Virus
Episodes
In this clip, Dr. Eran Elinav explains the new field of bacteriophages and how they could be combined with probiotics to generate personalized therapies.
In this clip, Dr. Roger Seheult describes ivermectin and its possible role against COVID-19.
In this clip, Dr. Roger Seheult clarifies the ambiguity surrounding how physicians report deaths and comorbidities from COVID-19.
-
In this clip, Dr. Eran Elinav explains the new field of bacteriophages and how they could be combined with probiotics to generate personalized therapies.
-
Is Ivermectin treating silent parasitic infections in people with COVID-19 in developing countries ClipIn this clip, Dr. Roger Seheult describes ivermectin and its possible role against COVID-19.
-
In this clip, Dr. Roger Seheult clarifies the ambiguity surrounding how physicians report deaths and comorbidities from COVID-19.
-
In this clip, Dr. Roger Seheult discusses concerns about whether vaccines were rushed or can lead to more harmful forms of the virus.
-
In this clip, Dr. Rhonda Patrick discusses the relationship between vaccines and viral evolution.
-
In this clip, Dr. Roger Seheult describes how treatment modalities differ between the two distinct phases of COVID-19 illness.
-
In this clip, Dr. Roger Seheult discusses the biological plausibility of incorporating heat hydrotherapy into the treatment of COVID-19.
-
Dr. Roger Seheult discusses the roles of vaccines, vitamin D, and heat therapy in the prevention of COVID-19.
-
In this clip, Dr. Rhonda Patrick discusses whether COVID-19 disease causes permanent lung damage.
-
In this clip, Dr. Rhonda Patrick describes the effect of sex hormones on immune function.
-
In this clip, Dr. Rhonda Patrick describes the effect of sex hormones on immune function.
-
In this clip, Dr. Rhonda Patrick discusses how omega-3 fatty acids participate in resolving inflammation during an immune response.
-
In this clip, Dr. Rhonda Patrick discusses the trace element zinc and its role in the immune system.
-
In this clip, Dr. Rhonda Patrick describes how vitamin C is involved in immunity.
-
In this clip, Dr. Rhonda Patrick discusses how vitamin A is involved in mounting an immune response.
-
In this clip, Dr. Rhonda Patrick details the critical role that vitamin D plays in the immune response.
-
In this clip Dr. Rhonda Patrick discusses how deficiencies or insufficiencies in micronutrients might negatively affect immune function.
-
In this clip, Dr. Rhonda Patrick explains how allergens in the environment may shape the immune system during early life.
-
In this clip, Dr. Rhonda Patrick describes how the body's microbiome affects immune function.
-
In this clip, Dr. Rhonda Patrick discusses how a lack of sleep impacts the immune response.
-
In this clip, Dr. Rhonda Patrick discusses how the quantity and quality of antibodies against a virus might lead to negative outcomes.
-
In this clip, Dr. Rhonda Patrick discusses the role that genetics plays in the immune system.
-
In this clip, Dr. Rhonda Patrick discusses the active area of investigation surrounding the immune response to the SARS-CoV-2 virus.
-
In this clip, Dr. Rhonda Patrick discusses the evidence surrounding how long the virus resides in the human body.
-
In this clip, Dr. Rhonda Patrick discusses what cross-immunity is and how it may be relevant for SARS-CoV-2.
-
COVID-19 Vitamin D Nutrition Exercise Microbiome Sleep Vitamin C Omega-3 Inflammation Immune System Virus Micronutrients Vitamin E Vaccine Genetics Testosterone Estrogen Zinc Fiber AutoimmunityCOVID-19 Q&A Part 2: Rhonda Patrick, Ph.D. answers subscriber questions in a multi-part series.
-
COVID-19 Q&A Series Part 1: Rhonda Patrick, Ph.D. addresses subscriber questions in this multi-part series.
Topic Pages
News & Publications
-
Each year, millions of people sustain a traumatic brain injury (TBI), often resulting in serious, long-term consequences. Research indicates that even one head injury is linked to a higher risk of developing dementia, with the risk increasing further after two or more. A recent study found that TBIs can reactivate dormant herpes simplex virus type 1 (HSV-1), driving neuroinflammation and contributing to the development of Alzheimer’s.
Researchers created a three-dimensional model of the human brain. Then, they subjected HSV-1-infected and non-infected brain tissue to multiple blows, emulating TBIs and their ensuing pro-inflammatory effects.
They found that repeated mild blows to HSV-1-infected tissues reactivated the virus, triggering inflammatory processes in the brain and driving the buildup of amyloid-beta and phosphorylated tau—proteins linked to brain damage and memory loss. These harmful effects worsened with additional injuries but didn’t occur in uninfected tissue.
These findings demonstrate that viral reactivation in the brain may contribute to the development of Alzheimer’s. HSV-1 is the virus responsible for causing cold sores and genital herpes. It infects approximately 80% of people by age 60 and is commonly found in the brains of older adults. In people with the APOE4 gene, HSV-1 markedly increases the risk of Alzheimer’s.
-
Most people recover from COVID-19 within a few weeks of symptom onset. However, some 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, characterized by chronic fatigue, brain fog, and other neurocognitive symptoms.
Scientists don’t fully understand what causes PASC, but viral persistence, chronic inflammation, hypercoagulability, and autonomic dysfunction likely play roles. A recent study links these drivers to a single cause: low serotonin levels.
Researchers analyzed the blood of participants enrolled in a long-term study of COVID-19 and PASC. They found that the participants had low serotonin levels post-infection, and those levels predicted whether a person recovered fully or developed PASC.
Then, using a mouse model of COVID-19, they demonstrated that viral inflammation altered genetic pathways regulating serotonin absorption in the gut – the primary source of the body’s serotonin. They also showed that serotonin depletion impairs vagal nerve activity, in turn reducing hippocampal activity and driving neurocognitive dysfunction. Giving the mice a selective serotonin reuptake inhibitor (SSRI, a drug that promotes serotonin uptake in the gut) improved their cognitive function.
These findings suggest that low serotonin levels drive the symptoms associated with PASC and highlight the potential for SSRI treatment following COVID-19 illness. Learn about the symptoms of PASC (“long-haul COVID”) in this clip featuring Dr. Roger Seheult.
-
The unique balance of gut viruses, termed the virome, may hold the secret to centenarians' longevity, new research proposes. healthsciences.ku.dk
The gut virome – the collection of viruses inhabiting the gut – plays a crucial role in shaping the immune system and defending against infections throughout the lifespan. A new study shows that centenarians' viromes differ from those of younger people, potentially contributing to their longevity.
Researchers examined the gut viromes of centenarians and compared them with those of younger people. Then they analyzed the viruses' auxiliary metabolic gene activity. Auxiliary metabolic genes are found in bacteriophages – viruses that infect bacteria. They help viruses manipulate their host cells' metabolism to facilitate viral replication.
They found that the centenarians exhibited more diverse viromes than younger people. In addition, the centenarians' viromes demonstrated increased lytic activity, indicating that their viromes were more active in infecting and destroying bacterial cells. Finally, they found that the centenarians' gut viruses possessed an abundance of auxiliary metabolic genes involved in sulfate metabolism, the byproducts of which promote gut integrity and pathogen resistance.
These findings suggest that centenarians' viromes differ markedly from those of younger people in terms of makeup and activity, potentially contributing to centenarians' healthspan and longevity. Learn more about the role gut microbial populations play in human health in this episode featuring Dr. Eran Elinav.
-
Blocking the body's antiviral immune response holds promise for Alzheimer's disease prevention. medicalxpress.com
The immune system plays important, and sometimes surprising, roles in brain health. A new study in mice found that blocking components of the antiviral immune response may make the brain more resilient to the effects of abnormal tau – potentially preventing Alzheimer’s disease and other forms of dementia.
Tau is a protein found in the brain. Abnormal tau can form aggregates called tau tangles – one of the defining characteristics of Alzheimer’s disease – activating antiviral response pathways and interfering with normal brain function and cognition.
Researchers studied the effects of exposure to abnormal tau on microglia, the brain’s resident immune cells. They found that when microglia were exposed to abnormal tau, the mitochondria became “leaky,” releasing their DNA into the cellular fluid. The immune system inappropriately interpreted the leaked DNA as a viral attack, triggering an immune response that promoted the release of type-I interferon, a cytokine that drives the antiviral immune response. Interrupting the pathways involved in this response restored normal brain function.
These findings suggest that suppressing the inappropriate immune response to abnormal tau exposure could provide a means to prevent or treat the tau-associated pathologies common in Alzheimer’s disease and dementia. Learn about other strategies to reduce the risk of Alzheimer’s disease in this episode featuring Dr. Dale Bredesen.
-
Estradiol enhances anti-viral responses in the genital tract of mice infected with herpes simplex virus type 2. (2016) www.sciencedaily.com
From the article:
“If this pathway can be verified in women, then we have laid the foundation to address a number of important public health issues, particularly whether some hormonal contraceptives may be better than others for women who are at higher risk of acquiring sexually transmitted infections, such as in Sub-Saharan Africa, where both HIV-1 and HSV-2 infection rates are high.”
As part of the study, researchers implanted estradiol-releasing pellets into female mice whose ovaries had been removed. The mice then received two rounds of an HSV-2 vaccine, followed by a high dose of the virus.
The researchers saw that the majority of the mice survived and showed less severe disease symptoms, compared to a control group that was not immunized. Further analysis of the molecular pathways underpinning this defensive mechanism revealed that estradiol primes dendritic cells in the vaginal tract to initiate anti-viral T cell immunity.
More specifically, the researchers reported an increase in anti-viral activity unique to the vaginal tract and not found in any other mucosal lining of the body.
-
Estrogenic compounds reduced flu virus replication in nasal cells from women but not men. (2016) www.sciencedaily.com
From the article:
To examine how estrogen affected the flu virus’s ability to replicate, the research team gathered nasal cells – the cell type that the flu virus primarily infects – from male and female donors. The researchers exposed the cell cultures to the virus, estrogen, the environmental estrogen bisphenol A and selective estrogen receptor modulators (SERM), which are compounds that act like estrogen that are used for hormone therapy.
The researchers found that estrogen, SERM compound raloxifene and bisphenol A reduced flu virus replication in nasal cells from women but not men. They also observed that the estrogens initiated their antiviral effects through estrogen receptor beta. Receptors are protein structures that molecules bind with to induce cells to respond.
According to Klein, “Other studies have shown that estrogens have antiviral properties against HIV, Ebola and hepatitis viruses.”
[…]
“But, premenopausal women on certain kinds of birth control or post-menopausal women on hormone replacement may be better protected during seasonal influenza epidemics,” she says.
-
Infection-induced interleukin-6 secretion in mice increases the risk for schizophrenia- and autism-like behaviors in offspring. (2007) www.sciencedaily.com
From the article:
It has been known for some time that schizophrenia is more common among people born in the winter and spring months, as well as in people born following influenza epidemics. Recent studies suggest that if a woman suffers even one respiratory infection during her second trimester, her offspring’s risk of schizophrenia rises by three to seven times.
[…]
To prove this, they triggered an artificial immune response in pregnant mice–giving them a faux case of the flu. The trigger they used was a snippet of double-stranded RNA called poly(I:C), which fools the immune system into thinking there has been an infection by an RNA virus.
A single, mid-gestation injection of poly(I:C) creates a strong immune response in a pregnant mouse. When her offspring reach adulthood, they display behavioral and tissue abnormalities similar to those seen in schizophrenia in humans.
Though there might be some disagreement over what it means for a mouse to be schizophrenic, these abnormalities are generally marked by inappropriateness of response and difficulty in coping.
[…]
The team tried injecting the pregnant mice with individual cytokines, rather than with poly(I:C). It turned out that after a single dose of a specific cytokine known as interleukin-6 (or IL-6), a mouse would give birth to offspring who, at maturity, exhibited the familiar schizophrenia- and autism-like behaviors.
To confirm the role of IL-6, Steve Smith, the lead researcher, gave fake colds (poly(I:C)) to two groups of pregnant, IL-6-free mice. One group had received anti-IL-6 antibodies which blocked IL-6; the other consisted of so-called IL-6 knockout mice (mice whose genetic makeup prevents them from synthesizing IL-6). In both groups, offspring grew up normal, showing that IL-6 is necessary for the maternal poly(I:C) treatment to alter fetal brain development and subsequent behavior in the offspring.
-
Managing phage therapy to help save lives medicalxpress.com
Genomic analysis reveals important insights regarding bacteriophage therapy for multidrug resistance bacteria.
In recent decades, antimicrobial resistance – the ability of a microorganism to resist the effects of a drug – has emerged as a serious public health concern. Multidrug-resistant Acinetobacter baumannii is a rapidly emerging pathogen in the health care setting, where it causes infections that include sepsis, pneumonia, meningitis, urinary tract infection, and others. A recent study analyzed the genomes of multidrug-resistant Acinetobacter baumannii and the bacteriophages used against it.
Bacteriophages (often referred to simply as “phages”) are viruses that infect bacteria. They are abundant in the human gut and exert disparate effects on human health, as seen in their potential roles in resolving bacterial infections and in the pathogenesis of Parkinson’s disease. Bacteriophages are species-specific and typically only infect a single bacterial species or even specific strains within a species. In 2016, physicians in the United States used bacteriophage therapy to successfully treat a patient with multidrug-resistant Acinetobacter baumannii. During bacteriophage therapy, both the phages and their bacterial hosts replicate and evolve, which can drive resistance to the phages and impair resolution of the infection.
The current study analyzed the genomes of the phages used in the treatment as well as their bacterial target. Their analysis revealed that not only were eight of the nine phages related (minimizing their effectiveness due to redundancy), but phage resistance emerged as early as the second day of treatment, highlighting the importance of genomic analysis of phages prior to treatment.
These findings add to the growing body of evidence to support the use of bacteriophages against drug-resistant microbes. Learn more about bacteriophages in this interview featuring gut microbiome expert Dr. Eran Elinav.
-
A type of virus present in the gut microbiota is associated with better cognitive ability in humans, mice and flies www.sciencedaily.com
Bacteriophages may influence the capacity to learn and remember information.
The gut microbiome plays many roles in human physiology, including aspects of brain and neurological health. Because the overall microbial makeup of the microbiome stabilizes around the age of three years, reconfiguring an unfavorable balance with dietary measures or via fecal microbial transplantation has shown limited success. In recent years, scientists have turned to bacteriophages as a possible means of restoring imbalances. Interestingly, bacteriophages may serve other purposes, as demonstrated in findings from a recent study showing that bacteriophages may influence an animal’s ability to learn and remember information.
Bacteriophages (often referred to simply as “phages”) are viruses that infect bacteria. They are abundant in the human gut and exert disparate effects on human health, as seen in their potential roles in resolving bacterial infections and in the pathogenesis of Parkinson’s disease. Bacteriophages are species-specific and typically only infect a single bacterial species or even specific strains within a species. The dominant bacteriophages in the human gut are those of the Caudovirales and Microviridae families.
The study involved more than 1,000 adult participants enrolled in the Ageing Imagenoma Project, an ongoing study of aging patterns among healthy adults (50 years and older) living in Girona, Italy. Participants completed food questionnaires and underwent a battery of cognitive tests, with special emphasis on executive function, one of the key domains of cognitive function.
Investigators collected fecal samples from the participants and measured the viral species present. Interestingly, participants who consumed higher quantities of dairy products tended to have more Caudovirales bacteriophages in their guts. The researchers transplanted fecal samples from the participants into the guts of mice and performed cognitive tests on the mice. Mice that received fecal transplants from participants with more Caudovirales viruses performed better on the cognitive tests than mice that received transplants with fewer Caudovirales.
Next, they fed fruit flies either ordinary whey powder (a dairy product that contains bacteriophages) or sterilized, virus-free whey powder. Then they duplicated the experiment using isolated bacteriophages. In both scenarios, production of genes in the flies' brains that are associated with memory increased.
These findings suggest that bacteriophages, especially those of the Caudovirales family, influence aspects of cognitive function and underscore the potential for capitalizing on the beneficial roles of viral species in the human gut. Learn more about bacteriophages in this interview featuring gut microbiome expert Dr. Eran Elinav.
-
Not getting enough sleep increases common cold risk. jamanetwork.com
Sleep plays roles in many aspects of human health, including immune function. Not getting enough sleep can drive a chronic inflammatory state, increasing a person’s risk for both acute and chronic diseases. Findings from a 2009 study demonstrate that not getting enough sleep increases a person’s risk for developing a common cold.
The average person experiences two to three colds every year, most of which are caused by rhinoviruses. Working adults in the United States tend to lose nearly nine work hours per cold due to absenteeism and on-the-job productivity losses. Adults caring for a child under the age of 13 years tend to lose at least one hour of work per cold. Together, these productivity losses equate to nearly $25 billion per year.
The study involved 153 healthy men and women between the ages of 21 and 55 years. Over a period of two weeks, participants kept sleep diaries in which they reported how long they slept each night and how rested they felt upon waking. They also reported their “sleep efficiency,” the ratio of the total time spent asleep versus the total amount of time spent in bed. The study investigators then quarantined the participants and exposed them to RV-39, a type of rhinovirus that causes colds. They monitored the participants for five days to see if they developed cold symptoms.
The investigators found that participants that had less than seven hours of sleep (on average) were three times more likely to develop a cold than those that had eight or more hours of sleep. Participants with less than 92 percent sleep efficiency were nearly six times more likely to develop a cold than those with 98 percent or higher sleep efficiency.
These findings suggest that not getting enough sleep or having poor sleep efficiency increases a person’s risk for developing illnesses the common cold. Many people experience difficult falling or staying asleep, increasing their risk for colds and other diseases. Learn how cognitive behavioral therapy benefits people with sleeping problems.
-
Epstein-Barr virus is one of the most common human viruses in the world. It is the primary cause of mononucleosis (often called “mono”) – a highly infectious disease that affects mostly teenagers and young adults. Findings from a recent study suggest that Epstein-Barr infection increases a person’s risk for developing multiple sclerosis.
Multiple sclerosis is an autoimmune disorder characterized by the progressive destruction of myelin – the insulating sheath that surrounds nerves and facilitates neural transmission. The disease affects approximately 3 million people worldwide and is twice as likely to manifest in women than men. Symptoms of multiple sclerosis typically appear between the ages of 20 and 50 years.
The study investigators analyzed blood samples from more than 10 million active duty military personnel, collected during routine health exams over a period of 20 years. From this group, they identified 801 personnel who had been tested for Epstein-Barr virus and later developed multiple sclerosis while on active duty. The investigators looked for the presence of antibodies in the blood samples that signaled past Epstein-Barr infection, as well as a protein called neurofilament light chain, a marker of myelin degeneration.
They found that the average age at which personnel were diagnosed with Epstein-Barr infection was 20 years; multiple sclerosis onset typically occurred approximately ten years later. The risk of developing multiple sclerosis later in life was 32 times higher after having experienced Epstein-Barr infection during young adulthood. Levels of neurofilament light chain were higher among the military personnel who had experienced Epstein-Barr infection.
These findings suggest that Epstein-Barr virus is the causal factor in the development of multiple sclerosis and underscore the need for developing vaccines against the virus. Although there is no cure for multiple sclerosis, evidence suggests that the fasting-mimicking diet may be beneficial in treating the condition. Learn about the fasting-mimicking diet in this episode featuring Dr. Valter Longo.
-
Influenza infection may increase a person's risk for Parkinson's disease. www.the-scientist.com
Parkinson’s disease, a neurodegenerative disorder that affects the central nervous system, is caused by destruction of nerve cells in the part of the brain called the substantia nigra. Symptoms of Parkinson’s disease typically manifest later in life and are characterized by tremors and a shuffling gait. Findings from a new study indicate that influenza infection may increase a person’s risk for Parkinson’s disease.
Bacterial and viral infections typically resolve quickly, but in some cases, they elicit long-term adverse effects on human health. For example, streptococcus bacterial infection, which causes strep throat, increases a person’s risk for rheumatic fever, causing fatigue, joint pain, and a dangerous buildup of fluid around the heart. Similarly, human papilloma virus infection, a generally mild sexually transmitted disease, can increase a person’s risk for certain types of cancer. And a growing body of evidence indicates that infection with SARS-CoV-2, the virus that causes COVID-19, is associated with 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.”
The authors of the current study drew on data from the Danish National Patient Registry, a longitudinal registration of detailed administrative and clinical data used exclusively for research. They analyzed more than 61,000 patient records spanning nearly 40 years (1977 to 2016) to identify people who had been diagnosed with influenza and/or Parkinson’s disease.
They found that more than 10,000 people had been diagnosed with Parkinson’s disease during the study period. Those who were diagnosed with influenza (but not other viral infections) were 73 percent more likely to be diagnosed with Parkinson’s more than ten years later, compared to people who had never had an influenza diagnosis. When the researchers restricted the time frame of when the people were diagnosed with influenza to the peak influenza season (when it was less likely to be a false-positive diagnosis), the association with Parkinson’s disease was even stronger.
These findings suggest that influenza infection increases the risk of developing Parkinson’s disease. The authors of the study posited that the mechanisms that drive this association may be related to inflammatory responses during a viral infection that could promote subsequent neurodegeneration, but they caution that their findings were observational and therefore not causal.
-
T cells may be key to providing long-lasting immunity to SARS-CoV-2. www.sciencedaily.com
Much remains unknown about SARS-CoV-2, the new coronavirus responsible for the on-going COVID-19 pandemic. Two important questions revolve around why some people become severely ill while others experience no symptoms, and the associated implications for long-term immunity. Findings from a recent study suggest that prior exposure to related coronaviruses may affect the production of T cells that affect disease severity and immunity.
SARS-CoV-2 belongs to the Coronaviridae family of RNA viruses. There are six coronaviruses known to infect humans, having effects that range from severe pneumonia (SARS-CoV-1 and MERS-CoV) to the “common cold”.
A healthy person infected with a virus mounts a coordinated immune response involving distinct cell types that work together to neutralize the invading pathogen. The adaptive immune system includes T cells that kill virus-infected cells and display antigens (viral fragments) to B cells, which in turn produce antibodies against the virus. Research demonstrates that T cells persist in the body longer than antibodies. For example, 11 years after recovering from SARS-CoV-1 infection, memory T cells were still present, while antibodies were undetectable two to three years after the disease resolved.
Proteins are highly conserved among related coronaviruses. The current study investigated whether the blood of people who had recovered from SARS-CoV-1 or SARS-CoV-2 contained immune factors that would react to isolated SARS-CoV-2 viral proteins.
The authors of the study identified SARS-CoV-2 virus-specific memory T cells in the blood of people who had recovered from COVID-19. The authors then analyzed the blood of 15 SARS-CoV-1 resolvers, 17 years after infection. They observed that all individuals possessed viral-specific T cells that responded not only to SARS-CoV-1 viral proteins but also to SARS-CoV-2 proteins. These results suggest that T cells provide long-lasting protection and offer some cross-protection between SARS-CoV-1 and SARS-CoV-2. The researchers even detected SARS-CoV-2 specific T cells in 19 out of 37 people unexposed to either SARS-CoV-1 or SARS-CoV-2, suggesting they had encountered a related coronavirus, possibly one responsible for the “common cold”.
These findings suggest that T cells produced against SARS-CoV-2 will provide long-term immunity. This research also supports the idea that prior infection with a related coronavirus affords some immunity against SARS-CoV-2 infection, and might explain the variations observed in infection rates and disease severity.
-
Cancer cells hijack the body's inflammatory response to protect themselves from viruses. www.crick.ac.uk
Oncolytic viruses target and kill cancer cells without harming healthy cells by promoting an immune response against a tumor. However, they only work in a minority of patients. Findings from a new study identify potential mechanisms underlying the varied response to oncolytic virus therapies.
The authors of the cell study investigated the role of cancer-associated fibroblasts, a type of cell involved in the body’s immune and inflammatory responses. They infected cancer cells with herpes simplex virus, the only FDA-approved oncolytic virus, to determine how the fibroblasts mediate the tumor’s response to the virus.
They found that when fibroblasts come in contact with cancer cells, they activate pathways that mediate the expression of proinflammatory cytokines such as interferon beta-1. Interferons are proteins produced by the body’s cells as a defensive response to viruses. The ensuing inflammation prevents the virus from invading and replicating in the cancer cell, undermining the pathogen’s efficacy.
These findings identify potential mechanisms that mediate the body’s response to oncolytic viruses and suggest that targeting the pathways that mediate the expression of proinflammatory cytokines might be useful in future cancer therapies.
-
Critical elements of the body’s immune system are T-cells, a class of lymphocytes that promote an appropriate immune response and actively engage in the destruction of pathogens. Findings from two new studies suggest that people who are infected with SARS-CoV-2, the virus that causes COVID-19, have T-cells that target the virus.
The first of the two studies analyzed blood samples collected 20 to 35 days after the onset of symptoms in 20 non-hospitalized COVID-19 patients who were no longer symptomatic. All of the COVID-19 patients that were tested carried SARS-CoV-2 specific helper T-cells and nearly three-quarters carried natural killer T-cells.
The authors of the study also investigated whether people who haven’t been infected with SARS-CoV-2 might have immunity to the virus by analyzing blood samples from 2015 to 2018, well before the pandemic began. They found that roughly half of the samples had helper T-cells that recognized SARS-CoV-2.
Similar results were found in the second study, which analyzed blood samples from 18 people with COVID-19. Their findings demonstrated that 83 percent of COVID-19 patients carried helper T-cells and 35 percent of uninfected people carried helper T-cells. The authors of both studies suggested that this cross-reactivity likely stems from a previous infection with coronaviruses that cause colds.
These findings suggest that a subset of the population might be better equipped to fight of infection from SARS-CoV-2 due to previous exposure to other coronaviruses.
-
Gut bacteria use flavonoids to prime the body's immune response and protect against influenza. Press release: https://www.sciencedaily.com/releases/2017/08/170803141048.htm
Gut bacteria process bioactive plant-based dietary compounds and, in turn, produce metabolites not synthesized by their human hosts. Many of these metabolites influence human health by regulating physiological processes such as nutritional homeostasis, energy expenditure, and immunity. A 2017 study demonstrated that microbial metabolites produced from flavonoids modulate the body’s response to influenza infection.
Flavonoids are bioactive compounds present in a variety of fruits and vegetables. More than 4,000 flavonoids have been identified in the human diet. When gut bacteria called Clostridium orbiscindens break down flavonoids, they produce a metabolite known as desaminotyrosine (DAT). DAT helps the body produce interferon, a signaling molecule that activates the immune system.
The authors of the rodent study gave mice DAT for seven days and then infected them with influenza. The mice continued to receive DAT for 14 days post-infection. A control group of mice received no DAT.
The mice that received the DAT exhibited lower levels of viral RNA and less epithelial damage and apoptosis in their lungs. They also experienced less weight loss and were less likely to die from their infection than control mice. Interestingly, if mice were given DAT two days post-infection, they had worse outcomes than the mice who received DAT before infection, suggesting that DAT primed the immune system for an appropriate response to an immune challenge.
These findings suggest that dietary compounds can boost immune function and highlight the importance of regular consumption of these protective compounds to prime the immune system.
Press release: https://www.sciencedaily.com/releases/2017/08/170803141048.htm
-
A 2008 article by Dr. Anthony Fauci identifies pneumonia as primary cause of death for 1918 pandemic victims, raising alarm about future pandemics. www.sciencedaily.com
The global influenza pandemic of 1918 was the deadliest in history, claiming the lives of more than 50 million people worldwide. Although the cause of the outbreak has been attributed to infection from the H1N1 virus, a 2008 study co-authored by Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, suggested the primary cause of death among those infected was pneumonia.
Fauci and his colleagues conducted an extensive review of the scientific literature detailing the pathological and bacteriological evidence regarding the pandemic, derived from the findings of more than 8,000 autopsies. Then they examined preserved lung tissue samples from 58 of those autopsies to determine the cause of death.
They found that the death rate followed an age-specific, W-shaped curve, with the highest peaks occurring among infants and elderly people and a slightly lower peak occurring among young adults between the ages of 20 and 40 years old. Examination of the tissue samples revealed that severe acute bacterial pneumonia was present in nearly every case as either the primary pathological feature or coincidental to other features commonly associated with influenza infection, including serious injury to the tissues of the respiratory tract.
The primary pathogens identified in the samples were pneumococci, streptococci, and staphylococci – bacteria that commonly reside in the throat and upper respiratory tract and typically pose no harm. However, the injurious tissue changes that accompanied the primary viral infection created an environment conducive to secondary bacterial infection and subsequent pneumonia. Also present in the samples were Bacillus influenzae, bacteria that often facilitate the infiltration of other pneumonia-causing bacteria.
Taken together, these findings suggest that pandemic preparedness should include the stockpiling of antibiotics and bacterial vaccines.
-
SARS-CoV-2 replicates in the throat, making it more contagious than other coronaviruses. www.eurekalert.org
COVID-19 is highly contagious, spreading rapidly from person to person, primarily through respiratory droplets produced when an infected person coughs or sneezes. A recent study indicates that SARS-CoV-2, the virus responsible for COVID-19, replicates in the throat, increasing its transmissibility.
The authors of the study followed nine patients who presented with symptoms of COVID-19. They collected nose and throat swabs and sputum samples from the patients to test for the presence of SARS-CoV-2 throughout the course of their illness and up to four weeks after the onset of symptoms. They found that the swabs and sputum samples showed high levels of infectious viral particles – an indication that, unlike related coronaviruses, SARS-CoV-2 didn’t need to travel to the lungs to replicate. Instead, it rapidly replicated in the throat in the early days of infection, producing a high viral load. These findings suggest that people with SARS-CoV-2 infection can transmit the virus before they are aware that they are infected.
The authors noted that sputum samples with fewer than 100,000 copies of viral RNA didn’t contain any infectious viral particles, suggesting that patients who achieve this benchmark by day 10 of their illness can be discharged to isolation at home. This is critical information for overburdened hospitals and healthcare providers trying to determine when to discharge patients.
-
An open-label pilot trial found that the antimalarial drug hydroxychloroquine may be useful in the treatment of COVID-19. mediterranee-infection.com
A number of randomized controlled trials are currently underway investigating various antiviral therapies for the treatment of COVID-19. Findings from a very small open-label study recently published in the Journal of Antimicrobial Agents found that hydroxychloroquine decreased viral nasopharyngeal levels of SARS-CoV-2 virus in COVID-19 patients in only three to six days in most patients.
Hydroxychloroquine is a common antimalarial drug that is also used to treat rheumatoid arthritis and lupus. In 2017, it was the 128th most prescribed medication in the United States with more than five million prescriptions. It is relatively safe with a few side effects. This Wikipedia article provides an overview of hydroxychloroquine.
In vitro studies in 2004 and 2005 showed that hydroxychloroquine is a potent inhibitor of SARS-CoV, the virus that causes severe acute respiratory syndrome, or SARS. A later study found that hydroxychloroquine improved survival rates in newborn mice infected with a related coronavirus.
The current study involved 32 confirmed COVID-19 patients who were administered 600 milligrams of hydroxychloroquine daily for six days. Some patients also received the antibiotic azithromycin. Nasopharyngeal samples taken on day six of treatment indicated that 70 percent of the hydroxychloroquine-treated patients had cleared the virus compared with 12.5 percent in the group receiving standard of care. All of the patients who received both the antibiotic azithromycin and the hydroxychloroquine cleared the virus from nasopharyngeal samples.
Azithromycin is an antibiotic that has been shown to have antiviral activity against some viruses like Ebola in animal studies. The safety profile of taking both hydroxychloroquine and azithromycin needs to be determined.
In addition, randomized-controlled trials need to confirm whether these therapeutics are effective for the treatment of COVID-19. Large randomized-controlled trials are underway in China and the US. You can read more about those trials here.
-
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.
-
More than 10 percent of people with COVID-19 are infected by someone who has the SARS-CoV-2 virus but is asymptomatic. www.eurekalert.org
A critical factor in containing SARS-CoV-2, the virus that causes COVID-19, is understanding how quickly the virus spreads. Findings from a new study indicate that the SARS-CoV-2 spreads quickly due to its short serial interval, often before carriers are symptomatic.
Serial interval refers to the amount of time between when a primary case (someone who is infected) develops symptoms and when a secondary case (the person they infect) develops symptoms. Some diseases, such as Ebola virus disease, have long serial intervals so containment is relatively easy despite the virulence of the virus. Other diseases, such as influenza, have short serial intervals, which contributes to their spread.
The authors of the study reviewed 468 COVID-19 reports of disease transmission that occurred during a three-week period in mainland China, outside of Hubei Province. Each report provided information about when symptoms first appeared in both the primary and secondary cases, as well as where the transmission likely occurred.
They found that the average serial interval for SARS-CoV-2 was approximately four days and more than 12 percent of disease transmissions occurred when the primary case was asymptomatic. These findings point to the importance of limiting exposure to the virus and can inform policymakers on which interventions might be more useful.
-
Potential targets for immune responses to novel coronavirus have been identified, a crucial step in vaccine development. www.eurekalert.org
Coronaviruses, a genus of the Coronaviridae family, are enveloped viruses with a large positive-strand RNA genome. The recently identified SARS-CoV-2, the cause of the disease known as COVID19, is one of seven coronaviruses known to infect humans. Others include SARS-CoV (which causes severe acute respiratory syndrome, or SARS) and MERS-CoV (which causes Middle East respiratory syndrome, or MERS). A team of scientists recently identified several epitopes in the SARS-CoV-2 virus, a crucial step in vaccine development strategies.
Epitopes are regions on viral proteins that immune cells bind to drive a targeted immune response. Most epitopes are approximately five or six amino acids in length. A typical full-length viral protein sequence may contain many different epitopes to which antibodies can bind.
The authors of the study drew on data from the Immune Epitope Database as well as Virus Pathogen Resource, a compilation of information about known pathogenic viruses. The team compiled known epitopes from other coronaviruses, mapped the corresponding regions to SARS-CoV-2, and used the information to predict likely epitopes.
They identified several specific regions in SARS-CoV-2 that have high homology to the SARS virus, indicating that SARS-CoV is the closest related virus to SARS-CoV-2. Specifically targeting these epitopes may generate immunity to related coronaviruses and promote resistance to viral evolution.
-
Exposure to influenza viruses during childhood may provide partial lifelong protection against distantly related influenza. www.eurekalert.org
Early life environmental exposures play key roles in our ability to launch an effective immune response due to a phenomenon referred to as “immunological imprinting” – the process by which the immune system fights infections after previous exposure to a pathogen. A commonly held theory was that previous exposure to an influenza virus conferred no immunological protection against subsequent exposure. However, new data suggest that immunological imprinting due to exposure to subtypes of influenza viruses during childhood may provide partial lifelong protection against other subtypes.
Influenza is a highly contagious respiratory infection caused by the influenza virus. Complications from influenza sicken or kill hundreds of thousands of people worldwide each year. Although children and elderly people are typically among the most vulnerable to influenza infection, some subtypes of influenza disproportionately affect young, healthy adults.
The authors of the study analyzed large surveillance data sets from the Arizona Department of Health Services, spanning 22 years of influenza seasons. The Centers for Disease Prevention and Control define “influenza season” as occurring between epidemiological week 40 (usually early October) of one year and week 39 of the subsequent year.
Their analysis revealed that immunological imprinting shapes a person’s seasonal influenza risk and emphasized that childhood exposures can imprint a lifelong immunological bias toward particular influenza subtypes. However, newer antibody responses acquired later in life did not provide the same strength of protection as responses imprinted in childhood following the first exposure. The authors of the study postulated that the low mortality rates associated with some influenza subtypes may increase as cohorts of exposed people age.
Link to study: https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008109
-
Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease www.frontiersin.org
Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer’s disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD. Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia—are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD. It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.
-
Summary Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive evidence has not been presented. Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also difficult to resolve. We constructed multiscale networks of the late-onset AD-associated virome, integrating genomic, transcriptomic, proteomic, and histopathological data across four brain regions from human post-mortem tissue. We observed increased human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) from subjects with AD compared with controls. These results were replicated in two additional, independent and geographically dispersed cohorts. We observed regulatory relationships linking viral abundance and modulators of APP metabolism, including induction of APBB2, APPBP2, BIN1, BACE1, CLU, PICALM, and PSEN1 by HHV-6A. This study elucidates networks linking molecular, clinical, and neuropathological features with viral activity and is consistent with viral activity constituting a general feature of AD.
-
Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection www.sciencedirect.com
Summary
Amyloid-β peptide (Aβ) fibrilization and deposition as β-amyloid are hallmarks of Alzheimer’s disease (AD) pathology. We recently reported Aβ is an innate immune protein that protects against fungal and bacterial infections. Fibrilization pathways mediate Aβ antimicrobial activities. Thus, infection can seed and dramatically accelerate β-amyloid deposition. Here, we show Aβ oligomers bind herpesvirus surface glycoproteins, accelerating β-amyloid deposition and leading to protective viral entrapment activity in 5XFAD mouse and 3D human neural cell culture infection models against neurotropic herpes simplex virus 1 (HSV1) and human herpesvirus 6A and B. Herpesviridae are linked to AD, but it has been unclear how viruses may induce β-amyloidosis in brain. These data support the notion that Aβ might play a protective role in CNS innate immunity, and suggest an AD etiological mechanism in which herpesviridae infection may directly promote Aβ amyloidosis.