve been exposed to similar coronaviruses.

A recent study from Karonliska Institute in Sweden, which has not yet been peer reviewed, found that many people who suffered mild or asymptomatic COVID-19 have T-cell-mediated immunity – even when antibodies can’t be detected. The authors believe this can prevent or limit reinfection, estimating that one-third of people with symptomless COVID-19 could have this kind of immunity. But it is not clear yet how it works and how long it lasts.

If this is the case, it is very good news – meaning public immunity to COVID-19 is probably significantly higher than antibody tests have suggested. Some have argued it could create “herd immunity” – whereby enough people have been infected to become immune to the virus – with an infection rate as low as 20%, rather than the widely accepted 60-70%. This claim, however, is still controversial.

Immune response to COVID-19 is complex, with the full picture likely to extend beyond antibodies. Larger studies over longer periods of time must now be done on both T-cells and antibodies to understand how long-lasting the immunity is and how these different components of COVID-19 immunity are related.

Number of cases

The reporting of coronavirus cases varies drastically around the world. Some regions are reporting that less than 1% of people have been infected, and others that over half the population has had COVID-19. One study, which has been peer reviewed, estimated that only 35% of symptomatic cases have been reported in the US, and that the figure is even lower for some other countries.

When it comes to estimating true prevalence, scientists use just one of two main approaches. They either test a sample of people in a population for antibodies and directly report those numbers, or predict how the virus has affected a population using mathematical models. Such models have given very different estimates.

Research led by the University of Toronto in Canada, which hasn’t been peer reviewed yet, assessed blood test data from people across the world and discovered that the proportion who have had the virus varies widely across countries.

We don’t know why. There could be real differences due to the age, health or spread of each population – or in policies to control virus transmission. But it is very likely it’s down to differences in the methodology, such as antibody tests (serological testing): different tests have different sensitivity.

Antibody studies suggest that only 14% of people in the UK have had COVID-19, compared with 19% in Sweden and 3% in Yemen. But that excludes T-cells. If they provide a reliable guide to infection, the number may be much higher – potentially close to herd immunity in some regions – but this is hugely debated.The Conversation

Manal Mohammed, Lecturer, Medical Microbiology, University of Westminster

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Alzheimer’s disease: protective gene uncovered in human cell model – bringing promise for new drug discoveries

Our method could someday potentially detect the disease before it starts developing in a person’s brain.
Robert Kneschke/ Shutterstock

Dean Nizetic, Queen Mary University of London

Every three seconds, someone in the world develops dementia. The most common form of dementia is Alzheimer’s disease. While researchers have identified a number of risk factors that are linked to dementia – including genetics, smoking, and high blood pressure – there is currently still no cure.

Part of the reason for this is because of how complicated it is to test potential Alzheimer’s drugs. In order to conduct clinical trials participants need to have symptoms. But by the time symptoms appear, it’s usually too late for treatments to have a large effect as many of their brain cells have already died.

But our latest research developed a new human cell model that is able to rapidly simulate the development of Alzheimer’s disease in the lab. This allowed us to identify a gene, called BACE2, that is naturally able to suppress the signs of Alzheimer’s disease in human brain cells. Our research is the result of around five years’ work, and was the collaborative effort of teams based in London, Singapore, Sweden and Croatia.

Researchers already know a lot about which genes cause Alzheimer’s disease or make someone more likely to develop it. These genes contribute to certain toxic proteins accumulating in the human brain. So our team thought that the opposite must also be true: our brain cells must also have proteins that can naturally slow down the development of Alzheimer’s.

One gene that can definitely cause Alzheimer’s disease is a gene found on the 21st pair of human chromosomes that is responsible for making the amyloid precursor protein (APP). Research shows that 100% of people born with just one extra copy of the APP gene (called “DupAPP”) will develop dementia by age 60.

People with Down’s syndrome are born with three copies of APP because they have a third 21st chromosome. But by age 60, only 60% of them will develop clinical dementia. We wanted to know why some people with Down’s syndrome have delayed development of – or never develop – Alzheimer’s dementia compared to those who have one extra DupAPP gene.

The simple answer for this is because they have an extra dose of all other genes located in chromosome 21. We believed that there could be some dose-sensitive genes on chromosome 21 that, when triplicated, protect against Alzheimer’s disease by counteracting the effects of the third APP gene.

These genes must then appear to delay the onset of clinical dementia in some people with Down’s syndrome by approximately 20 years. Studies have even shown that any future drug able to delay dementia onset by just five years would reduce the prevalence of Alzheimer’s in the general population by half.

We re-programmed cells, turning them into brain cells.
arrideo/ Shutterstock

To study the potential of the extra genes, we took hair follicle cells from people with Down’s syndrome and re-programmed the cells to become like stem cells. This allowed us to turn them into brain cells in a Petri dish.

We then grew them into 3D balls of cells that imitated the tissue of the grey matter (cortex) of the human brain. The 3D nature of the culturing allowed misfolded and toxic proteins to accumulate, which are crucial changes that lead to Alzheimer’s disease in the brain.

We found all three major signs of Alzheimer’s disease (plaque build-up in the brain, misfolded “tau” proteins and dying brain neurons) in cell cultures from 71% of people with Down’s syndrome who donated samples. This proportion was similar to the percentage of clinical dementia among adults with Down’s syndrome.

We were also able to use CRISPR – a technology that allows researchers to alter DNA sequences and modify a gene’s function – to reduce the number of BACE2 genes from three copies to two copies on chromosome 21. This was only done in cases where there were no indications of Alzheimer’s disease in our cellular model. Surprisingly, reducing the number of BACE2 genes on chromosome 21 provoked signs of the disease. This strongly suggest that having extra copies of a normal BACE2 gene could prevent Alzheimer’s.

The protective action of BACE2 reduces the levels of toxic amyloid proteins. This was verified in our cellular models, as well as in cerebrospinal fluid and post-mortem brain tissue from people with Down’s syndrome.

Our study provides proof that natural Alzheimer’s-preventing genes exist, and now we have a system to detect new potential protective genes. Importantly, recent research showed the protective action of BACE2 might also be relevant to people who don’t have Down’s syndrome.

Our results also show that all three signs of Alzheimer’s disease can be potentially detected in cells from live donors. Though this requires a lot more research, it means we may be able to develop tests that identify which people are at higher risk of Alzheimer’s disease by looking at their cells.

This would allow us to detect the disease before it starts developing in a person’s brain, and could make it possible to design personalised preventative treatments. However, we are still a long way from reaching this goal.

Most importantly, our work shows that all three signs of Alzheimer’s disease detected using our model could be prevented by drugs known to inhibit the production of the toxic amyloid protein – and this can be detected in as little as six weeks in the lab. We hope our discovery could lead to the development of new drugs aimed at delaying or preventing Alzheimer’s disease, before it causes brain cell death.The Conversation

Dean Nizetic, Professor of Cellular and Molecular Biology, Queen Mary University of London

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Sodom found? The quest for the lost city of destruction – Part 1

By Brian Nixon

Special to ASSIST News Service

I met Dr. Steven Collins in the reception area of Trinity Southwest University in Albuquerque, where he serves as provost and professor. Instead of staying at the school, we headed off to a local coffee shop.

Dr. Collins didn’t look like your average jet-setting archeologist: no Indiana-Jones leather jacket, hat, or whip. Instead, Steve wore jeans, sandals, and a “Life is Good” t-shirt. And for Steve, that motto is playing out in his own life.

With his newest discoveries in Jordan, life is turning out very good for the unassuming archeologist from New Mexico.

I first got word of his recent finding at Calvary of Albuquerque, where Steve sat down for an interview with Senior Pastor, Skip Heitzig. Steve brought some convincing evidence of a monumentally significant find. Dr. Collins contends that he may have discovered the historic city of Sodom.

Steve told me in our interview that his interest in the location of Sodom began in 1996. Then, Steve was working on a dig in the West Bank north of Jerusalem, the site of biblical Ai, but was also leading archeology tours in the Near East.

It was on one of these trips that Steve began to question the traditional site of Sodom, what is known as the “Southern Theory.” This theory attributes the site of Sodom to the southern region of the Dead Sea.

“I began to read Genesis 13-19, and realized that the traditional site did not align itself with the geographical profile described in the text,” Steve told me.

“Now let me say,” he continued, “that many scholars don’t have a high view of Scripture. Some even frown upon using biblical texts as a tool for location designation. My philosophy is that the text is generally reliable and can—and should—be used (at bare minimum) as a basic guide for a geographical profile.”

“When I read how the author of Genesis described the area of Sodom and then looked at the area of the traditional site in the Southern region, I said: ‘This cannot be the place. There are too many differences of description.’

“Sadly, because of my work at the site of Ai, I was unable to really investigate and do research on my initial thoughts. So I let it sit for over five years.”

The geographical point at issue, according to Steve, is how the text in Genesis describes the region of the Kikkar, understood as “the disc of Jordan.”

Dr. Collins continued, “When the Bible uses the description of Kikkar, it is only referring to the circular region of the Jordan Valley east of Jericho and north of the Dead Sea.”

“This region is the breadbasket of the area, full of freshwater and farmland,” he explained. “All of this is interesting to me because Kikkar can also mean “flat bread,” like a tortilla here in New Mexico.”

So what’s the issue?

According to Collins, “The traditional “Southern Theory” site of Sodom does not have the geographical parallels described in the text. Namely: 1. One can see the whole area from the hills above Jericho (Bethel/Ai), 2. It must be a well-watered place (described, “like Egypt.”), 3. It has a river running through it (the Jordan), and 4. It must follow the travel route of Lot” (who went to the other side of the Jordan, eastward, away from Jericho.)

Though the traditional site does not have any of these geographical indicators, the site in Jordan, Tel-al-Hamman, does. How did Dr. Collins become aware of this site? That is a fascinating story in and of itself—which we’ll turn to in Part 2.

Report from the Christian Telegraph