February 23, 2021
Throughout the pandemic, cases have been reported of children experiencing a hyper-inflammatory response after a COVID-19 infection (1, 2). What was first described as a cluster of intense symptoms, has since come to be known as Multisystem Inflammatory Syndrome in Children (MIS-C).
The pool of data around SARS-CoV-2 infection and MIS-C is still small, and a lack of consistency in clinical presentations of MIS-C make it easy for clinicians to misdiagnose symptoms for other conditions where hyperinflammation is prevalent, like Kawasaki disease, toxic shock syndrome, and macrophage-activation syndrome (MAS). Due to the general ambiguity around MIS-C’s cause and development, as well as its mechanisms for tissue damage, the CDC and WHO have constructed different clinical criteria for the diagnosis of MIS-C (3).
The American Academy of Pediatrics (AAP) recently published the results of an international survey detailing MIS-C cases from April-June 2020. Data was provided from 33 hospitals and included 183 pediatric patients ages 1.2 months to 18 years. In the clinical presentations of MIS-C, all patients presented with a fever (>100.4 F) and over 60% had gastrointestinal symptoms. The second most common symptom was cardiovascular. These findings coincide with previously published reports and classification criteria for MIS-C; other common clinical manifestations include dermatologic/ mucocutaneous symptoms, cardiovascular symptoms, respiratory symptoms, and neurologic symptoms (4). Examples can include rash, swelling of hands and/or feet, change to oral mucosa, pink eye, and swollen lymph nodes. It is unknown why a hyperimmune response occurs, and why autoantibodies against endothelial, gastrointestinal, and immune cells are produced. One study conducted by the Icahn School of Medicine found that MIS-C may share some pathophysiology with autoimmune disease.
114 of the 183 patients included in the AAP survey tested positive for current or recent SARS-CoV-2 infection (3). Patients who did not test positive for COVID but presented symptoms concurrent to MIS-C may have experienced a COVID-19 exposure 2-6 weeks prior to the onset of symptoms (4).
Continued research studying this occurrence will help to shed light on the long-standing damage this hyperimmune response may have on the body. Additionally, as criteria for clinical diagnosis is standardized, children experiencing MIS-C can have more immediate access to tailored therapies and treatment, to mitigate the often severe symptoms that accompany MIS-C.
February 16, 2021
In early February 2021, Janssen Pharmaceutical Companies of Johnson & Johnson requested emergency authorization by the FDA to distribute their COVID-19 vaccine. Come the end of the month, the FDA will be reviewing their request; if approved, the Janssen COVID-19 vaccine could be rolled out across the U.S. as early as the end of March.
According to the press release on their website, this single shot vaccine is “85% effective overall in preventing severe disease, demonstrat[ing] complete protection against COVID-19 related hospitalization and death as of Day 28” (1).
Within the trial, “moderate” COVID was defined as having received a lab-confirmed COVID diagnosis as well as experiencing the following symptoms: pneumonia, DVT (deep vein thrombosis), shortness of breath and/or abnormal oxygen and respiratory rates. “Severe” COVID includes “signs consistent with severe systemic illness, admission to an intensive care unit, respiratory failure, shock, organ failure or death” (1).
No anaphylaxis was observed during the clinical trials, and overall serious adverse events reported were actually higher from placebo groups than those who received the vaccine. While the population size was not released, it was confirmed that immunocompromised participants were in the study (1).
Janssen’s COVID-19 vaccine uses an inactive virus to deliver SARS-CoV-2 proteins to the body. These proteins are recognized as invaders by the body, signaling the production of antibodies as an immune response. This particular vaccine uses an adenovirus (which causes the common cold) as a vector (a device used to deliver genetic material) containing incomplete genetic material of the coronavirus. The genetic makeup cannot replicate; therefore, patients are not at risk for infection of SARS-CoV-2 from inoculation (2).
Rheumatology International recently published a scientific review on the range of SARS-CoV-2 vaccines as they pertain to autoimmune inflammatory diseases. As of January 2021, there has been “no experience of viral-vector based vaccines against infectious agents in patients with [autoimmune inflammatory disorders]” (3). While this may spark initial concern, available data on vector-based vaccines in immunocompromised patients shows that these vaccines are not only well tolerated, but even more, severe adverse events are unlikely to occur (4). At the time of publication, only patients with rheumatic diseases have been included as an autoimmune disease population group in the most recent stage of clinical trials. While “well-known vaccines can provide guidance and partial confidence for the use of the ‘new vaccines,’” including more varied population groups going forward will ensure vaccine efficacy and safety for those living with autoimmune disease (3).
February 11, 2021
The B.1.1.7 coronavirus variant was first identified in the UK this past fall, emerging in Colorado soon thereafter. According to the CDC, there have been upwards of 1,000 cases caused by the B.1.1.7 variant across 34 states as of February 9, 2021. California and Florida, two states that have taken vastly different approaches for containing the novel coronavirus, have both reported the highest numbers of B.1.1.7 cases.
While a preliminary report by the UK government’s NERVT advisory group indicates “there is a realistic possibility that…B.1.1.7 is associated with an increased risk of death,” research has yet to officially state if the B.1.1.7 variant causes more severe COVID symptoms (1). That being said, this variant has the potential to become the dominant strain of SARS-CoV-2, as its mutation is associated with a higher transmission rate than its predecessors. According to preliminary data, the B.1.1.7 variant is doubling in frequency every 9-10 days across the U.S. Moderna and Pfizer have released preliminary data verifying that their vaccines are likely to neutralize the B.1.1.7 variant; however, the efficacy rate may be negatively affected.
For regularly updated information and news on coronavirus mutations and variants, check out this comprehensive tracker created by The New York Times.
February 10, 2021
On February 8, the NIH released a news statement announcing the implementation of a Phase 3 clinical trial for a new combination of antibodies as a therapy treatment for COVID-19.
“Antibodies are infection-fighting proteins naturally made by the immune system… [they] prevent viruses from infecting cells, usually by binding to the surface of the virus” (1). AZD7442 antibodies are the third antibody combination to be studied in patients currently hospitalized for COVID-19, being tested under a “master protocol” which allows investigators to trial multiple antibody combinations at the same time. This means less patients are receiving the placebo while providing a more robust pool of results on the efficacy of antibodies as a therapeutic measure.
AZD7442 antibodies work for a longer period of time once administered in patients infected with COVID, and may also function as a preventative measure against SARS-CoV-2.
February 6, 2021
Recent studies have demonstrated the distinct relationship between the infectious disease COVID-19 and autoimmune disease. The review titled “COVID-19 and Autoimmune Diseases” by Yu Liu, Amr Sawalha, and Qianjin Lu delves into the most recent research on the similarities, which include: dysregulated immune responses, the promise of immunomodulatory drugs to treat both conditions, the detection of certain autoantibodies, and the development of autoimmune diseases after SARS-CoV-2 infection. Investigating the relationship between these diseases is critical in preventing and treating COVID-19, as well as understanding the risks for individuals living with autoimmune disease.
In some individuals, SARS-CoV-2 infection triggers immune system dysregulation with the overproduction and release of pro-inflammatory cytokines and, in effect, damage to one or multiple organ systems. Cytokines are proteins that signal the immune system to fight infection, but in excess they indicate the breakdown of self-tolerance. Similarly, autoimmune disease involves increased levels of pro-inflammatory cytokines, a loss of immune tolerance, and subsequent organ injury. As stated in the review, this parallel story between COVID-19 and autoimmune disease suggests that medications effective in treating autoimmune disease can have a similar impact on COVID-19. In fact, immunomodulatory drugs targeting excess cytokines (such as corticosteroids) are now being used to dampen the immune response in autoimmune disease as well as in severe COVID-19 in cases. While aiding in treatment of the disease, the fact that SARS-CoV-2 triggers immune dysregulation may also “have important implications in the development of vaccine strategies against this virus,” state the authors of the review (1).
Another likeness between autoimmune diseases and COVID-19 is the release of autoantibodies, which are proteins that can target and attack the body’s own immune system and organs (2). Antinuclear antibodies (ANA) and antiphospholipid antibodies (APL) are examples of autoantibodies found in both autoimmune disease and COVID-19 patients. The results of one study “showed that 45% of the [COVID-19] patients were positive for at least one autoantibody and patients with positive autoantibodies tended to have a worse prognosis” (1).
We are also beginning to learn that a loss of immune tolerance from COVID-19 can lead to full-blown autoimmune diseases such as Guillain-Barre syndrome (GBS) and systemic lupus erythematosus (SLE) (1). While more of these post-infection autoimmunity cases are likely to be discovered, researchers are still unsure whether individuals with preexisting autoimmune diseases are at higher risk of SARS-CoV-2 infection in the first place. Studies around the world have returned with conflicting results, and thus no clear consensus on the issue.
As the scale is poised to tip in either direction, the authors of the review urge autoimmune disease patients to continue physical distancing, washing their hands, wearing masks, and sticking to their medical protocols – including any prescribed immunosuppressive drugs – to prevent flare-ups and avoid potential organ damage. While there are still unknowns about COVID-19 and its connection to autoimmune diseases, the evolving clues about their relationship bring us hope in understanding and characterizing COVID-19.
February 3, 2021
While COVID-19 short-term impacts have been identified, the long-term effects of the disease are still widely unknown. Many new studies have shed some light on the potential long-term consequences of COVID-19, focusing on autoimmunity. A recent study from The University of Stanford School of Medicine directly links COVID-19 to autoimmunity and autoantibody development. This suggests that severe cases of COVID-19 can lead to a progression of “symptomatic classifiable autoimmunity in the future” (1). The linking of coronavirus to an increase in autoimmunity indicates significant concerns, especially for those with autoimmune diseases, whose immune systems are already impacted.
Many autoantibodies were found in this study’s COVID-19 patients, but the most common was Immunoglobin G (IgG) autoantibodies. IgG antibodies make up most of our blood’s antibodies, protecting us from infection, meaning that IgG autoantibodies pose potential threats as they could be pathogenic. The study used protein chips to track protein interactions that measure distinct IgG autoantibodies associated with connective tissue disease (CTD), anti-cytokine antibodies (ACA), and anti-viral antibody response.
This study’s findings signify that over 58% of the COVID-19 patients had at least one ACA that targeted interferons (IFN), which are proteins that inhibit virus replication. This emphasizes that the autoantibodies produced by infection from COVID-19 attack the vital proteins needed to protect the immune system. This study also measured autoantibodies levels throughout the patient’s sickness period, distinctly showing that the levels of autoantibodies increased in many patients over time. This is particularly important because it demonstrates that infection from COVID-19 can lead to the development of new autoantibodies.
Throughout this pandemic, many discoveries have been found, including one linking COVID-19 to autoimmunity. Such studies are leading scientists to a better understanding of the COVID-19 virus and the rise to autoimmunity and other diseases.
January 25, 2021
A coronavirus variant (called P.1) that was first detected in Brazil was just confirmed by the Minnesota Department of Health as being the first documented case of the variant in the United States. (1) This variant has been particularly worrying scientists because of the mutations it has that let the virus spread faster and evade the immune system more effectively. This evolution could make it easier for COVID-19 survivors to contract the disease again and could potentially impede the effectiveness of vaccines. (2) While this is a daunting premonition, Marion Pepper, an immunologist at the University of Washington, wants us to remember that “even though everyone is obviously concerned about a virus evolving, your memory B cell responsiveness also evolves over time.” (3)
So, let’s talk about these hero memory B cells – how do they actually help fight our battles? The main function of the memory B cells is to retain and recall an infection (when presented with one that the body has experienced before) and react accordingly by producing corresponding antibodies. This sounds great, but what about when the body is presented with a new virus variant like the P.1 variant? The way these cells keep up with ever-evolving viruses is by randomly generating new antibodies that are similar to ones they’ve created in the past. (3) This essentially gives our immune system an unlimited defense arsenal. For more information on memory B cells, check out this great summary created at Arizona State University.
January 19, 2021
These are truly novel times that we are experiencing, and the scientific community is no different. Interest in messenger RNA (mRNA) continues to grow within the medical community, especially since the developments of breakthrough COVID-19 vaccines. It is important to note that even after 30 years of research, mRNA vaccines have never before been approved for use in any disease, until now (1). However, researchers in Germany recently used mRNA technology to reduce disease activity in mice with Experimental Autoimmune Encephalomyelitis (EAE), a disease similar to multiple sclerosis (2).
mRNA vaccines involve using a small strand of distinct genetic material that carries the instructions for building a specific part of a cell. In the case of COVID-19, the mRNA vaccine contains instructions for building the virus’s “spike” protein. When a person receives the mRNA vaccine for the virus that causes COVID-19, their own cells are able to build the spike protein. This ramps up an immune system response against the virus.
This response is especially important when it comes to battling the virus that causes COVID-19 because the SARS-CoV-2 virus in particular has the ability to dampen the immune system response while it is still replicating. This can lead to infected individuals spreading the virus to others while still asymptomatic. This technique has never been seen before. Virologist Benjamin tenOever of the Icahn School of Medicine at Mount Sinai stated that “it’s something I have never seen in my 20 years of studying viruses” when discussing the virus’ ability to commandeer cells’ genomes (3).
Although it may be quite a while before human clinical trials become a possibility, this research is significant. It shows the potential of mRNA vaccines to treat disease-specific autoimmunity without relying on therapies that suppress immune system function as a whole.
January 12, 2021
As distribution continues, experts are working diligently to uncover everything we need to know about the safety and efficacy of the emerging COVID-19 vaccines. The CDC advises the following: “People with autoimmune conditions may receive an mRNA COVID-19 vaccine. However, they should be aware that no data are currently available on the safety of mRNA COVID-19 vaccines for them. Individuals from this group were eligible for enrollment in clinical trials.” (1)
Despite lingering questions and uncertainties, there is one concern that researchers have been able to adequately address: Do vaccines cause autoimmune diseases? Check out Deplatform Disease’s article outlining what we already know about immunological function, autoimmune disease, and the science of vaccines. (2)
January 7, 2021
Recent developments concerning the COVID-19 virus are leading to an increase in questions and unknowns about it. While various vaccines are being distributed across the globe, recent findings on SARS-CoV-2 variants are worrying many. Some of these variants are known to spread faster and transmit more efficiently than other variants of the virus. Three of the most wide-spread variants are the UK variant (D614G), the Y453F mutation found in minks, and the N501Y cluster spreading in England. The research article “Genetic Variants of SARS-CoV-2—What Do They Mean?” explains that while the specific manifestation of these variants differs, the Y453F brings into question other evolutionary challenges, such as an abundance of a new COVID-19 from other mammals to humans. What makes these coronavirus variants even more worrisome is that they are advanced concerning “viral replication, transmission, and escape immunity,” making them even more difficult to contend with than the original COVID-19 virus (1).
One primary concern is the vaccine effectiveness of these variants. The variants are mostly mutations in the spike protein; therefore, scientists have to consider if the vaccines, which stimulate an immune response to the spike protein, are still effective. Thus far, the major consensus regarding vaccine effectiveness is that since current vaccines target the entire spike protein, they are effective regardless of the few changes in the variant. It is also important to note that while the mutations are considered efficient for the virus, they can make it inefficient in the future. To be certain, the evolution of SARS-CoV-2 must be carefully monitored over time. In addition, regulation of mask mandates and physical distancing guidelines is essential in stopping the spread of COVID-19 and all of its variants.
December 22, 2020
Signs or symptoms that continue or develop after a COVID-19 infection is known as long COVID. A recent study indicated that as many as 1 in 20 people will develop an illness that persists for weeks or months after they’ve had COVID-19. (1) Long COVID symptoms vary greatly from person to person, and in some cases, bear a close resemblance to autoimmune-related diseases like myalgic encephalomyelitis (ME/CFS).
Researchers across the world are working to answer key questions, like who is at risk for long COVID? What is the link between COVID-19 and autoimmune disease? What are the most useful treatments for long COVID? Check out our latest article, “Understanding Long COVID” for a breakdown of this condition and how the experts are working to address it.
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