Category: Covid-19

Glen Nowak, associate dean for research and graduate studies at Grady College, has been appointed to a newly established committee by The National Academies of Sciences, Engineering, and Medicine. The committee is tasked with reviewing the Centers for Disease Control and Prevention's COVID-19 Vaccine Safety Research and Communications. (Photo: Sarah Freeman)

Glen Nowak, professor and associate dean for research and graduate studies at Grady College of Journalism and Mass Communication, has been appointed to a National Academies of Sciences, Engineering, and Medicine (NASEM) committee that will review the Centers for Disease Control and Preventions (CDC) COVID-19 Vaccine Safety Research and Communications .

Over the course of this year and the first half of 2025, this ad hoc NASEM committee of experts will be evaluating the systems, methods, processes, and communication efforts of the CDC Immunization Safety Offices (ISO) regarding the safety of COVID-19 vaccines during the 2020-2023 public health emergency. The CDC used multiple COVID-19 vaccine safety monitoring systems during the public health emergency to assess and ensure vaccine safety and foster public confidence in authorized and licensed vaccines. One of the purposes of the review is to provide recommendations for sustaining, maintaining, and strengthening CDC ISOs current vaccine safety monitoring systems moving forward.

It is an honor to be invited to be a member of this NASEM review committee, said Nowak. As the COVID-19 pandemic showed, vaccines are a major part of preventing and reducing the considerable harm to people and society that new highly infectious viruses can quickly cause. However, we also know achieving high public acceptance and use of new vaccines requires communicating about the safety and effectiveness. I look forward to being involved in this effort to provide recommendations to strengthen vaccine safety communication.

Nowak, who also serves as co-director of the Grady Colleges Center for Risk & Health Communication, brings much health and vaccine-related communication expertise to the committee. Much of his professional experience and academic research has focused on infectious and vaccine-preventable disease communication. Before rejoining the UGA faculty in January 2013, Nowak worked 14 years at the CDC, including six years as Associate Director of Communication for the National Immunization Program and six years as CDC Director of Media Relations. He has also authored or co-authored over 50 peer-reviewed journal articles, many of which involve health and vaccine-related communication. He is one of three Grady College faculty members to serve as co-editors of the book Advancing Crisis Communication Effectiveness: Integrating Public Relations Scholarship with Practice.

Nowak holds a Bachelor of Science degree in economics and communications from the University of Wisconsin-Milwaukee, an M.A. degree in journalism and a Ph.D. in mass communications from the University of Wisconsin-Madison.

Author: Shannon Lorusso, sel67411@uga.edu

Contact: Glen Nowak, gnowak@uga.edu

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Grady College faculty member appointed to national COVID-19 committee - Grady - Grady College

A new study in the Journal of Infectious Diseases uses data from 1,988 SARS-CoV-2positive US Military Health System beneficiaries to define the characteristics and clinical patterns observed in patients with long COVID, or post-COVID condition (PCC), grouping patients into three phenotypes based on clusters of symptoms.

The authors of the study said they wanted to use machine learning to analyze data on clinical symptoms 6 months post-infection to identify new definitions for PCC. The longitudinal study took place from March 2020 through May 2022. Case-participants tested positive for COVID-19 during the study period and completed a survey approximately 1, 3, 6, 9, and 12 months after their first positive test.

At each time point, participants were asked about the duration and severity of their symptoms, the authors said.

"To identify distinct PCC clusters based on differing symptomatology, we utilized a machine learning clustering algorithm of survey responses to identify patterns that differentiated participants based on their reported symptoms," they wrote.

3 symptom clusters identified

In total, the authors said three symptom-based clusters were identified: a sensory cluster (loss of smell and/or taste), a fatigue/difficulty-thinking cluster, and a difficulty-breathing and exercise-intolerance cluster.

"Cluster 1 (Sensory) was characterized by a higher frequency of sensory symptoms such as loss of smell and/or taste, Cluster 2 (Fatigue/Difficulty thinking) was characterized by a higher frequency of fatigue (including mental and physical fatigue) and difficulty thinking (e.g., brain fog), and Cluster 3 (Difficulty breathing/Exercise intolerance) was characterized by a higher frequency of difficulty breathing symptoms (e.g., shortness of breath) and exercise intolerance (e.g., difficulty exercising)," they said.

Of the 1,988 participants included in the study, 60.4% were men, and 69.5% were 18 to 44 years old. Seventy-three percent had no significant comorbidities prior to SARS-CoV-2 infection, and 9.6% were hospitalized due to acute COVID-19 infection.

The authors also found that certain comorbidities were linked to certain PCC symptoms, for example, obesity during COVID-19 infection was linked to difficulty breathing in the PCC period. Everyone in the sensory cluster was treated as an outpatient during COVID infection.

"The sensory cluster was less likely to be vaccinated (15.6%) compared to the fatigue/difficulty thinking (36.2%) cluster and the difficulty breathing /exercise intolerance (39.1%) cluster," the authors said.

This study underscores that PCC is not a single condition but, rather, a multisystemic condition with distinct symptom-based phenotype

In an editorialon the study, researchers from the University of Cambridge write, "This study underscores that PCC is not a single condition but, rather, a multisystemic condition with distinct symptom-based phenotypes that have specific risk factors and perhaps unique early inflammatory profiles."

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New study aims to define long COVID through phenotypes of patients - University of Minnesota Twin Cities

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The union representing Cargill employees at its High River plant was seeking about $20 million in damages

Published Jun 19, 2024 Last updated 23hours ago 4 minute read

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Cargill wont have to pay about $20 million in damages for how it handled the first months of the COVID-19 pandemic and subsequent outbreak which claimed the lives of two employees and one workers father.

The decision ends a four-year-long battle between the major meat producer and its employees union, which came in the wake of the three deaths and 951 COVID-19 cases connected to the meat-processing plants workforce the largest single outbreak recorded during the pandemic.

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The three deaths linked to the outbreak were Hiep Bui, a 67-year-old shop steward; Benito Quesada, a 51-year-old shop steward; and Armando Sallegue, the 71-year-old father of a Cargill employee.

In his June 10 decision, Arbitrator James Casey wrote that the limited and rapidly changing information around the virus during the first months of the pandemic was a factor that weighed heavily on his conclusion Cargill largely met its obligations to ensure the health and safety of its High River employees.

When the pandemic broke, public health authorities determined food processing plants such as Cargills slaughterhouse were critical services and werent required to close. (At the time, Cargills High River plant provided about 30 per cent of Canadas beef and 40 per cent of Albertas supply.)

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But the logistics of safely running a meat-packing plant were challenging: A centre like Cargills requires large numbers of employees working close together on an open production line, making it a high-risk transmission area. On the advice of public health bodies, Casey wrote, Cargill had instituted by late February 2020 a series of safety measures to protect workers against droplet transmission and physical contact the two prevailing ways the scientific community believed COVID-19 was transmitted at the time.

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That approach did not take into account the then-unknown reality COVID-19 could spread through airborne or aerosol transmission, which was established much later in the pandemic, Casey wrote. In April 2020, he noted, Alberta Health Services (AHS) wrote in its Frequently Asked Questions page that COVID-19 was not an airborne illness.

Employers, unions, governments and public health authorities had to make it up as they went along, he wrote.

The plants first case was confirmed on April 6, prompting the United Food and Commercial Workers (UFCW) Local No. 401 representing Cargill employees to call for a temporary two-week closure. Across North America, 30 UFCW employees had already died. At the same time, members of High Rivers Filipino community wrote to the mayor imploring him to convince Cargill to close the plant.

The fear in the community was intense, Casey wrote. Soon after, swaths of employees stopped coming to work while AHS set up a Cargill Task Force to try to control the outbreak, though the public health body believed the risk of transmission at the plant was relatively low. AHS greater concern, Casey wrote, was transmission from employees living together and carpooling.

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On April 22, 2020, two days after the first employee was killed by the virus, Cargill temporarily closed the plant due to low attendance. Two days later, UFCW filed the grievance, claiming Cargill wasnt meeting its obligation to provide a safe work environment.

The plant reopened in early May. On May 12, the union announced the death of a second employee. Little more than a month later on June 19, 2020, AHS determined the Cargill outbreak had resulted in 902 COVID-19 cases the largest in Canada in the first year of the pandemic. More than 1,500 cases were eventually linked to the outbreak, with 951 employees testing positive about half the plants entire workforce.

In its grievance filing for that two-month period, UFCW demanded Cargill pay each employee $10,000 and pay the union $100,000. Because there were about 2,000 employees in the bargaining unit, the union was seeking about $20 million in damages.

The eventual 19-day arbitration saw the union call eight witnesses and Cargill bring six witnesses. It is fair to say, that the parties have left no stone unturned in the intense examination of Cargills actions, Casey wrote.

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The central issues in the arbitration were the state of public health knowledge at the time, and whether Cargills safety measures were effective given the mode of virus transmission.

Casey eventually concluded that Cargill followed advice of public health authorities which was in line with what was known at the time about COVID-19. While the union argued this advice was mistaken and therefore didnt protect employees, Casey wrote that Cargill and health authorities were relying on limited information at the time.

It is not appropriate to second-guess Cargills decision based on current scientific knowledge about COVID-19 and current regulatory advice, he wrote.

Casey noted that Cargill did fail to comply with its obligations to communicate with the Joint Health and Safety Committee to identify hazards and address those hazards, which is a direct contravention of the Occupational Health and Safety Act. While he said awarding damages for this breach wouldnt be appropriate, he added the company failed to comply with its collective agreement in a narrow but important way.

He dismissed the remaining grievances.

Cargill and UFCW Local 401 did not immediately respond to Postmedias request for comment.

Alberta RCMP announced in January 2021 that it was investigating Quesadas death. Mounties confirmed to Postmedia on Wednesday that the file was closed and Quesadas death was deemed non-criminal.

mscace@postmedia.com X: @mattscace67

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Cargill avoids damages for handling of early days of COVID-19 that left two employees dead, 951 with virus - Calgary Herald

A team of scientists has identified previously unrecognized immune responses that explain why some individuals do not contract COVID-19.

The experts utilized single-cell sequencing to investigate immune reactions to SARS-CoV-2 in healthy volunteers as part of the worlds first COVID-19 human challenge study.

The research was led by researchers from Wellcome Sanger Institute, University College London (UCL), Imperial College London, and the Netherlands Cancer Institute.

The study involved 36 volunteers exposed to the virus, with detailed monitoring revealing unique immune responses associated with resisting infection.

This was an incredibly unique opportunity to see what immune responses look like when encountering a new pathogen in adults with no prior history of COVID-19, in a setting where factors such as time of infection and comorbidities could be controlled, said co-first author Rik Lindeboom, a researcher at the Netherlands Cancer Institute.

These findings shed new light on the crucial early events that either allow the virus to take hold or rapidly clear it before symptoms develop, noted study senior author Marko Nikoli, a clinical scientist fellow at UCL.

We now have a much greater understanding of the full range of immune responses, which could provide a basis for developing potential treatments and vaccines that mimic these natural protective responses.

Using single-cell sequencing, the researchers generated a dataset of over 600,000 cells. They discovered immediate virus detection responses, including activation of specialized mucosal immune cells and a reduction in inflammatory white blood cells.

Individuals who cleared the virus immediately showed unique innate immune responses, influenced by high pre-exposure activity of the gene HLA-DQA2. Those who developed sustained infections had a rapid blood immune response but a slower nasal response.

As were building the Human Cell Atlas we can better identify which of our cells are critical for fighting infections and understand why different people respond to coronavirus in varied ways, said Sarah Teichmann, co-founder of the Human Cell Atlas.

Future studies can compare with our reference dataset to understand how a normal immune response to a new pathogen compares to a vaccine-induced immune response.

The study also identified patterns in T cell receptors, offering insights for targeted T cell therapies.

Shobana Balasingam from Wellcome emphasized the value of human challenge models in understanding the bodys response to infectious diseases, highlighting the need for such studies in low-resource settings to develop effective tools and treatments.

This research provides critical insights into immune mechanisms that allow some individuals to avoid COVID-19, offering potential pathways for improved therapeutic strategies and vaccine designs.

By understanding these natural protective responses, scientists can better inform the development of treatments and preventive measures for COVID-19 and other infectious diseases.

COVID-19, caused by the SARS-CoV-2 virus, invades the body through a multi-step process.

Initially, the virus enters the body primarily through the respiratory system, as people inhale droplets containing the virus from an infected persons coughs, sneezes, or speech. The virus can also enter through the eyes, nose, and mouth.

Once inside, the virus targets specific cells in the respiratory tract by using its spike protein to bind to ACE2 receptors on the surface of these cells, which are abundant in areas such as the lungs, heart, kidneys, and intestines.

Upon binding to the ACE2 receptor, the viruss membrane fuses with the host cell membrane, allowing the viral RNA to penetrate the host cell.

Inside the host cell, the viral RNA takes control of the cells machinery, directing it to replicate the viral RNA and produce viral proteins necessary for creating new virus particles. These new viral particles are then assembled within the host cell.

Once assembled, the new viral particles are released from the host cell and proceed to infect neighboring cells, thereby spreading the infection throughout the body.

The bodys immune system responds to this invasion, often leading to inflammation and symptoms associated with COVID-19, such as fever, cough, and difficulty breathing.

In severe cases, this can result in complications like pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure, as the immune systems response can cause significant tissue damage.

The study is published in the journal Nature.

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Some people have unique immune responses that block Covid - Earth.com

Rare types of cancer are showing up in higher numbers since the Covid-19 pandemic. Doctors suspect that the virus itself may be contributing to the higher cancer rates, despite a solid connection not yet being established. The pandemic may have permanently altered the bodies of those infected, making them more susceptible to cancer. Those affected include people who were otherwise previously healthy.

Doctors have identified a marked increase in late-stage rarer cancers in people who had otherwise been healthy. Lung, blood and colon cancer, especially, have been rising in younger people. Specifically, medical experts have observed a rise in new cancer patients, multiple patients with multiple cancers, couples and siblings developing cancer within months of each other and cancer patients relapsing after years of remission.

The trend has been particularly noticeable since the Covid-19 pandemic. "This is an observation that has piqued the researchers' and clinicians' interest, that, is there an association with Covid, especially long Covid and cancer?" Dr. Suraj Saggar, chief of infectious disease at Holy Name Hospital in Teaneck, New Jersey, said to Fox 5 New York.

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Cancer is caused by errors in genetic code within cells. "The human body is made up of trillions of cells in a constant state of growth, repair and death," said The Washington Post. "Most of the time, cells with damaged DNA fix themselves, or simply disappear. Sometimes, they start collecting mistakes in their genetic code and rampage out of control into tumors."

What is more alarming is the prevalence of people suffering from more than one type of cancer. "Having multiple forms of cancer at the same time has also become more prevalent. Cancers typically start in one part of the body and spread," the Post said. "It's rare for discrete cancers to begin in different parts of the body during a short window."

Some scientists posit that the Covid virus itself could be contributing to the higher numbers of cancer diagnoses, especially for those who are suffering from long Covid. "The idea that some viruses can cause or accelerate cancer is hardly new," said the Post. "Scientists have recognized this possibility since the 1960s, and today, researchers estimate 15% to 20% of all cancers worldwide originate from infectious agents such as HPV, Epstein-Barr and hepatitis B."

Because "infection with SARS-CoV-2 occurs in several organs either directly or indirectly, it is expected that cancer stem cells may develop in multiple organs," said a 2023 study published in the journal Biochimie. Lung, colorectal, pancreatic and oral cancer could particularly be exacerbated.

While not officially confirmed, the virus is said to cause full-body inflammation. "Inflammation triggers many genetic changes in a genome that can create a propensity of developing cancer in certain individuals," Dr. Kashyap Patel, CEO of Carolina Blood and Cancer Care Associates, said to News Nation. "We are completely under-investigating this virus," Douglas C. Wallace, a geneticist and evolutionary biologist at the University of Pennsylvania, said to the Post. "The effects of repeatedly getting this throughout our lives is going to be much more significant than people are thinking."

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Covid may have made rare cancers more common - The Week

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Excerpt from:

The relationship between SARS-CoV-2 infection and type 1 diabetes mellitus - Nature.com

Yesterday in Nature Communications a study shows cancer that patients who are up to date on vaccines and have received COVID-19 boosters are more protected against death and serious complications than unvaccinated patients.

Cancer patients were not included in key randomized clinical trials on vaccine efficacy (VE), the authors of the study write, but they are at increased risk of death and serious illness from COVID-19 infections. Those especially at risk include lung cancer patients, those with hematologic cancer, and those undergoing chemotherapy.

The authors said prospective data on immunogenicity following initial vaccination have shown that cancer patients develop protective antibodies against SARS-CoV-2 but in lower rates than the general population.

In the study, Spanish researchers looked at data from clinical registries on 184,744 cancer patients in Catalonia, Spain. Half of the patients (92,372) had received at least the first complete immunization series, and the other half (92,372) had not been vaccinated at the time of the study.

All participants had received a cancer diagnosis from 2015 to 2020. The most common cancers included were breast, prostate, and colorectal.

The proportion who received one, two, and three (booster) doses of COVID-19 vaccines were 87.2%, 84.9%, and 68.2%, respectively, the authors said.

The researchers found that cancer patients had 51.8% (95% confidence interval [CI], 40.3% to 61.1%) and 58.4% (95% CI, 29.3% to 75.5%) protection against COVID-19 hospitalization and COVID-19 death, respectively after full (two-dose) vaccination and 77.9% (95% CI, 69.2% to 84.2%) and 80.2% (95% CI, 63.0% to 89.4%) after a booster dose.

Protection from booster doses was high, hovering around 75%, the authors said, but waned significantly by 120 days post-injection.

"Patients should be encouraged to get vaccinated if not and boosted if they have had only two doses," the authors concluded. "Because of the higher risk of breakthrough infections, hospitalizations, and death compared to healthy individuals, patients with cancer should be prioritized in future additional dose studies and vaccination campaigns."

Patients should be encouraged to get vaccinated if not and boosted if they have had only two doses.

In an ISGlobal press release on the study, co-senior author Otavio Ranzani, MD, PhD, said the results "clearly demonstrate that vaccination against COVID-19 significantly reduces mortality and serious complications among cancer patients, especially those who have received the booster dose."

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Study suggests cancer patients should stay current on COVID-19 boosters - University of Minnesota Twin Cities

This study aimed to investigate the expression of microRNAs in leukaemia patients and their association with CD markers. Our results showed significant differences in the expression of microRNAs between AML patients and individuals in the control group. A strong correlation between microRNAs was observed, indicating that the presence of one microRNA led to increased expression of other microRNAs. Additionally, we found that MicroRNA16, MicroRNA21, and MicroRNA221 expression levels exhibited significant differences between AML patients with a history of COVID-19 infection and individuals without an infection history. Moreover, significant fold changes were observed between microRNA expression levels, and the CD markers among AML patients were positive for COVID-19. Finally, the upregulation of MicroRNA137 in AML patients was identified as a novel diagnostic biomarker that may aid in diagnosing, prognosis, and assessing treatment response for AML patients.

The diagnosis and classification of AML require a meticulous approach, as the World Health Organization (WHO) advised, encompassing a comprehensive blend of clinical history, morphological evaluation, cytogenetic/molecular genetic analysis, and immunophenotyping. Nonetheless, the absence of cytogenetic/molecular analyses in numerous healthcare facilities underscores the utility of cytomorphological evaluation supplemented by immunophenotyping, which proves adequate for expedited diagnosis and classification of AML (de Morais et al., 2022).

MicroRNAs are often deregulated in the cancerous process of body cells, and some of them enhance tumorigenesis and cancer progression by increasing tumour growth, angiogenesis, invasion, and immune evasion. The expression level of microRNAs in cancer can be used to predict patient prognosis and clinical response to treatment26,27. Since most of the microRNAs are intracellular, circulating microRNAs have been found in different body fluids and are identified as new cancer biomarkers. This study showed that the expression of microRNAs in AML patients increased significantly, and their role in the prognosis of AML disease was well established, similar to other studies28,29.

AML patients often have standard karyotypes30. They are a heterogeneous group from the molecular point of view, and these molecular differences are related to the prognosis of the disease. Therefore, it is crucial to identify new molecular markers and validate their promising future in treating the disease31. One of these essential markers is FLT3. It has been determined that it can be introduced as a valuable marker for diagnosing AML. In this study, we showed that the frequency of FLT3 mutation in AML patients was higher than in the control group and functions as an essential marker in the diagnosis and prognosis of AML disease; these results are consistent with the previous studies32,33,34,35. Fluorescence in situ hybridisation (FISH) diagnosis was used to detect chromosomal abnormalities in patients with AML, and based on the results of this study, FISH was able to show chromosomal abnormalities and disorders in patients with sufficient accuracy. Previous studies have investigated that the diagnostic strategies of FISH in diagnosing AML can be used as an efficient and powerful tool compared with other methods36. Additionally, FISH can be used as one of the standard methods for detecting microRNA expression, which was utilised in this study and effectively demonstrated the expression of microRNAs. Other studies have also shown the reliability of FISH as a method for detecting microRNA expression levels, which is consistent with the present studys findings. This technique has consistently proven its effectiveness in accurately assessing and quantifying the expression of microRNAs, confirming the results obtained in this research37,38.

Recent investigations have unveiled a variety of microRNAs that are dysregulated in AML and play roles in disease pathogenesis. Among these miRNAs are hsa-miR-16, hsa-miR-497, and hsa-miR-125, which have been implicated in regulating NRAS gene expression and cellular processes relevant to cancer development and progression (Hussen et al., 2021, Kipkeeva et al., 2022).

The BCR gene is a key player in the pathogenesis of several cancers, including AML. It encodes a protein regulating cell growth, differentiation, and survival. Dysregulation of the BCR gene, often through chromosomal translocations, can lead to the formation of oncogenic fusion proteins that drive leukemogenesis (Boucher et al., 2023). In the context of AML, aberrant expression of microRNAs has been implicated in disease progression. Specifically, miRNAs such as hsa-miR-16, hsa-miR-497, and hsa-miR-125 have been identified as potential regulators of gene expression and cellular processes relevant to cancer development. These miRNAs may target the BCR gene, influencing its expression levels and activity. Dysregulation of hsa-miR-16, hsa-miR-497, and hsa-miR-125 could thus contribute to aberrant BCR signaling and AML pathogenesis (Szczepanek, 2020). Understanding the regulatory interactions between genes and these miRNAs in AML patients is crucial for elucidating the molecular mechanisms underlying the disease and identifying potential therapeutic targets. Targeting the dysregulated expression of these miRNAs or modulating gene activity may represent promising strategies for AML treatment. Further investigation into the functional roles of hsa-miRNAs in gene regulation and AML pathogenesis is needed to validate their potential as therapeutic targets or diagnostic biomarkers.

Here, for the first time, we identified that the changes in the association between some of the microRNAs and CD1a, CD2, and CD11b were the most apparent alterations among AML patients after infection with COVID-19. Some of these findings are aligned with and confirmed by the previous study of a systematic screening of genetic events in AML patients, which shows that the expression of CD markers CD1a, CD2, and CD11b in AML patients is significantly increased39. The present study is also consistent with the analysis of Li et al.40, which shows increased expression of CD markers CD1a, CD2, and CD11b in Mixed-phenotype acute leukaemia (MPAL) patients, and they have revealed that these three CD markers are among the CD markers that have the highest expression and have the most changes.

The present study evaluated the levels of various cytokines in AML using flow cytometry for diagnostic purposes. Flow cytometric immunophenotypic analysis was conducted on all patients. The expression levels of CD99, CD33, CD45, CD13, HLA-DR, CD64, CD11c, and CD117 ranged from 54.58% to 90.56% in all cases. Meanwhile, MPO, CD38, CD36, CD15, CD34, CD11b, and CD2 exhibited expression levels between 24.48% and 45.06%, with the remaining CD markers showing expression levels below 20% in all cases. These findings were consistent with previous studies on AML (Rasheed et al., 2021, Piero et al., 2022). Previous researchers noted that markers such as MPO, CD13, CD33, CD15, and CD117 are specific to myeloid cells, while CD11c, CD64, CD14, and CD36 indicate monocytic lineage. Additionally, markers like CD19, CD22, CD10, CD79a, and CD20 are associated with B-lymphoid cells, while CD1a, CD2, CD3, CD4, CD5, CD7, and CD56 are linked to T-lymphoid/natural killer cells. Moreover, CD34, CD45, CD99, HLA-DR, Terminal deoxynucleotidyl transferase (TdT), and CD38 are commonly used as progenitor markers for diagnosing and classifying AML (Weir and Borowitz, 2001, Peters and Ansari, 2011).

Haematopoiesis is a highly regulated process controlled by complex molecular events that concurrently regulate hematopoietic stem cells commitment, differentiation, proliferation, and apoptosis. Substantial evidence now exists to demonstrate that microRNAs modulate haematopoiesis at the level of proliferation and differentiation and act as regulators of hematopoietic cell activity41. Differential expression of microRNAs in malignant cells compared to normal cells can be justified by their gene placement in cancer-related genomic regions, epigenetic mechanisms, and alterations in their processing mechanisms42,43. It has been established that variable expression of microRNAs plays a crucial role in leukemogenesis, and each cytogenetic alteration in AML is associated with the expression of a specific microRNA9,44. Generally, MicroRNA16 is a tumour suppressor that inhibits cell proliferation and induces apoptosis45. MicroRNA21 regulates immune responses in the body46, while MicroRNA125a, MicroRNA125b, and MicroRNA155 regulate hematopoietic stem cell activity8. MicroRNA192 plays a role in cell cycle arrest47, whereas MicroRNA221 induces cellular apoptosis48 and MicroRNA15a reduces apoptosis49. MicroRNA497 regulates cell proliferation50. In this study, the expression levels of these microRNAs were reported, and it was determined that they significantly impact disease progression. The increased expression levels of these microRNAs in AML patients are consistent with the findings of other studies that have reported higher expression of these microRNAs51,52. However, we presented for the first time the expression levels of microRNA and its correlation with CD markers in AML patients who were COVID-19 positive.

Considering that the expression patterns and levels of microRNAs can be used in disease prognosis and therapeutic responses23, the observed differences in the expression levels of microRNAs between AML patients and healthy individuals in this study are consistent with the results of other studies that have reported significant changes in the expression of microRNAs in various patients28,53. The decreased expression of microRNAs in the presence of CD markers and the concurrent decrease in CD marker expression in the presence of other CD markers align with the findings of studies by Shahrabi et al.11 and Gbarowska et al.54.

In a systematic review by Reyes-Long et al. (2023), they have demonstrated that microRNA expression levels differ between COVID-19 positive and negative patients, and these differences may be associated with the upregulation or downregulation of specific microRNAs55. Additionally, in the study by Shi et al. (2022), differences in microRNA expression among patients are observed56. The present study also found that the expression levels of microRNAs differed between COVID-19 positive and negative patients, and some microRNAs exhibited increased expression. The upregulation of microRNAs may not only be attributed to COVID-19 infection or vice versa but potentially due to the host's immune response to the virus57. Furthermore, considering the distinct expression levels of microRNAs in COVID-19 positive and negative patients, these changes in the expression levels of microRNAs could serve as suitable biomarkers58,59.

Identifying new types of microRNAs can be highly valuable and informative in understanding the mechanisms underlying various diseases, guiding therapeutic interventions, and promoting overall health improvement60,61. In the present study, microRNA 137 was identified as a novel biomarker involved in AML progression. MicroRNA137 plays a vital role in the evolution of the nervous system, the development of schizophrenia, and the maintenance of cellular homeostasis62,63. The present study showed an increased expression of MicroRNA137 in AML patients, while its expression was reduced in individuals who tested positive for COVID-19. However, a study by Wang et al. (2020) aimed to investigate the interaction between TRIM25 and MicroRNA137 and uncover their potential mechanisms in the progression of malignant AML. In that study, it was shown that there was a significant reduction in MicroRNA137 in blood samples of AML patients3. Cellular functional assays confirmed that the loss of MicroRNA137 substantially enhanced the invasion, migration, and proliferation abilities of AML cells. At the same time, overexpression of MicroRNA137 hindered the invasion, migration, and proliferation of AML cells. These findings indicated the tumour-suppressive role of MicroRNA137 in AML. However, further research is necessary due to the novelty of this microRNA. The precise significance and therapeutic target potential of MicroRNA137 may change as more is discovered about the molecular mechanisms behind AML and the involvement of microRNAs. Notably, research on MicroRNA137 and its role in AML is still underway. Targeting MicroRNA137in AML treatment may offer further therapeutic benefits, which will be further explored in subsequent research and clinical trials.

The present study demonstrated an increase in fold changes and microRNA expression in individuals who tested positive for COVID-19, and this increase was observed across all examined microRNAs. These findings are consistent with the results of studies conducted by Donyavi et al.59, Farr et al.64, and Li et al.65. This observation led us to understand that increased correlations for the expressions of genes in the cancer networks associated with decreased correlations for the expressions of genes in the standard networks might serve as valid biomarkers for early diagnosis of tumorigenesis and cancer progression. Finally, the identification of different MicroRNAs, the discovery of their target sequences, and the investigation of their gene expression pattern change in various cancers, including AML, along with their association with different cytogenetic abnormalities in AML patients, can provide a basis for more precise disease investigations, drug design, and the development of novel treatments for various types of cancer, including AML.

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The impact of COVID-19 on microRNA and CD marker expression in AML patients | Scientific Reports - Nature.com

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Recently, scientists found that some people who suffered from COVID-19 had auto-antibodies targeting their own type 1 interferons, which are important immune signaling proteins. Now, researchers conducted an in-depth study on 123 Japanese COVID-19 patients to clarify just how common these auto-antibodies are among severe cases and how they affect the immune system. Their findings could shed light on the role of auto-antibodies in exacerbating COVID-19 severity.

Even though COVID-19 manifests as a mild and short-lived disease in most people, some suffer extremely severe symptoms; in the worst cases, these patients die due to complications such as respiratory failure or thromboembolism. It is well-known that factors such as age and underlying medical conditions like diabetes or immunodeficiencies increase vulnerability to severe COVID-19. However, some patients still experience severe COVID-19 without any apparent reason.

One possible explanation may lie in auto-antibodies, which are antibodies that erroneously target specific proteins produced by ones own body. In normal circumstances, type I interferons (or t1-IFNs) play a crucial role in the bodys defense against viral infections; they interfere with viral replication and help mobilize the immune system. However, auto-antibodies against t1-IFNs can neutralize their activity, compromising the bodys defense mechanisms. While detecting these auto-antibodies was uncommon before COVID-19, there have been multiple reports of severe COVID-19 patients bearing them since the pandemic started. Could auto-antibodies targeting t1-IFNs be more common than previously thought?

To answer this question, a research team, including Lecturer Chiaki Iwamura from Chiba University, Japan, investigated whether and how auto-antibodies targeting t1-IFNs are related to COVID-19 severity by analyzing blood samples from 123 Japanese patients. Their findings were published in Volume 44 of theJournal of Clinical Immunologyon April 22, 2024. This research was co-authored by Dr. Kiyoshi Hirahara and Dr. Koutaro Yokote from Chiba University, as well as Dr. Ami Aoki from Niigata University.

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To shed some light on how auto-antibodies to t1-IFNs affected COVID-19 patients, the researchers then conducted RNA sequencing and B cell receptor analyses. These experiments showed that conventional dendritic cells and canonical monocytes, two types of white blood cells, exhibited attenuated IFN signaling for patients in which auto-antibodies were present. Moreover, B cells (yet another type of immune cell) in these patients had fewer SARS-CoV-2-specific receptors, implying reduced effectiveness in combating an infection.

Overall, these findings highlight the importance of looking at auto-antibodies to t1-IFNs in more detail when facing viral epidemics. People with auto-antibodies to t1-IFNs are more susceptible not only to SARS-CoV-2 but also to common viruses such as influenza and to unknown viruses that may emerge in the future, warns Dr. Iwamura, Thus, we hope to collaborate with companies to develop a system to detect auto-antibodies to t1-IFNs in the blood. Ideally, we would develop a test to examine the presence of these auto-antibodies in regular health checkups so that people will be able to know whether they have them with little burden.

Reference:Aoki A, Iwamura C, Kiuchi M, et al. Suppression of type I interferon signaling in myeloid cells by autoantibodies in severe COVID-19 patients. J Clin Immunol. 2024;44(4):104. doi: 10.1007/s10875-024-01708-7

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here.

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Autoantibodies Contribute to Severe COVID-19 by Impairing Immune Responses - Technology Networks

Maternal distress during COVID-19 linked to reduced neonatal brain volumes | Image Credit: sebra - sebra - stock.adobe.com.

There is a link between maternal psychological distress and regional neonatal brain volumes, according to a recent study published in JAMA Network Open.1

Fetal brain development is impacted by intrauterine stressors, influencing the growth and development of a child. Data has indicated maternal psychological distress as a stressor of early brain development, potentially lowering cognitive scores and increasing negative temperament up to 2 years of age.

Maternal stress has also been linked to other negative birth outcomes.2 One study reported significantly increased composite stress, anxiety, and depression (SAD) scores among women with unpredicted birth complications. Women with these complications also had increased hair cortisol concentration, which is associated with SAD scores.

The prevalence of psychological distress significantly increased during the COVID-19 pandemic, with pregnant women also impacted.1 During this time, fetal brain development was linked to reduced cerebral white matter, hippocampal, and cerebellar volumes, but the enduring effects of these prenatal alterations are unclear.

Investigators conducted a study to evaluate the impact of prenatal maternal mental health with neonatal brain development during the COVID-19 pandemic. Participants included mother-infant dyads undergoing magnetic resonance imaging (MRI) studies.1

Women with multiple gestational pregnancy, documented chromosomal abnormalities, congenital infection, maternal contraindications to MRI, or documented COVID-19 infection were excluded from the analysis. Self-reported data obtained included race, ethnicity, maternal age, and education level.

Maternal distress measures such as the Spielberger State Anxiety Inventory (SSAI), Spielberger Trait Anxiety Inventory (STAI), and Perceived Stress Scale (PSS) were used to determine maternal distress. Psychological distress was determined by an SSAI score over 40, STAI score over 40, or PSS score over 15.

A 3T MR scanner (Discovery MR750; GE Healthcare) and 8-channel high-resolution brain array were used to conduct neonatal MRI studies. The DrawEM (Developing Brain Region Annotation With Expectation-Maximization) tool was used to process volumetric brain measurements.

There were 223 dyads enrolled, with 64 excluded from the final analysis. A median gestational age of 39.6 weeks and median maternal age of 34.5 years were reported.1

Of mothers, 27.7% were Hispanic, Asian, or multiracial, 17% were Black, and 55.3% were White. A college or graduate degree was reported in 81.8% and employment as business professionals in 70.4%.

Maternal age, employment education level, neonatal sex, head circumference, gestational age, and weight at birth did not differ between cohorts. However, the gestational age when receiving a postnatal MRI was higher in the pandemic cohort vs the prepandemic cohort, at 44.9 weeks vs 41.9 weeks, respectively.

The pandemic cohort presented with increased SSAI, STAI, and PSS scores vs the prepandemic cohort. Anxiety, stress, and pooled psychological distress rates were 21.1%, 24.7%, and 28.4%, respectively, in the prepandemic cohort vs 61.8%, 69.1%, and 72.7%, respectively, in the pandemic cohort.1

White matter volume was significantly reduced among neonates born during the pandemic period vs the prepandemic period, with a difference of -0.41 cm3. However, differences were not reported for amygdalar, hippocampal, and cerebellar volumes.

White matter was significantly reduced among infants of mothers with increased psychological distress in both cohorts, with a difference of -0.36 cm3. Additionally, right hippocampal and left amygdalar volumes were reduced by -0.35 cm3 and -0.49 cm3, respectively.

An inverse association was reported for cerebral white matter and left amygdalar volumes with increased maternal psychological distress when adjusting for pandemic effects, at -4.94 cm3 and -0.03 cm3, respectively.

These results indicated a link between maternal psychological distress during the COVID-19 pandemic and decreased volumetric brain growth in offspring. Investigators recommended further studies about the long-term impact on offspring development.1

Reference

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Maternal distress during COVID-19 linked to reduced neonatal brain volumes - Contemporary Obgyn