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COVID-19

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Posted on October 21st 2024 (7 months)

Dr. Rhonda Patrick discusses her supplement stack, avoiding microplastics, creatine for brain health, and mRNA vaccine autoimmunity risks.

Posted on April 3rd 2022 (about 3 years)

In this clip, Dr. Rhonda Patrick reviews the recently published data on children's susceptibility to COVID-19.

Posted on April 3rd 2022 (about 3 years)

In this clip, Dr. Rhonda Patrick describes the different blood types and how they influence immunity.

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News & Publications

  • Supplemental vitamin C and arginine reduce symptoms associated with long COVID, a new study shows. People who took the combined supplements experienced less fatigue and performed better during exercise.

    Researchers gave people with long COVID either a combination of liposomal vitamin C and arginine or a placebo for four weeks. They measured their walking speed, strength, and endothelial function before and after the intervention.

    They found that those who took the vitamin C/arginine combination improved on measures of speed, strength, and endothelial function compared to those who took the placebo. They were also less likely to report experiencing fatigue.

    Vitamin C is an essential nutrient that exerts robust antioxidant properties. Evidence suggests that liposomal formulations of vitamin C are more bioavailable than conventional forms. Learn more about vitamin C in our overview article. Arginine is an amino acid that plays roles in vasodilation. Evidence suggests that arginine metabolism is altered in the setting of COVID-19.

  • Sulforaphane may be beneficial for the prevention and treatment of coronavirus infections.

    Sulforaphane is a bioactive compound derived from certain cruciferous vegetables, including broccoli (especially broccoli sprouts) and red kale. Robust evidence from epidemiological, clinical, rodent, and in vitro studies indicates that sulforaphane exhibits antioxidant, anti-inflammatory, and antiviral properties. Findings from a recent study suggest that sulforaphane is beneficial for the prevention and treatment of coronavirus infections.

    Coronaviruses are a group of related viruses that cause illness in birds and mammals, including humans. Members of this group include SARS-CoV-1 (which causes severe acute respiratory syndrome, or SARS), MERS-CoV (which causes Middle East respiratory syndrome, or MERS), SARS-CoV-2 (which causes COVID-19), and HCoV-OC43 (which causes the common cold), as well as others.

    The investigators conducted a two-part study involving cultured cells and mice. First, they exposed the cells to sulforaphane for one to two hours and then infected them with SARS-CoV-2 and HCoV-OC43. They also assessed the effects of sulforaphane on previously infected cells. They found that sulforaphane roughly halved the replication of the two viruses in both scenarios. Then they repeated the experiment, but they added remdesivir, an antiviral medication commonly used to treat COVID-19, to the sulforaphane and found that the compounds worked in a synergistic fashion to potently reduce viral replication.

    Next, they gave mice sulforaphane prior to infecting them with SARS-CoV-2 and gauged the compound’s effects. They found that sulforaphane decreased viral replication in the animals' lungs by 1.5 orders of magnitude – a 30-fold reduction – compared to infected mice that didn’t receive sulforaphane. The mice that received sulforaphane also exhibited less lung inflammation, one of the hallmarks of COVID-19 and a driver of poor disease outcomes.

    These findings demonstrate that sulforaphane may be beneficial for preventing or treating COVID-19 while modulating inflammation that typically accompanies the illness. Learn about other strategies that reduce the risk of COVID-19 infection in this episode featuring Dr. Roger Seheult.

  • Vitamin D is a fat-soluble vitamin that plays key roles in several physiological processes, including immune function. Robust evidence demonstrates links between poor vitamin D status and severe outcomes following infection with SARS-CoV-2, the virus that causes COVID-19. Now, findings from a recent study suggest that poor vitamin D status prior to infection with SARS-CoV-2 increases the risk of severe disease and/or death from COVID-19.

    During an infection, vitamin D deficiency can lead to over-expression of renin (an enzyme produced in the kidneys) and subsequent activation of the renin-angiotensin-system, a critical regulator of blood pressure, inflammation, and body fluid homeostasis. Disturbances in this system can drive poor outcomes, such as acute respiratory distress syndrome and death in COVID-19. Research suggests that supplemental vitamin D during hospitalization with COVID-19 improves outcomes. Vitamin D levels may drop during a viral infection, however, so measuring pre-infection status provides a more accurate assessment of the vitamin’s protective effects.

    The authors of the study reviewed the medical records of 253 patients whose vitamin D levels had been measured two weeks to two years prior to testing positive for COVID-19. They categorized the patients according to disease severity (critical, severe, moderate, or mild). They classified the patients' vitamin D status as deficient, below 20 nanograms per milliliter (ng/ml); insufficient, 20 to 29.9 ng/ml; adequate, 30-39.9 ng/ml; or high-normal, above 40 ng/mL.

    They found that patients categorized as having critical or severe COVID-19 disease were 14 times more likely to have pre-infection vitamin D deficiency than patients with moderate or mild disease. Patients with vitamin D deficiency were more likely to have coexisting illnesses, such as diabetes, high blood pressure, and chronic obstructive pulmonary disease and were 11 times more likely to die from COVID-19, compared with those who had vitamin D sufficiency.

    These findings suggest that pre-infection vitamin D deficiency markedly increases the risk of critical or severe disease and death in patients with COVID-19. Learn more about the importance of vitamin D in COVID-19 in this episode featuring frontline physician Dr. Roger Seheult.

  • Scientists have identified an emerging pattern of associations between SARS-CoV-2 (the virus that causes COVID-19) and Parkinson’s disease. For example, the loss of smell is one of the most common symptoms reported in SARS-CoV-2 infection, but it is also an early symptom of Parkinson’s disease, often preceding diagnosis by many years. In addition, some recent case reports describe patients who presented with probable Parkinson’s disease after recovering from severe SARS-CoV-2 infection. Now, evidence from a recent study suggests that the SARS-CoV-2 nucleocapsid protein drives aggregation of alpha synuclein, a hallmark of Parkinson’s disease.

    SARS-CoV-2 nucleocapsid proteins are helical structures that are housed within the viral membrane. They encapsulate SARS-CoV-2’s genome, protecting it from the host cellular environment. The virus produces large quantities of nucleocapsid proteins once inside an infected cell because they play critical roles in virion assembly and viral replication.

    Alpha synuclein is a type of neuronal protein that regulates synaptic vesicle movements and neurotransmitter release. Its aggregation, a progressive process that spreads from cell to cell, impairing brain function, is a dominant feature in the pathophysiology of Parkinson’s disease.

    The authors of the report assessed alpha synuclein aggregation in both the absence and presence of the SARS-CoV-2 spike protein (the virus’s primary infectious particle) and the nucleocapsid protein. They found that in the absence of any SARS-CoV-2 proteins, aggregation naturally occurred after about 10 days. The spike protein had no effect on aggregation time, but following exposure to the nucleocapsid protein, aggregation occurred in less than one day – more than 10 times faster than normal.

    Then they studied the effects of the nucleocapsid protein in a cell model of Parkinson’s disease. They injected some of the cells with nucleocapsid protein (about the amount one would expect during SARS-CoV-2 infection) and alpha synuclein and injected some with alpha synuclein alone. They found that twice as many cells injected with both proteins died compared to those injected with alpha synuclein alone.

    These findings suggest that the SARS-CoV-2 nucleocapsid protein drives aggregation of alpha synuclein and promotes cells death in a model of Parkinson’s disease. Learn more about Parkinson’s disease in this episode featuring Dr. Gizelle Petzinger.

  • The World Health Organization (WHO) recently issued warnings about Omicron, a newly emerged variant of SARS-CoV-2, the virus that causes COVID-19. Omicron is driving a substantial uptick in the number of COVID-19 cases in South Africa and other nations. The first U.S. case was recently detected in a fully-vaccinated person living in California, and several other states are now reporting Omicron cases.

    The WHO has classified Omicron as a variant of concern. To be considered a variant, a virus must have sufficient mutations to change a portion of its genetic code. Variants of concern further exhibit a wide range of characteristics that differ from the parent strain, including changes in transmissibility, disease severity, clinical presentation, immune response, or response to treatments and vaccines.

    Several SARS-CoV-2 variants have been identified, including Delta, a variant of concern that first emerged in India in December 2020 and has at least 13 mutations. Delta is currently the dominant form of the virus in the U.S. By contrast, the Omicron variant has approximately 50 mutations, roughly 30 of which are present in the spike protein, the major surface protein that SARS-CoV-2 uses to enter cells, where it can replicate.

    Scientists do not yet know the consequences of these mutations, which have the potential to increase transmissibility or reduce vaccine effectiveness. Early reports from Israeli health officials suggest that Omicron is highly transmissible but elicits only mild symptoms in fully vaccinated people.

    Although the WHO and governing bodies worldwide have responded quickly to the news of Omicron’s emergence, determining the full extent of the variant’s effects on human health may take several weeks. Public health containment strategies such as being vaccinated, wearing masks, washing hands, and physically distancing remain essential to reducing the spread of COVID-19.

  • Current approved treatment protocols for COVID-19 involve provision of supportive care, such as supplemental oxygen or mechanical ventilation, and administration of remdesivir, an antiviral drug. Results of a recent phase 3 clinical trial demonstrate that REGEN-COV, a combination of the monoclonal antibodies casirivimab and imdevimab, improves outcomes in people who have COVID-19.

    Monoclonal antibodies are proteins that mimic the body’s natural antibodies. They are mass-produced in a laboratory setting and help the body combat harmful pathogens such as viruses. In late 2020, the Food and Drug Administration granted emergency use authorization for REGEN-COV as a post-exposure treatment for patients meeting specific criteria based on robust data from phase 1 and phase 2 clinical trials. REGEN-COV has demonstrated activity against current variants of concern and those of interest, including the alpha, beta, delta, epsilon, gamma, and iota variants.

    The phase 3 trial involved three cohorts of non-hospitalized participants who had tested positive for COVID-19 less than 72 hours prior to entering the trial. Cohort 1 included participants who were 18 years of age or older (average age, 50 years); cohort 2 included participants who were younger than 18 years of age; and cohort 3 included participants who were pregnant. Investigators randomly assigned participants in cohort 1 to receive REGEN-COV at a dose of either 1,200 milligrams (600 milligrams of each antibody), 2,400 milligrams (1200 milligrams of each antibody), or a placebo, delivered via intravenous infusion. The investigators measured antibodies against SARS-CoV-2 in the participants' blood and categorized the participants as antibody-positive, antibody-negative, or other, if the test was inconclusive. They also measured the participants' viral load. Participants tracked their symptoms and reported them using a validated electronic diary.

    Because the trial for cohorts 2 and 3 is ongoing, this report included data for cohort 1 only. The trial demonstrated that 1.3 percent of participants who received the 2,400-milligram dose and 4.6 percent of participants who received a placebo required hospitalization or died; similarly, 1.0 percent of participants who received the 1,200-milligram dose and 3.4 percent of those who received a placebo required hospitalization or died. Participants with a high viral load were more likely to be hospitalized or die than participants with a low viral load. Symptom resolution among participants who received the monoclonal antibody treatment occurred four days earlier than those who received a placebo; similarly, viral load reduction was faster with monoclonal antibody treatment than with the placebo. Serious adverse events were rare and occurred more often among participants who received the placebo.

    These findings suggest that the combined monoclonal antibody treatment REGEN-COV demonstrates efficacy against COVID-19 and exhibits a strong safety profile. Learn more about COVID-19 treatments in this episode featuring Dr. Roger Seheult.

  • Since COVID-19’s emergence in late 2019, the disease has claimed the lives of nearly 5 million people worldwide. Scientists predict that SARS-CoV-2, the virus that causes COVID-19, will likely achieve endemic status in the coming years, so identification of strategies that bolster viral immunity and reduce negative outcomes is essential. Findings from a recent study suggest that optimal blood levels of vitamin D could markedly reduce the risk of death from COVID-19.

    Vitamin D regulates the expression of thousands of genes in the human body via its interaction with specialized cellular proteins called vitamin D receptors. Nearly all cell types involved in the body’s immune response (monocytes/macrophages, T cells, B cells, natural killer cells, and dendritic cells) possess vitamin D receptors. Consequently, vitamin D plays essential roles in the regulation of both innate and adaptive immune systems.

    The Endocrine Society defines optimal blood levels of vitamin D as 40 to 60 nanograms per milliliter (ng/mL). Unfortunately, approximately 40 percent of people living in the United States are vitamin D deficient, based on Endocrine Society standards. Deficiency is associated with poor bone health in adults and children as well as severe outcomes in COVID-19. Certain populations are at greater risk for deficiency, especially older adults, dark-skinned people (such as those of African or Hispanic descent), and people who have obesity, low education, or diabetes.

    The authors of the study analyzed data from one population-based study (which measured long-term vitamin D status in more than 400 million people worldwide) and seven clinical studies (which measured vitamin D levels post-infection). They used a machine learning model to compute the expected death rates among the patients based on characteristics such as the patients' age, sex, median vitamin D levels, and whether they had diabetes. The timeframe for the data collection preceded the advent of vaccines against COVID-19.

    The analysis revealed that people who had optimal vitamin D levels preceding SARS-CoV-2 infection were highly unlikely to die from their illness, suggesting that vitamin D reduces the risk of death from COVID-19. However, these findings were based on observational data, so interpretation of the findings must take into account the higher death rates associated with age and comorbidities (coexisting illnesses). Learn more about the role of vitamin D in COVID-19 in this episode featuring Dr. Roger Seheult.

  • Early data indicated that the Pfizer BioNTech mRNA vaccine demonstrated 90 percent efficacy in preventing infection from the alpha variant of SARS-CoV-2, the virus that causes COVID-19. The vaccine is typically administered in two doses, delivered three to four weeks apart. However, in the setting of vaccine shortages in some areas of the United States, some public health agencies have opted to deliver the vaccines on an extended interval. Findings from a recent study suggest that the vaccine elicits robust humoral immunity even when doses are delivered 16 weeks apart.

    Humoral immunity, also known as antibody-mediated immunity, is an aspect of the immune response to specific antigens. It occurs when foreign material, such as a pathogen, is detected in the body. Lymphocytes are the primary drivers of humoral immunity.

    The authors of the study measured humoral responses to two doses of the Pfizer BioNTech vaccine, delivered 16 weeks apart. The study included 22 people who had never been infected with SARS-CoV-2 and 21 people who had been infected. Among those who had previously been infected, ten participants did not receive a second dose, leaving 11 recipients of two doses. The authors collected blood samples for testing prior to the first dose, three weeks after the first dose, three months after the first dose, and three weeks after the second dose.

    They found that providing a second dose to previously infected people did not significantly improve humoral responses. However, humoral responses in people who had never been infected increased markedly after the delayed second dose, achieving levels comparable to those observed in previously infected people.

    These findings suggest that delaying the second dose of the Pfizer BioNTech vaccine as much as 16 weeks provides robust humoral immunity against SARS-CoV-2 infection. Learn more about COVID-19 vaccines in this episode featuring Dr. Roger Seheult and Dr. Rhonda Patrick.

  • SARS-CoV-2, the virus that causes COVID-19, binds to a receptor on a cellular receptor called angiotensin-converting enzyme 2 (ACE2) to enter the cell and replicate. This process markedly impairs ACE2 receptor function. Findings from a recent study suggest that antibodies for the ACE2 receptor develop after COVID-19 illness, driving long-term complications.

    Most people recover from COVID-19 illness within a few weeks of symptom onset. Some, however, experience long-term complications that last several weeks or months, a phenomenon previously referred to as “long COVID” and now known as “Post-Acute Sequelae after SARS-CoV-2 infection,” or PASC.

    Many of the acute symptoms of COVID-19 arise from overactivation of the body’s immune system following loss of ACE2 function. A key player in this overactivation is the renin-angiotensin-system, an important regulator of blood pressure, inflammation, and body fluid homeostasis. Disturbances in this system in the setting of SARS-CoV-2 infection can drive poor outcomes, such as acute respiratory distress syndrome and death in COVID-19.

    The authors of the study analyzed blood samples for the presence of ACE2 antibodies in 67 people who had a history of previous SARS-CoV-2 infection and 13 people with no history of infection. They also measured ACE2 levels and activity in the participants' blood.

    Whereas 81 percent of the participants with previous infection had antibodies against ACE2, none of the participants who had never been infected had antibodies. Even though ACE2 levels were comparable in both infected and non-infected participants, ACE2 activity was lower among participants with antibodies compared to those without antibodies.

    These findings suggest that following SARS-CoV-2 infection, antibodies against the ACE2 receptor can be detected in the blood. These antibodies, which likely form early in the disease process, impair ACE2 function, providing a potential mechanism for PASC. One limitation of this study is that the blood samples were de-identified, meaning that they carried no identifiers or information about whether the samples were from people who experienced long-term complications of COVID-19.

  • Current vaccines against COVID-19 provide powerful protection against the disease. Some evidence suggests that when people who have been infected with the original strain of SARS-CoV-2 (the virus that causes COVID-19) are vaccinated against the disease, they develop unusually robust immunity, a phenomenon known as “hybrid immunity.” However, a recent report describes findings that suggest many people infected with SARS-CoV-2 do not develop antibodies to the virus.

    The study involved 72 people who had tested positive for COVID-19 but were symptom-free for at least three weeks. The authors of the study tested the participants' blood for the presence of antibodies to the spike protein (the primary infectious particle of the SARS-CoV-2 virus) as well as other viral particles at the time of enrollment and at subsequent follow-up visits. They gathered information regarding the participants' demographics, viral load, and symptom severity.

    Two of the participants (3 percent) reported no symptoms, 13 (18 percent) reported mild symptoms, 48 (67 percent) reported moderate symptoms, and 9 (12 percent) reported severe symptoms. The authors' analysis revealed that 36 percent of the participants failed to develop detectable antibody levels against the SARS-CoV-2 spike protein or other infectious particles. Those who did not develop antibodies were on average 10 years younger and had lower viral loads than those who developed higher antibody levels.

    These findings indicate that the antibody response to SARS-CoV-2 infection is variable and subject to a variety of factors. Vaccines against COVID-19, on the other hand, provide predictable antibody responses. It is important to note that although antibodies are important components of the body’s immune response, cellular immunity plays a critical role, too. Learn more about COVID-19 vaccines in this clip featuring Dr. Roger Seheult.

  • SARS-CoV-2 mRNA vaccines (e.g., Moderna and Pfizer-N-BioTech) are effective in preventing infection and have even greater efficacy in preventing severe COVID-19 illness and hospitalization. However, many people in the United States received their vaccine early in 2021, more than six months before the time of this writing. Whether the protection afforded by vaccination lasts as time passes and more SARS-CoV-2 variants emerge is unclear. Findings of a report published in August provide insights into long-term immunity following vaccination or SARS-CoV-2 infection, concerns about emerging variants, and implications for vaccination boosters.

    During infection with a virus, the innate immune system immediately produces inflammation to fight the infection. Within days or weeks, the adaptive immune system produces antibodies that are specific to the virus. These antibodies bind to a small piece of the viral particle, called an antigen. White blood cells such as macrophages and neutrophils participate in the innate response, while B and T cells facilitate the adaptive response. Plasma B cells are responsible for producing antibodies; however, these cells steadily decrease in number over time. Memory B cells store the genetic information needed to produce virus-specific antibodies upon reinfection. Memory T cells are also responsible for “remembering” viruses in this way. Memory CD4+ T cells rapidly respond to reinfection to support inflammation and antibody production. Memory CD8+ T cells, also called cytotoxic T cells, bind to virus-infected host cells and order them to undergo apoptosis (i.e., programmed cell death).

    The authors of the report analyzed a set of 342 blood samples collected from 61 participants at one, three, and six months following vaccination. This group of participants included SARS-CoV-2 naive individuals (i.e., those who were never infected with the virus) and SARS-CoV-2 recovered individuals. The investigators measured the concentration of circulating antibodies that bind to the SARS-CoV-2 receptor binding domain protein and spike protein. They also measured the concentration of memory B cells and T cells and characterized these cells’ response when challenged with SARS-CoV-2 antigens.

    The concentration of serum antibodies declined over time, but was still detectable at six months post-vaccination. mRNA vaccination produced memory B cells that respond to the receptor binding domain protein of the Alpha, Beta, and Delta variants, called cross-binding memory. These memory B cells had significantly more hypermutation, the process by which B cells rearrange their DNA in order to produce antibodies to new antigens, and increased in concentration between three and six months post-vaccination. Cross-binding B cells were more common in SARS-CoV-2 recovered patients than naive patients. mRNA vaccination also increased memory CD4+ and CD8+ T cells.

    The immune response to mRNA vaccination and infection with the SARS-CoV-2 virus evolves over time, which may have implications for the future use of booster vaccines. These results should be considered with caution as this research has yet to be peer-reviewed.

  • COVID-19 is an acute illness caused by infection with the SARS-CoV-2 virus. Although most people recover from COVID-19 within a few weeks of presenting with symptoms, some experience long-term complications that affect multiple organs, including the heart, lung, kidney, skin, and brain. Findings from a recent study suggest that SARS-CoV-2 infection may promote neurodegenerative disease.

    Neurodegenerative diseases are chronic disorders of the central nervous system that are characterized by chronic progressive loss of neuronal structure and function. They often emerge in mid-to-late adult life and are increasingly common, affecting roughly 37 million people worldwide – a number expected to increase as human lifespan increases. Although scientists don’t fully understand the underlying causes of most neurodegenerative diseases, protein aggregation in the brain is a widely accepted contributing factor. Previous research has shown that the SARS-CoV-2 spike protein binds to heparin (a protein involved in blood clotting) and heparin binding proteins, accelerating the aggregation of proteins involved in neurodegeneration.

    Since many of the biological functions of a protein depend upon its affinity to bind with other proteins, the authors of the study used a web-based algorithm called HDOCK to gauge the binding affinity between the receptor binding domain of the SARS-CoV-2 spike protein between heparin and several aggregation-prone heparin-binding proteins implicated in neurodegenerative diseases, including amyloid-beta, alpha-synuclein, tau, and TAR DNA binding protein.

    They found that SARS-CoV-2 spike protein exhibited differing binding affinities for the various proteins. Heparin showed the highest affinity, with the others exhibiting affinity in decreasing order: prion, amyloid-beta, tau, TAR DNA binding protein, and alpha-synuclein.

    These findings suggest that the heparin-binding site on the spike protein facilitates the subsequent binding to amyloid proteins, potentially leading to neurodegeneration in the brain. Learn more about risk factors that drive Alzheimer’s disease, a type of neurodegenerative disease, in this episode featuring Dr. Dale Bredesen.

  • As the COVID-19 pandemic continues into its second year, a number of variants have emerged, such as the delta variant, which is a highly contagious SARS-CoV-2 variant first identified in India in December 2020. The increase in transmissibility - the ability of a disease to be passed from one individual to another - is due to mutations of the viral spike protein, which allows entry into human cells. Findings of a report released this week show that vaccines that were effective against the original SARS-CoV-2 strain are less effective against the delta variant.

    Viruses are small particles containing genetic material (RNA in the case of SARS-CoV-2) and a lipid capsule with protein structures on the surface. They do not contain the cellular machinery to create new viruses and depend on host cells for replication. Messenger RNA (mRNA) vaccines, such as the Pfizer-BioNTech and Moderna vaccines, work by delivering modified viral RNA encapsulated in a lipid membrane to human cells. These lipid droplets fuse with the lipid membranes of human cells in the respiratory tract and elsewhere and deliver mRNA to the inside of the cell. Once inside the cell, the vaccine mRNA directs the cell to produce more of the modified viral protein. This tricks the immune system into thinking these cells are infected and the body mounts an immune response that ultimately results in the production of antibodies that bind to the SARS-CoV-2 spike protein, preventing subsequent infection.

    Reports published before the emergence of the delta variant demonstrate an efficacy of 95 percent for the Pfizer-BioNTech vaccine and 93 percent for the Moderna vaccine against the original Wuhan Hu-1 strain. Because the delta variant has a modified spike protein, it is unclear if vaccines designed for the original SARS-CoV-2 spike protein will be effective against current and future variants.

    The authors analyzed data from patients of the Mayo Clinical Health System in Minnesota, Wisconsin, Arizona, Florida, and Iowa starting in January 2021, when the original SARS-CoV-2 strain was most prevalent, and ending in July 2021, when the delta variant was most prevalent. The study included more than 25,000 vaccinated participants and 25,000 unvaccinated participants matched for age, sex, race, ethnicity, state of residence, and history of prior SARS-CoV-2 testing.

    The delta variant prevalence in Minnesota increased from less than one percent in May 2021 to over 70 percent in July 2021; whereas the original strain prevalence decreased from 85 percent to 13 over the same period. The researchers found that the Moderna vaccine was between 81 and 91 percent effective and the Pfizer-BioNTech vaccine was between 69 and 81 percent effective against infection with the original SARS-CoV-2 virus prior to May 2021. These vaccines were also highly effective in preventing hospitalization from infection with the original virus with the Moderna vaccine showing 81 to 97 percent efficacy and the Pfizer-BioNTech vaccine showing 73 to 93 percent efficacy. By July, the total effectiveness in preventing infection decreased to 76 percent for the Moderna vaccine and 42 percent for the Pfizer-BioNTech vaccine, indicating a loss of efficacy over time as variants became more common.

    Next, the authors compared vaccine effectiveness across multiple states over the entire study period. In most states, the Moderna vaccine was twice as effective in preventing breakthrough infections than the Pfizer-BioNTech vaccine. This difference in effectiveness against breakthrough infections between the vaccines was highest in July, when the delta variant was most prevalent. This was especially true in Florida, where the risk of breakthrough infection was 60 percent lower after vaccination with the Moderna vaccine compared to the Pfizer-BioNTech vaccine. Across all dates, the Moderna vaccine was twice as effective in preventing COVID-19 associated hospitalization compared to the Pfizer-BioNTech vaccine.

    While both vaccines demonstrate effectiveness in preventing infection and hospitalization, their effectiveness has declined over time as the prevalence of SARS-CoV-2 variants increased. The authors suggested additional studies in large and diverse populations are needed to guide public health policy. This manuscript has yet to be peer-reviewed.

    Previous infection with the original strain of the SARS-CoV-2 along with vaccination creates what is known as “hybrid immunity.” People who have hybrid immunity have a broader and more robust antibody response, as observed in this trial, which is covered in this edition of the Science Digest.

  • The delta variant of SARS-CoV-2, the virus that causes COVID-19, is one of multiple variants to exhibit increased resistance to antibodies as well as higher transmissibility. It is unclear if vaccination or prior infection with the original Wuhan Hu-1 strain is effective against these emerging variants. But now, a new report suggests individuals who have recovered from infection with the original SARS-CoV-2 strain are protected from variants such as delta, especially following vaccination.

    A virus strain is considered the “parent” form of a virus. For example, SARS-CoV-1 and SARS-CoV-2 are strains of the broader SARS-CoV line of viruses. To be considered a variant, a virus must have sufficient mutations to change a portion of its genetic code. In the case of the delta variant, increased transmissibility is the result of genetic changes to the receptor binding domain, a portion of the viral spike protein. This protein enables viruses to enter cells and is the main target of SARS-CoV-2 vaccines. Its genetic change in the delta variant has scientists concerned that individuals who have recovered from the original virus or an early variant may not be protected against later variants with altered spike proteins.

    During infection with a virus, the innate immune system immediately produces inflammation to fight the infection. Within days or weeks, the adaptive immune system produces antibodies that are specific to the virus. These antibodies bind to a small piece of the viral particle, called an antigen. Plasma B cells are the white blood cells responsible for producing antibodies; however, these cells steadily decrease in number over time and do not protect against reinfection with the same virus. Memory B cells store the genetic information needed to produce virus-specific antibodies upon reinfection.

    The authors of the novel report recruited 63 participants between the ages of 26 and 73 years old who were convalescent, meaning they had recovered from SARS-CoV-2 infection. Some participants had received a vaccine (only mRNA vaccines were included) and others had not. The researchers collected blood samples from their participants at about six weeks, six months, and one year following infection in order to characterize their immune responses specifically to the receptor binding domain of the SARS-CoV-2 spike protein. Immunity measures included specificity (the number of antigens to which an antibody will bind), reactivity (the strength to which an antibody binds its antigen), and neutralizing activity (the antibodies' ability to block infection).

    Their analysis revealed that convalescent participants who had not been vaccinated maintained their plasma antibody levels 12 months following infection, providing protection from reinfection. Notably, convalescent participants who had received an mRNA vaccine had 30 times more antibodies and 50 times greater neutralizing activity against the original SARS-CoV-2 strain 12 months following infection than unvaccinated convalescent participants. Neutralizing activity against the alpha, beta, iota, and gamma variants was also ten times greater at 12 months compared to vaccinated individuals who have never had the virus. This means the immune system will react strongly if a vaccinated convalescent individual catches one of the viral variants.

    Antibody-producing B cells evolved over time in both vaccinated and unvaccinated convalescent participants; however, receiving an mRNA vaccine increased receptor binding domain antibodies eightfold. Without vaccination, convalescent participants lost a significant portion of antibodies that were specific for the receptor binding domain of the spike protein at six months post-infection, putting them at greater risk for reinfection. The authors showed that memory B cells continually mutate their antibody structures to increase reactivity and specificity over time, providing stronger immunity against a wider array of strains.

    The authors concluded that immunity in convalescent individuals is long lasting. Vaccination provides additional protection against SARS-CoV-2 variants in convalescent individuals. However, an article covered in this edition of the Science Digest suggests current mRNA vaccines may be less effective against the delta variant in vaccinated people who have never had a SARS-CoV-2 infection.

  • The delta variant of SARS-CoV-2, the virus that causes COVID-19, first emerged in India and has since become a global concern. To be considered a variant, a virus must have sufficient mutations to change a portion of its genetic code. The delta variant carries seven mutations. A recent report describes the effectiveness of the Pfizer-BioNTech and AstraZeneca vaccines against the delta variant.

    The Pfizer-BioNTech vaccine is mRNA-based. It contains the genetic instructions for synthesis of a single viral protein that stimulates the immune system to make antibodies against the SARS-CoV-2 spike protein. mRNA vaccine technology allows rapid scaling of vaccine production and facilitates modification if the virus mutates significantly. The AstraZeneca vaccine is adenoviral vector-based. It uses a modified version of the chimpanzee adenovirus (ChAdOx1) to deliver the genetic information that codes for the SARS CoV-2 spike protein. Adenovirus vector vaccines are currently being tested for numerous infectious agents, ranging from malaria to HIV. Both the Pfizer-BioNTech and AstraZeneca vaccines require two doses for optimal immunity.

    The authors of the report took two approaches to gauge vaccine effectiveness against the delta variant versus the alpha variant (the first SARS-CoV-2 form). First, they compared vaccination status in people who had symptomatic COVID-19 with vaccination status in people who reported symptoms but had a negative test. Next, they estimated the proportion of people with cases caused by the delta variant relative to those caused by the alpha variant, based on vaccination status. Nearly 80,000 people were included in the analysis.

    The authors found that the effectiveness of both vaccines was lower against the delta variant than against the alpha variant, but the Pfizer-BioNTech vaccine was at least 88 percent effective against delta after two doses, and the AstraZeneca vaccine was 67 percent effective after two doses. Notably, both vaccines were only 30 percent effective against the delta variant after only one dose.

    These findings indicate that the Pfizer-BioNTech and AstraZeneca vaccines against COVID-19 are highly effective against the delta variant and underscore the importance of obtaining both doses for optimal immunity. Learn more about COVID-19 vaccines in this clip featuring Dr. Roger Seheult.

  • Vitamin D deficiency in the setting of COVID-19 can lead to over-expression of renin (an enzyme produced in the kidneys) and subsequent activation of the renin-angiotensin-system, a critical regulator of blood pressure, inflammation, and body fluid homeostasis. Disturbances in this system can drive poor outcomes, such as acute respiratory distress syndrome (ARDS) and death in COVID-19. Findings from a recent study suggest that supplementation with calcifediol, an intermediate molecule in the production of the active form of vitamin D, reduces the risk of death due to COVID-19.

    Unlike other vitamins – trace nutrients that must be consumed in the diet – vitamin D is a steroid hormone that is produced in the body. Its synthesis occurs in a stepwise manner that begins in the skin following exposure to ultraviolet light and ends in the kidneys with the production of 1α,25-dihydroxyvitamin D, or 1,25(OH)2D, the active steroid hormone.

    The retrospective cohort study involved 537 patients living in Spain who were hospitalized with COVID-19 during a three-month period in early 2020. Of these patients, 79 received vitamin D treatment providing 532 micrograms (~21,000 IU) of calcifediol on the first day of their hospital stay, and 266 micrograms of calcifediol (~9,300 IU) on days 3, 7, 14, 21, and 28. The primary outcome measure was death during the first 30 days of hospitalization.

    During the study period, 20 percent of patients who did not receive vitamin D treatment died. More of the patients in the untreated group had chronic kidney disease, but fewer had diabetes, cancer, high blood pressure, or other cardiovascular diseases, compared to the treated group. They also had low oxygen saturation levels and were more likely to have elevated inflammatory markers. Twenty-five percent of this group developed ARDS. Only 5 percent of those who received vitamin D treatment died, and only 10 percent of these developed ARDS, even though the patients in this group were more likely to have comorbidities (coexisting health conditions) compared to the untreated group.

    These findings suggest that vitamin D reduces the risk of severe outcomes, including death, in patients with COVID-19. The authors of the study noted that this small study was observational in design, possibly limiting the interpretation of these findings. They also noted that although none of the patients in this cohort were assessed for vitamin D deficiency, most of the people who live in southern Spain tend to be deficient during the time of year when the study was conducted.

  • Nutritional status plays critical roles in fighting infections, influencing not only how well the body’s immune system works but also how pathogens behave in the body. Findings from a new study suggest that omega-3 fatty acids improve clinical outcomes in critically ill patients with COVID-19.

    Omega-3 fatty acids, such as eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and alpha-linoleic acid (ALA) are essential nutrients. They participate in a wide range of physiological functions, including immune responses. Evidence suggests that omega-3 fatty acids stabilize cell membranes, regulate immune function, impair hyper-inflammatory reactions, and reduce severe outcomes associated with infections, such as systemic inflammatory response syndrome and multiple organ dysfunction syndrome.

    The double-blind, randomized clinical trial involved 101 critically ill hospitalized patients (average age, 65 years) diagnosed with COVID-19. Twenty-eight of the patients received 1,000 milligrams of supplemental omega-3 fatty acids via enteral feeding daily for two weeks, commencing 24 hours after admission to the intensive care unit. The supplement provided 400 milligrams of EPA and 200 milligrams of DHA. The remainder of the participants received enteral feeding without supplemental omega-3 fatty acids. The study investigators collected the participants' anthropometric data, medical histories, dietary records, and biochemical measures of respiratory and renal function.

    The one-month survival rate was 21 percent among the patients who received the supplemental omega-3 fatty acids, versus 3 percent among those who did not receive the supplement. The supplemented group also had improved markers of respiratory and renal function, including higher arterial pH, bicarbonate, and urinary output levels and lower blood urea-nitrogen, creatinine, and potassium levels.

    These findings suggest that supplemental omega-3 fatty acids improve respiratory and renal function in critically ill patients with COVID-19. Although the study was sufficiently powered, the sample size was small, necessitating future studies with larger groups.

  • Global vaccination programs have administered more than 218 million COVID-19 vaccine doses across 99 countries, at roughly 6.15 million doses per day. A recent study shows that a single dose of two currently available vaccines reduces COVID-19-related hospitalizations.

    The authors of the prospective cohort study drew on data from the Early Pandemic Evaluation and Enhanced Surveillance of COVID-19 database, a compendium of information that links vaccination, primary care, testing, hospitalization, and death records for 5.4 million people living in Scotland. They conducted a statistical analysis to estimate effectiveness of a single dose of the Pfizer and Oxford-AstraZeneca vaccines against COVID-19-related hospitalization.

    The analysis revealed that a single dose of the Pfizer vaccine reduced the risk of COVID-19-related hospitalization by 85 percent at 28 to 34 days post-vaccination. A single dose of the Oxford-AstraZeneca vaccine reduced risk by 94 percent at the same time frame post-vaccination. The results were similar (81 percent reduced risk) when the authors limited the analysis to vaccine recipients over the age of 80 years.

    These findings suggest that a single dose of two currently available COVID-19 vaccines effectively reduces the risk of hospitalization due to the disease and underscore the importance of expediting vaccinations globally. This study is in pre-print and has not undergone peer-review.

  • The incidence, clinical characteristics, and severity of outcomes of COVID-19 in children differ from those seen in adults. Questions remain regarding whether these differences are due to decreased susceptibility or testing and whether infected children can infect others. Findings from a recent study suggest that children are less likely to develop and spread COVID-19.

    The authors of the study collected data from 637 households in which all members (3,353 total) had been tested for COVID-19 using polymerase chain reaction (PCR), a type of diagnostic test. A subset of 714 household members underwent serological testing for the presence of antibodies to the SARS-CoV-2 virus, the virus that causes COVID-19. They analyzed the data using mathematical modeling.

    The PCR data indicated that nearly half (1,510) of the household members tested positive for COVID-19, but children (defined as 20 years and younger) were half as likely to test positive compared to adults. Interestingly, the serological data revealed that PCR testing under-detected infections in children. The mathematical modeling data indicated that children were 43 percent less likely than adults to be infected with SARS-CoV-2. If infected, they were 63 percent less likely than adults to spread the infection.

    These findings suggest that low susceptibility and under-detection of positive cases in children contribute to the low number of COVID-19 cases in children. The authors of the study posited that their model could have application in other settings, such as nursing homes and schools, to help understand disease transmission and guide public health policy.

  • On December 18, 2020, the Food and Drug Administration granted emergency use authorization for the Moderna mRNA vaccine against SARS-CoV-2, the virus that causes COVID-19. In recent weeks, however, variants of the SARS-CoV-2 virus have emerged, raising questions about the vaccine’s efficacy. A recent report from Moderna summarizes their findings regarding the two variants.

    To be considered a variant, a virus must have sufficient mutations to change a portion of its genetic code. Several variants of the SARS-CoV-2 virus have emerged, but the most notable of these, B.1.1.7, first identified in the United Kingdom, and B.1.351, identified in South Africa, appear to be more virulent than previous variants. The B.1.1.7 variant has 17 mutations, eight of which are located in the spike protein, the major surface protein that the virus uses to gain access into cells. The B.1.351 variant has 10 mutations located in the spike protein.

    The Moderna group tested their vaccine’s capacity to produce neutralizing antibodies against the new variants. They determined that the two-dose vaccine was equally effective against the B.1.1.7 variant in terms of inducing neutralizing antibodies. The level of neutralizing antibodies was sixfold lower against the B.1.351 variant, but this level is still considered sufficient to provide protection against infection. Moderna is investigating whether a third dose (a “booster”) will provide even better immunity against the variants.

    The findings presented in this report have not been subjected to peer-review.

  • COVID-19 primarily manifests as a respiratory illness, but cardiovascular, gastrointestinal, and neurological symptoms have been reported in some cases. Although most of these symptoms are acute and resolve within a few weeks, many people experience long-term complications of the illness, a phenomenon referred to as “post-COVID-19 syndrome. A recent report describes the long-term neurological effects of COVID-19.

    Mounting evidence indicates that COVID-19 affects the neurological system. A previous report found that the range of acute neurological symptoms associated with COVID-19 included psychoses, delirium, encephalitis, strokes, and Guillain-Barré syndrome. Other evidence suggests that COVID-19 affects speech. A case report describes a woman who manifested stuttering and word-finding difficulties during her COVID-19 illness. A recent lay article described the occurrence of stutter several weeks after recovering from COVID-19. Neuroscientists posit that the inflammatory response that accompanies COVID-19 perturbs the brain neurocircuitry that controls speech.

    The most recent study investigating neurological phenomena associated with COVID-19 involved 165 people (average age, 65 years) who had been hospitalized for the illness and had recovered. Six months after discharge from the hospital, the patients were assessed for long-term neurological symptoms.

    The assessments revealed that more than one-third of the patients experienced long-term neurological abnormalities after COVID-19 illness. The most common complaints were fatigue, memory and attention problems, sleep disorders, and muscle pains. Others included depression, anxiety, visual disturbances, impaired sense of smell, and tingling or numbness. The patients who reported having cognitive deficits were more likely to have experienced worse respiratory symptoms and required longer hospitalization than those without cognitive problems.

    These findings suggest that COVID-19 is associated with a wide range of neurological disorders and many of these disorders manifest long after the original infection. The authors noted that since their study excluded patients with pre-existing neurological disorders, their findings might underestimate the full burden of neurological symptoms associated with COVID-19.

  • On March 11, 2020, the World Health Organization declared the global outbreak of SARS-CoV-2 infection, known as COVID-19, a pandemic. A recent report identifies the immunological characteristics of SARS-CoV-2 that will govern its transition from pandemic to endemic status.

    The epidemiological view of endemic disease is one that is continuously, predictably present in the human population. An endemic disease is in a steady state in which the infection does not die out and the number of infected people does not increase exponentially.

    The SARS-CoV-2 virus, the cause of COVID19, is one of seven coronaviruses known to infect humans. Four of these human coronaviruses are globally endemic and elicit mild symptoms, while the remaining two, SARS-CoV (which causes severe acute respiratory syndrome, or SARS) and MERS-CoV (which causes Middle East respiratory syndrome, or MERS), are associated with more severe disease outcomes and death.

    The authors of the report developed an epidemiological model based on key aspects of immunity, all of which centered on reinfection. These aspects included how susceptible a population is to reinfection, whether the disease weakens after reinfection, and how quickly the virus spreads after reinfection.

    The authors' analysis suggested that once SARS-CoV-2 becomes endemic, the disease profile will look considerably different than it does now, affecting primarily children, eliciting mild symptoms, and providing immunity against severe outcomes with future reinfection. In this scenario, vaccination might not be required. However, the current vaccines against SARS-CoV-2 will play a role in how fast the virus becomes endemic, especially if they induce short-lived immunity but reduce the severity of disease upon reinfection. The authors posited that as milder reinfections become more common, reliance on symptoms as a surveillance tool to curb the virus’s spread will become more difficult.

    These findings suggest that in the coming years SARS-CoV-2 infection will become endemic, but until then, public health containment strategies such as wearing masks and social distancing remain essential.

  • Anaphylaxis, sometimes referred to as anaphylactic shock, is a severe, potentially life-threatening reaction to an allergen. It affects the entire body, and its symptoms include skin rash, shortness of breath, nausea, vomiting, and anxiety, among others. A recent report describes the incidence of anaphylactic shock following immunization with the Pfizer-BioNTech coronavirus vaccine.

    The Pfizer-BioNTech vaccine, also known by its generic name tozinameran or its brand name Comirnaty, induces an immune response against SARS-CoV-2, the virus responsible for COVID-19. A clinical trial involving more than 43,000 people demonstrated that the vaccine has an efficacy rate of 95 percent in preventing the disease. The most common reactions to the vaccine were injection site reactions, fatigue, headache, muscle pain, chills, joint pain, and fever.

    The Centers for Disease Control and Prevention (CDC) report that some severe reactions have occurred. As of December 23, 2020, nearly 1.9 million people in the United States had received their first dose of Pfizer-BioNTech vaccine. Of these, 21 experienced anaphylaxis (a rate of 11.1 people per one million doses), including 17 in people with a documented history of allergies or allergic reactions, seven of whom had a history of anaphylaxis. The onset of anaphylactic symptoms in most of the people was 13 minutes (with a range of two to 150 minutes). The CDC reported that of the 20 people for whom follow-up information was available, all had recovered.

    The findings presented in this report suggest that the Pfizer-BioNTech vaccine has an excellent safety profile and is safe for most people. However, the CDC recommends that vaccination locations should take the following precautions: ensure that necessary supplies are available to manage anaphylaxis; screen potential vaccine recipients to identify those who require extra precautions; establish post-vaccine observation periods (15 to 30 minutes, depending on patient history); ensure that healthcare providers can recognize the signs and symptoms of anaphylaxis early; and immediately treat suspected anaphylaxis with epinephrine.

  • Omega-3 fatty acids ameliorate olfactory losses.

    The sellar and parasellar regions of the brain comprise a complex anatomical area located near the pituitary gland. Tumors in these regions often require resection using endoscopic nasal procedures, which are often associated with concomitant olfactory function losses. In some patients these losses persist long after the procedure and are sometimes permanent. Findings from a new study suggest that omega-3 fatty acids ameliorate olfactory losses associated with endoscopic nasal procedures.

    Omega-3 fatty acids are polyunsaturated fats that play essential roles in human health. They influence cell membrane integrity, affect the function of membrane-bound cellular receptors, and participate in a vast array of physiological functions. Omega-3 fatty acids are present in flaxseed, soybeans, canola oil, fish, and other seafood. They are also widely available as dietary supplements.

    The prospective, randomized controlled trial involved 87 patients with sellar or parasellar tumors who were undergoing endoscopic nasal resection. Roughly half of the patients received nasal saline irrigations (standard treatment) or nasal saline irrigations plus 2,000 milligrams of supplemental omega-3 fatty acids daily. The participants underwent a smell test before and at six weeks, three months, and six months after the procedure.

    At the six-week point, 25 percent of the patients in both groups had experienced a clinically significant loss in olfactory function. However, at three and six months post-procedure, the patients who took omega-3 fatty acids had less olfactory loss than patients without supplementation.

    The authors of the study suggested that the improvements they observed in the patients' olfactory function were due to omega-3 fatty acids' neuroprotective effects as well as their capacity to promote synaptic plasticity and neurotransmitter function. Interestingly, many people report olfactory losses with viral infections, including COVID-19. A new clinical trial is investigating whether omega-3 fatty acids can protect and even restore lost sense of smell in patients with COVID-19.

  • The primary cause of death from COVID-19 is acute respiratory distress syndrome (ARDS), a severe form of acute lung injury characterized by rapid breathing, shortness of breath, and a low blood oxygen level. The authors of recent review posit that moderate fever protects against ARDS in COVID-19.

    The body’s fever response is a hallmark of infection and inflammation. An increase in core body temperature of a few degrees (no higher than ~102°F) is generally recognized as safe and improves survival from and resolution of many infections. For example, evidence indicates that people who take medications to reduce fever associated with influenza are 5 percent more likely to die. Conversely, extremely high fever in the setting of systemic inflammation is harmful. Notably, the fever response is diminished in older adults.

    Fundamental to the fever response is a short-term accumulation of heat shock proteins (HSP), a class of proteins that play important roles in providing protection from lung injury. HSPs increase markedly with fever but require a “cool-down” period to maintain their effectiveness. In COVID-19 illness, the increase in HSPs is transient, lasting only about two hours after the onset of fever.

    The authors of the review hypothesized that allowing patients with COVID-19 to experience brief (two hour) periods of fever, followed by administration of medications to reduce fever would maintain the highest levels of protective HSPs. They cautioned that their hypothesis must be tested in large, randomized clinical trials, however.

    The authors also suggested that strategies that promote HSP activation may provide protection against COVID-19. Sauna use, in particular, induces long-term activation of HSPs and is associated with reduced risk of developing certain chronic or acute respiratory illnesses, such as pneumonia. Findings from large epidemiological studies indicate that men who used the sauna four to seven times per week were 41 percent less likely to develop pneumonia than men who used the sauna less often or not at all. Read more about sauna use in our overview article.

  • Coronaviruses comprise a group of related viruses that cause illness in birds and mammals, including humans. While some coronaviruses cause fairly benign illness (such as the common cold), others can cause serious, even life-threatening disease (such as SARS-CoV-2, which causes COVID-19). As the number of COVID-19 cases continues to increase globally, identifying strategies to reduce or prevent its spread is essential. Findings from a recent study indicate that ordinary healthcare products may be useful in reducing viral load of coronaviruses.

    Viral load refers to the quantity of virus particles present in an organism following exposure. With most viruses, higher viral loads are associated with worse outcomes.

    The authors of the study assessed the merits of several healthcare products, including a saline nasal rinse, a 1 percent solution of baby shampoo, peroxide oral rinses, and mouthwashes in reducing viral load. They tested the products against human coronavirus 229e, a human respiratory pathogen with a structure similar to that of SARS-CoV2, by incubating the virus in the presence of the solutions for 30 seconds, one minute, and two minutes at room temperature.

    They found that the baby shampoo solution inactivated more than 99.9 percent of the virus after two minutes. The mouthwashes and oral rinses were similarly effective, with some products inactivating more than 99.9 percent of virus after 30 seconds and some inactivating 99.99 percent of the virus after 30 seconds. They found no benefit from using the saline nasal rinse.

    These findings suggest that ordinary household healthcare products are useful in preventing viral load of a coronavirus similar to SARS-CoV-2. Such products may be beneficial in reducing or preventing transmission of COVID-19.

  • Zinc is an essential nutrient that plays key roles in immune function. Sources of zinc include red meat, poultry, nuts, beans, and seafood. Findings presented at the recent European Society of Clinical Microbiology and Infectious Disease Conference on Coronavirus Disease suggest that zinc provides protection against COVID-19.

    The study involved 249 adults (average age, 63 years) who had been hospitalized in early 2020 for COVID-19-related treatment. The authors of the study analyzed blood samples from the patients to determine their serum zinc levels and inflammatory status, as measured by interleukin-6 (IL-6).

    The analyses revealed that 21 of the patients died from complications associated with COVID-19. The average zinc level among the patients 61 micrograms per deciliter (mcg/dL). (Normal serum zinc concentrations range between 70 and 100 mcg/dL.) Poor zinc status was linked with worse outcomes. Zinc levels among patients who survived averaged 63 mcg/dL, but among those died, levels averaged 43 mcg/dL, suggesting that zinc plays an important role in improving outcomes of COVID-19. Lower zinc levels also correlated with higher levels of IL-6, indicative of systemic inflammation.

    It’s noteworthy that zinc exists as a divalent cation (a positively charged ion) and cannot enter cells without a transporter. Uptake of zinc requires an ionophore, a molecule that can transport ions across a lipid membrane. Quercetin, a bioactive compound present in a variety of fruits and vegetables, especially apples and onions, is a zinc ionophore. Consuming zinc-rich foods along with quercetin-rich foods may boost zinc’s effectiveness. You can read more about quercetin in our overview article.

  • Antibodies defend cells from bacteria and viruses by neutralizing pathogens' biological effects. Antibodies that neutralize SARS-CoV-2, the virus that causes COVID-19, are important tools in treating or even preventing the disease. Researchers have identified a tiny component of an antibody that neutralizes SARS-CoV-2 by blocking its capacity to bind to the angiotensin converting enzyme 2 (ACE2) receptor.

    SARS-CoV-2 exploits the ACE2 receptor to gain entry into cells. A specific region of the virus called a spike protein binds to a cell’s ACE2 receptor, and the virus injects its genetic material – RNA – into the cytosol. Once inside, the virus hijacks the body’s natural replicating processes to promote viral reproduction.

    The researchers identified the component, called Ab8, from a library of 100 billion potential candidates. They conducted in vitro and animal studies to confirm its effectiveness and used electron microscopy to determine how Ab8 worked.

    They found that Ab8 completely neutralized SARS-CoV-2 in vitro and in mice and hamsters. The authors of the study speculated that Ab8’s small size might facilitate its delivery as an inhaled or intradermal drug. These findings demonstrate that Ab8 shows promise as a therapeutic and preventive drug against COVID-19.

  • Several factors increase the risk of death due to COVID-19, including hypertension, obesity, male sex, advanced age, living at a northern latitude, and coagulopathy. Interestingly, poor vitamin D status is associated with all of these factors. Findings from a small, retrospective study revealed that vitamin D deficiency was a common feature among the majority of COVID-19 patients with severe outcomes.

    The study involved COVID-19 patients treated in the intensive care unit (ICU) at a tertiary care academic medical center in the United States. Of 20 COVID-19 patients for whom vitamin D levels were available, 13 were treated in the ICU. Of those, 11 (nearly 85 percent) were vitamin D deficient. All of the ICU patients under the age of 75 were vitamin D deficient.

    The authors of the study noted that COVID-19-related death and vitamin D deficiency are more common among African Americans. They also suggested that vitamin D deficiency contributes to the severity of COVID-19 outcomes via impairment of the immune system and prothrombotic effects.

  • A cytokine storm is an excessive release of pro-inflammatory molecules that occurs during severe COVID-19 and is a common cause of death. A new study suggests that vitamin D could reduce the risk of developing a cytokine storm and decrease COVID-19 mortality.

    Vitamin D is a fat-soluble vitamin that plays essential roles in numerous physiological processes including the regulation of blood pressure, calcium homeostasis, and immune function. Previous work on other coronaviruses demonstrates that vitamin D can counteract a cytokine storm by strengthening the innate immune response and inhibiting the adaptive immune system from over-responding to a viral infection. COVID-19 mortality varies across countries and age groups, with the elderly being particularly susceptible.

    Previous research has suggested a connection between vitamin D deficiency and C-reactive protein (CRP), a protein that increases in the blood in response to inflammation and infection. Furthermore, elevated blood levels of CRP are indicative of severe COVID-19. The current study used large-scale data to investigate whether there is an association between vitamin D deficiency and the severity of COVID-19.

    The authors of the study examined COVID-19 data from patients in ten countries, together with vitamin D and CRP data from previous studies. They estimated that patients with normal vitamin D levels had a 15.6 percent reduced risk of severe COVID-19 compared to patients with severe vitamin D deficiency.

    These findings suggest that vitamin D could suppress the cytokine storm in COVID-19 patients and reduce disease severity. More research is needed to determine if these findings hold true when vitamin D levels are measured directly.

  • Infection with SARS-CoV2, the virus that causes COVID-19, disproportionally affects men more than women in terms of both incidence and severity. Some evidence indicates that men are more than twice as likely to die from COVID-19 than women. Findings from a new study suggest that the testes serve as reservoirs for the virus due to increased expression of the ACE2 receptor.

    The ACE2 receptor is widely distributed among the body’s tissues. SARS-CoV2 exploits ACE2 to gain entry into cells by binding to a cell’s ACE2 receptor and injecting its genetic material into the cytosol, where it can replicate.

    The study involved 68 patients (48 males, 20 females) who had been diagnosed with COVID-19. The patients, who were between the ages of 3 and 57 years, underwent daily testing via oropharyngeal/nasopharyngeal swab to assess their viral load. The testing revealed that females cleared the virus roughly two days earlier than males.

    The authors of the study then examined tissue expression patterns of ACE2 as reported in RNA expression databases. They found that testicular tissue is one of the highest sites of ACE2 expression. Ovarian tissue has very low ACE2 expression. These findings suggest that males have delayed viral clearance of SARS-CoV2 due to high expression of ACE2 receptors in testicular tissue, which serves as a reservoir for the virus.

  • Current options for addressing cardiovascular complications of COVID-19. Although COVID-19 commonly presents as a respiratory infection, the illness targets multiple organ systems, including the cardiovascular system. In one study, patients with cardiac injury accounted for nearly one-fourth of severe cases of COVID-19. A recent article describes the inflammatory aspects of COVID-19, identifies current therapies used in regard to cardiac injury, and suggests guidelines for clinical practice.

    The authors of the article identify three primary drivers of cardiac injury in COVID-19: direct viral infection to cardiac tissues, cytokine storm, and aggravation of preexisting cardiovascular disease. They posited that direct infection of cardiac tissue might be related to increased expression of angiotensin-converting enzymes-2 (ACE2) receptors in the heart. SARS-CoV-2, the virus that causes COVID-19, exploits ACE2 to gain entry into cells. Cytokine storm can occur in COVID-19 when SARS-CoV-2 infection provokes an excessive immune response that, in turn, induces multiple organ dysfunction. COVID-19 infection severely burdens the cardiovascular system, aggravating preexisting cardiovascular morbidities and triggering grave events, such as exacerbation of heart failure or acute coronary syndromes.

    The authors also suggest that targeting inflammation – the underlying cause of the aforementioned drivers of cardiac injury – is critical to preserving cardiac health in COVID-19. They identify various drugs currently in use that target the central pathways associated with inflammation; balance the body’s immune responses; and reduce inflammation.

  • Known complications of COVID-19 illness include acute respiratory failure, pneumonia, and acute kidney failure, among others. Recent findings now indicate that people with COVID-19 are at higher risk of complications associated with thrombotic events.

    Thrombotic events can occur when the procoagulant (clotting) forces and anticoagulant and fibrinolytic forces are disrupted. These events can affect multiple organ systems. Common manifestations of thrombotic dysfunction include deep venous thrombosis (blood clots in the legs) or pulmonary embolism (blood clots in the lungs), or disseminated intravascular coagulation (a systemic, life-threatening blood clotting disorder).

    Reports from two hospitals in France indicate that pulmonary embolism occurred in 23 to 30 percent of critically ill COVID-19 patients – considerably higher than is commonly observed in critically ill patients without COVID-19. A single case report described thrombotic events that affected a patient’s lungs, brain, and kidneys. These findings suggest that early monitoring via imaging tests and treatment with anti-clotting factors is critical for COVID-19 patients.

    Interestingly, omega-3 fatty acids might be useful as prophylactic measures against thrombotic events. Previous research indicates that omega-3 fatty acid intake of 4.7 grams or more per week from either fish or supplements reduced lower venous thromboembolism risk 22 to 26 percent and reduced pulmonary embolism risk 39 to 60 percent.

  • Vitamin D is a fat-soluble vitamin that plays critical roles in several physiological processes, including blood pressure regulation, calcium homeostasis, and immune function. Approximately 70 percent of people living in the United States have low vitamin D levels. Findings of a study presented at a 2016 scientific conference suggested that vitamin D insufficiency is associated with increased risk for developing acute respiratory distress syndrome (ARDS).

    ARDS is a severe form of acute lung injury characterized by rapid breathing, shortness of breath, and a low blood oxygen level and can lead to respiratory failure and death. It commonly occurs with viral illnesses, including influenza and COVID-19.

    The retrospective study, which drew on data collected as part of a multicenter randomized controlled trial, involved 476 patients diagnosed with ARDS. The patients' vitamin D status was assessed upon admission to the hospital. Vitamin D levels less than 20 ng/ml were considered “low.”

    The assessments indicated that approximately 90 percent of the patients had low vitamin D levels, even when the data were adjusted for age and severity of illness. The patients with low vitamin D levels spent an average of six days longer on mechanical ventilation compared to patients with higher levels. These findings suggest that poor vitamin D status contributes to increased risk for developing ARDS and influences disease outcomes associated with ventilator needs.

  • Chloroquine and hydroxychloroquine are antimalarial drugs currently being used under Emergency Use Authorization as treatments for COVID-19. Recently published data from a mouse study suggest that these drugs carry a significant risk of death when either is given in combination with metformin.

    Metformin is a drug commonly used to treat type 2 diabetes. It is the fourth most commonly prescribed medication in the United States, with more than 80 million prescriptions for the drug written yearly.

    Previous research has demonstrated that chloroquine and metformin, when used independently, exert anti-cancer effects. The current study investigated whether the two drugs, when used in combination, would have a synergistic effect against cancer.

    The authors of the study injected mice with saline, chloroquine, hydroxychloroquine, and/or metformin for four weeks. They found that the combination of chloroquine and metformin killed 40 percent of the mice. The combination of hydroxychloroquine and metformin killed 30 to 40 percent of the mice. All the treated mice exhibited high levels of lactate dehydrogenase and creatine kinase – indicators of tissue damage. Some of the mice treated with hydroxychloroquine and metformin exhibited signs of increased autophagy in their hearts, livers, and kidneys.

    These findings suggest that when chloroquine or hydroxychloroquine are given in combination with metformin, they can increase the risk of death in mice. Further clinical trials are needed to determine if these findings translate to humans.

  • People who have cardiovascular diseases such as coronary artery disease, atherosclerosis, or heart failure often have poor outcomes during acute illness. Cardiac injury commonly occurs with COVID-19 illness, exacerbating preexisting cardiovascular disease. A recent editorial summarizes the available data regarding adverse outcomes associated with cardiovascular disease and COVID-19.

    The authors of the editorial describe the findings from two recent studies conducted at a teaching hospital in Wuhan, China. One study compared the outcomes of hospitalized COVID-19 patients who had myocardial damage versus COVID-19 patients without myocardial damage. More than half (51 percent) of those with myocardial damage died while in the hospital, but only 4.5 percent of those without myocardial damage died in the hospital. Another study had similar findings, with higher death rates (59.6 percent) among patients with preexisting cardiovascular disease and elevated troponin (a marker of cardiac injury) compared to those with normal troponin levels (8.9 percent).

    The findings from these two studies suggest that cardiac injury commonly occurs in patients with COVID-19 and markedly increases risk of death among patients with preexisting cardiovascular disease. These patients might require more aggressive care than other patients.

  • At the time of this writing, the worldwide death toll from COVID-19 has exceeded 10,000 people. As spread of the disease escalates, a phase 1 clinical trial of an investigational vaccine using an RNA vaccine has begun in Seattle, Washington.

    Conventional vaccines typically employ antigens – inactivated disease-promoting organisms or proteins produced by a virus or bacterium. Antigens mimic the infectious agent to provoke an immune response and provide immunity from future exposures.

    RNA vaccines, on the other hand, utilize a messenger RNA (mRNA) strand that codes for a disease-specific antigen. The vaccine delivers the mRNA strand to the body’s cells, where the genetic information is used to produce the antigen. Similar to the conventional vaccine-derived antigen, these cell-derived antigens drive an immune response.

    The phase 1 clinical trial involves approximately 45 healthy men and women between the ages of 18 and 55 years. The study participants will be enrolled into one of three cohorts to receive either a 25 microgram (mcg), 100 mcg, or 250 mcg dose, via intramuscular injection in their upper arm. A repeat dose will be given four weeks later. The patients will be monitored via follow-up visits after the vaccinations to gauge the vaccine’s safety and effectiveness.

    The mRNA vaccine used in this trial, known as mRNA-1273, has shown promise in animal studies, but this is the first trial to test it in humans. Enrollment has already begun for the trial. If you live in the Seattle area and would like to participate, read this information.