In the past month, more than 1,000 scientific, public health, and legal experts have joined a call to global leaders to ensure access to COVID-19 vaccines for low- and middle-income countries.

“The COVID-19 pandemic will not be over for us until it is over for everyone,” the authors wrote in an open letter.

Now, a health expert in Argentina argues in the BMJ that, on top of supply problems, Latin American countries face an additional challenge due to a lack of publicly available data about vaccines from Russia and China.

Dr. Juan Víctor Ariel Franco, the editor-in-chief of BMJ Evidence-Based Medicine and a lecturer in research methodology, family medicine, and public health at the Instituto Universitario of the Hospital Italiano de Buenos Aires, in Argentina, points out that high-income countries have not had to face this difficulty.

“The lack of publicly available data on these vaccines adds another layer of inequality: We are administering vaccines to millions of individuals in Latin American countries for which we have little to no information beyond press releases,” he writes.

If the virus is allowed to spread unchecked in low- and middle-income countries, Dr. Franco warns, it will mutate into variants that evade the immune protection from vaccines.

Rollout of COVID-19 vaccines

Despite extreme political, economic, and social difficulties in Latin America, the rollout of COVID-19 vaccines started at the end of 2020 due to direct agreements between national governments and vaccine manufacturers.

Dr. Franco notes that the Pfizer-BioNTech and Oxford-AstraZeneca vaccines have been generally well-received because regulators such as the Food and Drugs Administration (FDA) and European Medicines Agency provided free access to the evidence on which they based their approvals.

However, he highlights an initial lack of information about the phase 3 trial of the Russian Sputnik V vaccine, which was distributed in Argentina between December 2020 and January 2021.

At the time, the only publicly available data was in a press release from the Gamaleya Research Institute of Epidemiology and Microbiology, in Moscow, which had developed the vaccine, and a two-page report from the Argentinian medicines regulatory agency.

Dr. Franco says that the publication of an interim analysis of the results in The Lancet in early February 2021 allayed some concerns, but the full protocol for the trial has still not been released.

In addition, he reports that the regulators in Argentina have not issued an independent evaluation of the results.

Vaccines from China

With the second wave of COVID-19 sweeping across the region and variants spreading unchecked, Dr. Franco notes that regulators in Latin America have now approved two more vaccines, made by Sinopharm and Sinovac, in China.

But they did this in the absence of publicly available technical reports on phase 3 clinical trials or published data, he writes.

Dr. Franco points out that there is “little or no information” about the effects of these vaccines in particular subgroups of people or whether these vaccines are as effective against variants.

This is particularly important, he says, given that their efficacy against the original strain could be as low as 50%.

“This would not be acceptable for high-income countries who sign deals with the main manufacturers and align their regulators’ power to guarantee quality control and transparency in the approval process,” Dr. Franco writes.

He observes that this openness by the regulators in high-income countries is maintained “even in the most sensitive cases,” as with concerns about a possible link between the AstraZeneca vaccine and adverse events.

Call for greater transparency

On their own, low- and middle-income countries do not have the power to negotiate access to the vaccines with more transparent data, Dr. Franco writes, “amid a brutal fight over vaccine doses” among high-income countries.

In his article, Dr. Franco calls for international collaborations — with the support of bodies such as the Pan American Health Organization and World Health Organization (WHO) — to ensure that all vaccine data are made available as soon as possible.

Given the global shortage, he concedes that low- and middle-income countries may have to deploy vaccines with lower efficacy:

“But this must be done with publicly available data and wide consultation to relevant stakeholders. We cannot afford to fuel anti-vaxxers, conspiracy theorists, and COVID-deniers in countries that are struggling to ramp up vaccination during a global crisis.”

Vitamin D plays a wide range of roles in the body, including regulating calcium levels, maintaining healthy bones and teeth, and supporting the immune system.

In addition to getting vitamin D from dietary sources, the body can make its own in the skin through exposure to sunlight.

However, it can be difficult for people with dark skin and those with low exposure to sunlight to maintain sufficiently high levels of the vitamin, especially during the winter months.

One studyTrusted Source found that, overall, about 42% of people in the United States were deficient in vitamin D. The figure rose to 82% among Black people and 70% among Hispanic people.

Accumulating evidence has shown that people with deficient vitamin D levels are more likely to test positive for SARS-CoV-2, which is the virus that causes COVID-19. They may also be more likely to develop severe disease.

This association may partly explain why the pandemic has disproportionately affected Black, Hispanic, and other non-white populations.

Clinical trialsTrusted Source have found that vitamin D supplements can help protect people against other respiratory infections resulting from viruses.

The research suggests that taking a vitamin D supplement can even reduce viral infections among people who are not deficient in the vitamin, based on the recommended intake in the current guidelines. These recommendations are based on the levels necessary to maintain healthy bones.

Dr. David Meltzer, Ph.D., and his colleagues at the University of Chicago, IL, wondered whether the same could be true of vitamin D and COVID-19.

Vitamin D blood tests

The researchers analyzed the medical records of 4,638 individuals who had a vitamin D blood test in the 12 months before having a PCR test for SARS-CoV-2 at the University of Chicago Medical Center (UChicago Medicine).

The researchers used the length of time since the vitamin D test and subsequent treatments to estimate the participants’ vitamin D levels 14 days before the PCR test.

In addition, they accounted for factors that are known to increase a person’s risk of COVID-19, such as age, sex, race, and medical conditions.

In total, 211 Black participants and 102 white participants tested positive for SARS-CoV-2.

The researchers discovered that among Black participants, the risk of testing positive was 2.64 times as high for those with a serum vitamin D level of 30–39.9 nanograms per milliliter (ng/ml) — a “sufficient” level — as it was for those with a level of at least 40 ng/ml.

In other words, there appeared to be a significant protective effect from having levels above the range that experts consider to be sufficient.

Among Black participants with a vitamin D level of at least 30 ng/ml, every incremental 1 ng/ml increase in the level of the vitamin led to a 5% decrease in the risk of testing positive for SARS-CoV-2.

“These new results tell us that having vitamin D levels above those normally considered sufficient is associated with decreased risk of testing positive for [SARS-CoV-2], at least in Black individuals,” says Dr. Meltzer, who is chief of hospital medicine at UChicago Medicine and lead author of the study.

“This supports arguments for designing clinical trials that can test whether or not vitamin D may be a viable intervention to lower the risk of the disease, especially in Persons of Color,” he adds.

There were no statistically significant associations between vitamin D levels and the risk of testing positive for SARS-CoV-2 among white individuals.

The researchers attribute this to the relatively low number of positive SARS-CoV-2 tests among white people in their sample.

Similarly, the numbers of participants from other racial groups, including Hispanic people, were too small to yield statistically significant results.

The study appears in the journal JAMA Network OpenTrusted Source.

Case for high dose supplements

“These results increase the urgency to consider whether increased sun exposure or vitamin D supplementation could reduce COVID-19 risk,” say the researchers in their paper.

They write that less than 5–10% of adults in the U.S. are likely to have vitamin D levels greater than 40 ng/ml. To attain these levels from taking a supplement — without increased sun exposure — would require more than the currently recommended daily dose.

“Lifeguards, surfers; those are the kinds of folks who tend to have more than sufficient vitamin D levels,” says Dr. Meltzer. “Most folks living in Chicago in the winter are going to have levels that are well below that.”

The National Institutes of Health (NIH) recommend 600 international units (IU), which equates to 15 micrograms (mcg), daily for adults aged 19–70 years. For adults aged 71 years and older, the recommended amount rises to 800 IU (20 mcg) daily.

In the United Kingdom, the National Health Service (NHS) recommends 400 IU (10 mcg) daily. It advises everyone to consider supplementing the vitamin during the fall and winter months but notes that those at high risk of deficiency should do so all year round.

Dr. Meltzer notes that although some studies have found that vitamin D improves immune function and decreases inflammation, the evidence has been mixed.

He believes this may be because researchers have been testing doses that are too low to boost the immune system.

“Based on these results, we think that earlier studies may have given doses that were too low to have much of an effect on the immune system, even if they were sufficient for bone health,” he says.

“It may be that different levels of vitamin D are adequate for different functions,” he adds.

A key limitation of the current study is that while it can demonstrate an association between vitamin D levels and SARS-CoV-2 infection risk, it cannot demonstrate that one causes the other.

To address this problem, researchers from the University of Chicago and Rush University in Chicago, IL, are conducting two clinical studies to learn whether taking a daily vitamin D supplement can help prevent COVID-19 or decrease the severity of its symptoms.

Socioeconomic inequality

Some of the results of the study were surprising. For instance, Black individuals with a vitamin D level of 20–30 ng/ml were not at an increased risk of COVID-19 compared with those with a level over 40 ng/ml.

Moreover, those with a level below 20 ng/ml seemingly had a lower COVID-19 risk than those with a level of 30–40 ng/ml. The authors suggest that potential variations in vitamin D treatment may explain these discrepancies, but they highlight that ongoing research is necessary in this area.

The authors of the new study also emphasize that social and economic inequities play a role in the increased susceptibility of Black people to COVID-19.

They write:

“The significant association of vitamin D levels with COVID-19 risk in Black individuals that was not found in white individuals could reflect their higher COVID-19 risk, to which socioeconomic factors and structural inequities clearly contribute.”

For decades, scientists have been hunting for a cure for the common cold, with little success.

However, recent research hints that this bothersome — though usually mild — infection may be a hidden ally in the fight against pandemic viruses such as influenza and SARS-CoV-2.

Human rhinoviruses (HRVs), which cause more than half of all common colds, are the most widespread respiratory viruses in humans.

Previous researchTrusted Source suggests that HRVs may have inhibited the spread of the influenza A virus subtype H1N1 across Europe during the 2009 flu pandemic.

Experts believe that the HRVs did this by inducing human cells to produce interferon, which is part of the body’s innate immune defenses against viral infection.

Research has shown that SARS-CoV-2 is susceptibleTrusted Source to the effects of interferon.

This finding led scientists at the MRC-University of Glasgow Centre for Virus Research in the United Kingdom to speculate whether HRVs could help combat the spread of SARS-CoV-2 and limit the severity of infections.

Human respiratory cells

To find out, the researchers infected cultures of human respiratory cells in the lab with either SARS-CoV-2, an HRV, or both viruses at the same time.

The cultures closely mimicked the outer layer of cells, called the epithelium, that lines the airways of the lungs.

SARS-CoV-2 steadily multiplied in the cells that the team had infected with this virus alone. However, in cells also infected with HRV, the number of SARS-CoV-2 virus particles declined rapidly until they were undetectable just 48 hours after the initial infection.

In further experiments, the scientists found that HRV suppressed the replication of SARS-CoV-2, regardless of which virus infected the cells first.

Conversely, SARS-CoV-2 had no effect on the growth of HRV.

To test their hunch that HRV was inhibiting SARS-CoV-2 by triggering the cells’ innate immune response, the researchers repeated their experiments in the presence of a molecule that blocks the effects of interferon.

Sure enough, the molecule restored the ability of SARS-CoV-2 to replicate in cells infected with HRV.

“Our research shows that human rhinovirus triggers an innate immune response in human respiratory epithelial cells, which blocks the replication of the COVID-19 virus, SARS-CoV-2,” says senior author Prof. Pablo Murcia.

“This means that the immune response caused by mild, common cold virus infections could provide some level of transient protection against SARS-CoV-2, potentially blocking transmission of SARS-CoV-2 and reducing the severity of COVID-19,” Prof. Murcia adds.

Mathematical simulation

The researchers used a mathematical simulation to predict how different numbers of HRV infections of varying lengths might affect the spread of SARS-CoV-2 through a population.

The results showed that the number of new SARS-CoV-2 infections in a population is inversely proportional to the number of HRV infections.

The model predicts that if the common cold virus were to become sufficiently widespread and persistent, it could temporarily prevent SARS-CoV-2 from spreading.

“The next stage will be to study what is happening at the molecular level during these virus-virus interactions to understand more about their impact on disease transmission,” says Prof. Murcia.

“We can then use this knowledge to our advantage, hopefully developing strategies and control measures for COVID-19 infections,” he adds.

The research appears in The Journal of Infectious Diseases.

In their paper, the researchers speculate that mild HRV infections might be mutually beneficial for the virus and its human hosts.

They write that the immune system may have evolved to allow HRV to replicate and transmit to new hosts. In return, the virus keeps more severe and potentially lethal viral infections at bay.

Real-world limitations

At the Science Media Centre in London in the United Kingdom, other scientists welcomed the research but flagged some potential limitations.

Gary McLean, who is a professor in molecular immunology at London Metropolitan University in the U.K., said that the major limitation was that the study involved just one of the 160 or more possible strains of rhinovirus.

He said there was no guarantee that each strain would have the same effect on SARS-CoV-2 infections.

He added that translating results from a lab experiment to real life is “very tricky,” saying:

“Although it is likely that a common cold virus, such as rhinovirus, would induce a strong innate immune response that could block SARS-CoV-2 infections, it would still require both infections to occur at a similar time.”

In addition, he pointed out that intensive infection control measures over the past year have made the common cold less prevalent, reducing the potential for HRV-triggered innate immunity to combat the spread of SARS-CoV-2.

SARS-CoV-2, which is the virus that causes COVID-19, is not the only zoonotic coronavirus. In fact, it is the third to have emerged since the turn of the century. It was preceded by severe respiratory syndrome (SARS) in 2003 and MERS in 2012.

There are likely to be more coronaviruses if the recent past is any indication. However, there are not currently many drugs that can effectively combat them.

Researchers have been racing to identify existing drugs that may be of use in this fight, with one team last year identifying 21 existing drugs as showing promise. Among these was a leprosy drug called clofazimine, which has proven effective against both SARS and MERS in laboratory experiments.

A new study from researchers at Sanford Burnham Prebys Medical Discovery Institute in San Diego, CA, and the University of Hong Kong in Pok Fu Lam suggests that it may also be useful in treating COVID-19.

Clofazimine exhibits antiviral properties against SARS-CoV-2 and limits the extreme inflammatory response that commonly occurs with COVID-19.

The study has undergone peer review and will soon appear in edited form in the journal NatureTrusted Source.

A drug that is well-known and safe

If researchers confirm clofazimine’s efficacy, experts could immediately deploy the drug against SARS-CoV-2 and COVID-19.

The Food and Drug Administration (FDA) have already approved it for use against leprosy, and it is on the World Health Organization (WHO)’s Model List of Essential Medicines. Experts have thoroughly vetted the drug for safety, though it is not currently available for sale in the United States.

Co-senior study author Dr. Sumit K. Chanda — of the Immunity and Pathogenesis Program at Sanford Burnham Prebys — says, “Clofazimine is an ideal candidate for a COVID-19 treatment. It is safe, affordable, easy to make, taken as a pill and can be made globally available.”

Dr. Chanda explains, “We hope to test clofazimine in a phase 2 clinical trial as soon as possible for people who test positive for COVID-19 but are not hospitalized,” adding:

“Since there is currently no outpatient treatment available for these individuals, clofazimine may help reduce the impact of the disease, which is particularly important now as we see new variants of the virus emerge and against which the current vaccines appear less efficacious.”

The effect of clofazimine

In the study, the researchers administered clofazimine to hamsters with SARS-CoV-2 and prophylactically (preventively) to other hamsters that did not yet have the virus.

Both groups that the researchers treated with clofazimine had less SARS-CoV-2 in their lungs after taking the drug.

Clofazimine also prevented the often deadly inflammatory overreaction that commonly occurs in humans. This is called the “cytokine storm.”

Co-senior study author Dr. Ren Sun, of the University of Hong Kong, reports, “The animals that received clofazimine had less lung damage and lower viral load, especially when receiving the drug before infection.”

Dr. Sun adds, “Besides inhibiting the virus, there are indications that the drug also regulates the host response to the virus, which provides better control of the infection and inflammation.”

The study suggests that clofazimine fights SARS-CoV-2 by doing two things: blocking the virus’s entry into cells and disrupting RNA replication of the virus.

A partner for remdesivir and more

The researchers also found that clofazimine, when they administered it to hamsters, worked synergistically with remdesivir. This is the most prominent drug currently in use as a COVID-19 treatment.

Since clofazimine is affordable and easy to make, it may help stretch the limited — and comparatively expensive — supply of remdesivir.

Considering experts’ concerns regarding future coronaviruses, it is equally exciting that clofazimine seems to prevent the in vitro replication of MERS in human lung tissue.

“Potentially most importantly, clofazimine appears to have pan-coronavirus activity, indicating [that] it could be an important weapon against future pandemics,” says co-senior study author Dr. Kwok-Yung Yuen, of Infectious Diseases at the University of Hong Kong.

Early in the pandemic, research showed that almost one-third of people with COVID-19 in intensive care experienced potentially fatal complications as a result of excessive blood clotting.

Another study found that many of these patients had unusually “sticky” blood that tended to coagulate easily.

“As we learned about the connection between blood clots and COVID-19, we knew that aspirin — used to prevent stroke and heart attack — could be important for COVID-19 patients,” says Jonathan Chow, M.D., assistant professor of anesthesiology and critical care medicine at the George Washington University School of Medicine and Health Sciences in Washington, D.C.

By “thinning” the blood, aspirin helps prevent the formation of clots, or thrombi, that can block the blood vessels supplying the heart, brain, lungs, and other vital organs.

One widely recognized limitation of aspirin as a preventive treatment is that it leads to a small increase in the risk of bleeding.

Given the low cost of aspirin and the evidence of its overall safety and efficacy in cardiovascular disease, however, Dr. Chow and his colleagues decided to conduct a pilot study of hospitalized patients with COVID-19.

Their analysis suggests that a low dose of aspirin shortly before or after hospital admission is associated with a significantly reduced risk of mechanical ventilation, admission to intensive care, and in-hospital mortality.

At the same time, the researchers found no evidence that aspirin increased the risk of bleeding.

“Aspirin is low cost, easily accessible, and millions are already using it to treat their health conditions,” says Dr. Chow. “Finding this association is a huge win for those looking to reduce risk from some of the most devastating effects of COVID-19.”

In addition to preventing clotting, aspirin reduces levels of an immune signaling molecule or cytokine called interleukin-6 (IL-6) in the blood. The molecule is associated with the immune overreaction, or “cytokine storm,” that can affect people with COVID-19 in intensive care.

The study features in the journal Anesthesia & Analgesia.

Study design

The authors emphasize that other researchers will need to conduct randomized controlled clinical trials to confirm their findings.

Their retrospective study analyzed the records of 412 adults with COVID-19 who were admitted to one of several hospitals in the United States between March 2020 and July 2020.

Of these people, 98 took aspirin in the week before admission or during the first 24 hours after admission. The researchers compared the outcomes for these individuals with those for the 314 people who did not take aspirin.

Among those taking aspirin, the median daily dose was 81 milligrams, and the median length of treatment was 6 days.

In their analysis of the data, the researchers accounted for other variables that scientists have shown to affect the severity of COVID-19, including age, sex, body mass index, race, hypertension, and diabetes.

After these adjustments, aspirin use was associated with a 43% reduced risk of intensive care unit admission, a 44% reduced risk of mechanical ventilation, and a 47% reduced risk of dying in the hospital.

While there was no evidence that aspirin increased the risk of bleeding, the authors recommend caution:

“Until a randomized controlled trial of aspirin is performed, it is imperative to exercise cautious optimism and deliberately balance aspirin’s known risks against its potential benefits in patients afflicted by COVID-19.”

Large and small clots

Interestingly, the researchers found no difference in overt thrombosis between the aspirin and non-aspirin groups. Overt thrombosis is the term for large blood clots that show up in standard diagnostic images.

However, they point out that the number of cases of thrombosis in the two groups was low, which limits the statistical reliability of this finding.

In addition, they note that small blood clots, called microthrombi, are difficult to spot without the use of more specialist, nonstandard imaging techniques.

The researchers acknowledge that their sample size was modest and that the study was observational, meaning that it could not prove that aspirin reduced the severity of COVID-19 in hospitalized patients.

The people who took aspirin may have received different medical treatments due to their underlying conditions, for example, which would skew the results.

The researchers were also unable to account for other medications that people may have been taking that could increase their risk of blood clots, such as birth control pills and hormone replacement therapy (HRT).