NeonPunk posted:

It has been awful busy for me this month but I'm sure everyone already saw that study showing that Covid antibodies causes ADE for dengue.

Gunshow Poophole posted:

sorry what? actually have not seen this

Zugzwang posted:

Cross-reactive antibodies != ADE

Given how many people have dengue antibodies in the world, and how many of them have gotten Covid, we'd probably have noticed ADE at this point.

NeonPunk posted:

(..)
Link to the study proper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9420930/

https://www.biorxiv.org/content/10.1101/2023.10.09.557914v1 posted:

Abstract
Dengue disease is highly prevalent in tropical and subtropical regions worldwide. However, its pathogenesis is still incompletely understood, particularly in comparison to other endemic viruses. Antibody-dependent enhancement (ADE) is a well-known phenomenon for dengue viruses. Given the recent surge in dengue cases and potential cross-reactivity with SARS-CoV-2 antibodies, this study explores the impact of anti-SARS-CoV-2 antibodies on DENV-2 infection.

The study assessed the cross-reactivity of SARS-CoV-2 antibodies with the DENV-2 Virus. Human convalescent plasma samples collected during different waves of COVID-19 and monoclonal and polyclonal antibodies raised against SARS-CoV-2 were examined for their potential to cause ADE of DENV-2 infection using cell-based assays. The study found that anti-SARS-CoV-2 antibodies acquired from natural infection in humans or through experimental immunization in animals were cross-reactive with DENV-2 and had the potential to enhance DENV-2 infection in K562 and U937 cells. In-silico and in-vitro studies indicated a strong interaction between SARS-CoV-2 antibodies and DENV-2 E-protein, providing a molecular basis for these findings. This study is the first to demonstrate that anti-SARS-CoV-2 antibodies can cross-react with DENV-2 and can enhance its infection through ADE. These findings have implications for SARS-CoV-2 vaccine development and deployment strategies in regions where dengue is endemic.

Summary Antibodies against SARS-CoV-2 (RBD and Spike) showed significant cross reactivity with DENV-2 (E protein). Also, anti-SARS-CoV-2-commercial antibodies, immunised animal sera and 46 human convalescent plasma samples (from different waves of pandemic) demonstrated antibody-dependent enhancement (ADE) of DENV-2 infection.

Platystemon posted:

WrasslorMonkey posted:

Do not maliciously bypass my PFC filter

Snowglobe of Doom posted:

I mentioned a while back that flesh-eating buruli bacteria ulcers were endemic here in Melbourne Australia and the numbers were increasing every year. In the last 12 months we've had 378 confirmed cases, with 40 cases in my local area

The good news: they're considering a vaccination program which will hopefully turn things around

The bad new: it's an oral bait BCG vaccine program for possums (which are suspected to be the zoonotic reservoir that acts as the vector between mosquitoes and humans) which is only at the proposal stage and they haven't even shown that this particular vaccine will protect possums from the disease yet, although it seems to work in mice.

Pingui posted:

That was a very confusing read, as the study you linked explicitly said they did not see ADE. You are looking for this preprint:
"SARS-CoV-2 antibodies cross-react and enhance dengue infection"

Strep Vote posted:

https://wellbefore.com/products/3d-kf94-style-kn95-pro-mask-with-adjustable-ear-loops

Trip report: with head straps, it fits like an aura but is more breathable, and fits my spouse's tall mug with a huge lower pocket under the chin. Awesome, comes in a very handsome denim as well as black, for those who are looking for an aura that doesn't stand out.

Pingui posted:

That was a very confusing read, as the study you linked explicitly said they did not see ADE. You are looking for this preprint:
"SARS-CoV-2 antibodies cross-react and enhance dengue infection"

Platystemon posted:

Imagine walking into the pharmacy for your moth juice and finding this scene:



I can’t believe that he’s an anti‐Semite, what with the octopus plushies and all.

quote:

Obviously I dont mean a personal doctor like rich people, but does anyone actually see the same doctor multiple times?

I usually just go to urgent care when I am sick and need meds to treat it (this was twice this year also its only $20 for me to go) or go to specialists directly through my insurance. I've found primary care doctors to be a waste of time and whenever I do go to one I never see that same one ever again. I have gone to see a couple per year to establish care but always have a bad experience.

I am not light on the medical visits either, I go to some sort of doctor 10-20 times or so per year and probably Should be using a pcp if I had one (for giving out referral and managing care) but do not. I dont need them for referral as I have ppo insurance, I can also order blood tests online and get them filled at the local labcorp. This isn't my preference but the only way I can get things to happen. Relying on pcp would take ages and often they don't even take me seriously.

I do not have a pcp I would call "mine" as in having some sort of relationship established. Rarely do I see the same person twice. I do have my psychiatrist though but we dont talk about my physical health or other problems.

Edit: This post has gotten me like a million notifications so I stopped responding to every comment. Sorry if I dont respond

A few things, no "mommy and daddy" dont need to make my appointments. I've made several appointments to several different primary cares within the last 7 years. Also they live several states away anyway

I am US based, west coast specifically.

I dont go to urgent care that much, only when sick. Its a $20 copay for me and generally a better experience than regular PCPs.

Also, yes I see the typo of "there" in the title

Also again this is the main point:

quote:

I do not have a pcp I would call "mine" as in having some sort of relationship established. Or seeing them multiple times.

And I have tried yes. Its a weird thing for some of yall to be so angry and make so many crazy assumptions. Relax, I am not making fun of your doctor.

Edit again: For the non Americans, urgent care is not the same as ER in the US. Basically just a no appointment clinic.

Platystemon posted:

Imagine walking into the pharmacy for your moth juice and finding this scene:



I can’t believe that he’s an anti‐Semite, what with the octopus plushies and all.

mawarannahr posted:

I thought every American had their doctor, their lawyer, and their accountant

mawarannahr posted:

I thought every American had their doctor, their lawyer, and their accountant

Skinnymansbeerbelly posted:

I mean, if, on a population level, the primary purpose of primary care doctors is to have someone regularly check blood pressure and make sure the population don't go all Scanners, aren't most people who don't have high blood pressure or some other trivially managed condition going to find their docs loving useless?

https://www.ajmc.com/view/covid-19-fallout-on-individuals-economy-and-health-system-to-last-for-years-white-paper-concludes posted:

COVID-19 Fallout on Individuals, Economy, and Health System to Last for Years, White Paper Concludes

The federal government may have declared an end to the public health emergency for COVID-19 on May 11, 2023,1 but the effects of this infectious disease that caused nearly 7 million confirmed deaths worldwide by October 20232 will not end for the US health care system anytime soon.

In fact, the effects of long COVID will exact both a public health and economic toll for years to come, according to a white paper developed in the summer of 2023.3

The white paper was produced following the Long COVID, Inflammation, and Cancer Conclave held May 11-12, 2023, in Charlotte, North Carolina, to bring together global researchers, health care experts, and philanthropists interested in understanding the long-term effects of COVID-19 across the health system.
(..)
The topics covered a range of issues around long COVID, also known as postacute sequelae of COVID-19 (PASC).5 Some speakers focused on identifying links between long COVID, microRNA, inflammation, and therapeutic interventions; others discussed COVID-specific microRNA detection, mitochondrial function in SARS-CoV-2 and cancer, methylation metrics, real-world data from community practice, and more, aiming to understand the long-term consequences of COVID-19 and its connection to cancer and other health conditions.
(..)
How Does Long COVID Affect the Body?
Long COVID or PASC is a complex, multi-organ illness that arises in individuals with a history of SARS-CoV-2 infection, typically emerging around 3 months after the onset of COVID-19 symptoms. These symptoms—which can last for months or years—cannot be attributed to another diagnosis and are often connected to ongoing inflammatory changes in multiple tissues. PASC affects up to 80% of individuals who have had COVID-19,7 with between 2.5% and 15% experiencing more prolonged symptoms.8 Notably, fatigue is the most frequently reported symptom, yet it is also a symptom for several other conditions, making it harder to pinpoint the cause.

Additionally, more severe cases of long COVID can lead to damage in various organ systems such as the lungs, heart, nervous system, kidneys, and liver, alongside conditions like thrombotic and cerebrovascular diseases, type 2 diabetes, and mental health impairments.9

Long COVID also intersects with cardiovascular disease (CVD) and patients with both conditions can display persistent symptoms such as dyspnea, fatigue, chest pain, and cough. Around 20% of patients continue to experience these symptoms 3 months after initial COVID-19 infection. As discussed during the conclave, the occurrence of COVID-19–associated myocarditis is estimated at 150 cases per 100,000 individuals, often resulting from multiple contributing factors.10 Chest pain remains a common CVD symptom for individuals with moderate to severe COVID-19 infection, with myocarditis and pulmonary embolism presenting as higher risks for these individuals compared with other CVD complications. Data from the US Department of Veterans Affairs database suggest there is an increased risk of heart failure, dysrhythmias, and stroke 1 year after SARS-CoV-2 infection.11

Neurological complications are also prevalent in long COVID, impacting up to a third of patients.12 These complications can affect either the central or peripheral nervous system and include fatigue, cognitive impairment, headache, mood disorders, smell and taste disorders, and sensorimotor deficits. Cognitive dysfunction caused by long COVID also influences attention, executive function, problem-solving, and decision-making, with memory impairment seen in many cases, even among younger individuals.13

Brain imaging studies have also revealed consistent changes across various brain areas, including the temporal lobe, hypothalamus, brain stem, and cerebellum.14 According to speakers at the conclave, COVID-19 infection may pose a risk for the development of neurodegenerative diseases, dementia, and mild cognitive impairments, even in relatively young adults.

Other significant health issues linked to long COVID include persistent cognitive and mental health disorders, muscle and joint pain, fatigue, inflammation, and multi-organ damage. Research suggests that approximately 70% of patients with long COVID experience damage to at least 1 organ, while studies on renal functions in veterans with COVID-19 indicate increased kidney damage risk.15

How Does Long COVID Affect Population Health?
It’s estimated that—based on a conservative estimate of 10% of individuals with COVID-19 developing more prolonged PASC—more than 65 million people globally are affected by long COVID.9 In the United States alone, more than 27 million people are presumed to have been affected by long COVID by spring 2023.16 PASC is prevalent across age groups and levels of disease severity, with most diagnoses occurring in patients aged between 36 and 50 years and a significant proportion of cases involving nonhospitalized patients with mild acute illness.9

What Is the Economic Impact of Long COVID?
The projected economic impact of long COVID is estimated to be around $3.7 trillion—more than $1 trillion over initial estimates made in 2020—with direct and indirect costs ranging from $140 billion to $600 billion annually.17 Nearly 60% of these costs are due to reduced quality of life, with the remainder due to reduced earnings and greater medical spending. This translates to about $11,000 per person.

As of August 2022, about 16 million working-age Americans aged 18 to 65 years were reported to have long COVID.18 Of this group, around 4 million were unable to work because of the condition, resulting in about $170 billion in lost wages.

PASC exerts an even bigger strain on the health care system, contributing to a yearly financial burden of nearly $400 billion in the United States, and is expected to remain one of the top 10 medical cost drivers for the next 5 years. As research has shown the neurological symptoms of long COVID, its impact on functional ability and workplace productivity is substantial. This has been seen particularly in cases of myalgic encephalomyelitis from long COVID, in which the persistence of neurocognitive symptoms led to estimated annual costs of $9000 per patient.17,19

Looking at both the workplace and the health care setting, long COVID can lead to a reduction in work hours for 46% of patients and a $6200 increase in annual emergency department visits and possibly more than 20 outpatient visits within a year.20

Does Long COVID Exacerbate Existing Disparities?
The short answer? Yes.

The longer answer? COVID-19 exacerbated existing inequalities among marginalized communities. This has led to a range of issues such as delayed diagnoses, reduced health care accessibility primarily driven by inadequate health insurance coverage in Black and Latinx populations, postponed or absent medical treatment, and heightened vulnerability to SARS-CoV-2 exposure, and that was only in the first year of the pandemic.21

Since then, research supported by the National Institutes of Health RECOVER program has uncovered disparities in the impact of long COVID symptoms across racial and ethnic groups in the United States, specifically among Black and Hispanic patients.22 It was found that Black and Hispanic Americans tend to experience a higher burden of symptoms and health issues related to long COVID compared with White patients.

In the study, racial and ethnic minority groups demonstrated significantly higher adjusted odds of being diagnosed with various symptoms and conditions affecting multiple organ systems compared with White patients. Notably, among nonhospitalized patients with COVID-19, Hispanic individuals had higher odds of long COVID diagnosed in 6 organ systems, while Black individuals had higher odds in 4 organ systems.

Among hospitalized patients, the disparities were even more pronounced, particularly when looking at patients’ endocrine and circulatory systems. For example, compared with White patients, Black patients were twice as likely to develop diabetes and 1.5 times more likely to experience chest pain within 30 to 180 days after infection. Similar disparities were observed among Hispanic individuals.22

According to researchers who conducted a cohort study from the RECOVER program, these disparities are likely influenced by a complex interplay of biological, environmental, and social factors, including variations in immunogenetics that affect immune profiles and cytokine levels.23 These findings underscore the importance of understanding and addressing the underlying reasons for these disparities in long COVID outcomes among different racial and ethnic groups.

What is the Link Between Long COVID and Cancer?
The connection between viral infections and cancer risk, dating back to the discovery of virus-associated lymphoma in 1964,24 underscores that around 15% to 20% of cancer cases stem from carcinogenic infections, primarily viral.25 At least 7 human oncogenic viruses—including Epstein-Barr virus, human papillomavirus, and hepatitis B and C viruses—are closely linked to various human cancers. Mechanisms contributing to this process are diverse, and include chronic inflammation, immune suppression, alterations in DNA modification, mitochondrial function, and activation of oncogenes and tumor suppressors. Additionally, tumorigenesis is linked to chronic inflammation and persistent infections, with viruses needing immune evasion mechanisms and infections inducing mild but lasting inflammation.26 Chronic inflammation also heightens mutation rates, elevating cancer risk.

Long COVID is characterized by inflammatory pathway activation, demonstrated by an early, intense inflammatory response alongside reduced anti-inflammatory activity and mitochondrial stress. Neutrophil dysfunction in even mild cases could heighten cancer susceptibility because of low-density neutrophil (LDN) increase, known for immunosuppression.27 The rise in LDNs correlates with poor T-cell response and disease severity, suggesting potential control limitations and altered neutrophil-to-lymphocyte ratio.

The lasting effects of residual virus cells may induce chronic inflammation and oxidative stress, leading to tissue and DNA damage.26 The spike protein of SARS-CoV-2 activates inflammasome and inflammatory pathways, particularly in older individuals, possibly contributing to age-related comorbidities and immune response impairment. This, coupled with immune evasion strategies of the virus, suggests long COVID’s potential as a risk factor for new cancer through various mechanisms, including chronic virus infection, inflammation, cell senescence, the oncogenic potential of SARS-CoV-2, and immunosuppression.

At the cellular level, the pathophysiology of long COVID involves immune imbalances, incomplete viral clearance, and potentially mitochondrial dysfunction.28 Recent evidence has also highlighted the virus’ targeting of mitochondria, disrupting their function. This occurs through virus-encoded proteins such as ORF-96 and ORF-3a, which alter mitochondrial genes and homeostasis, ultimately leading to apoptosis and the release of mitochondrial DNA. The degraded mitochondrial DNA, found at high levels in the blood, can predict poor COVID-19 outcomes. In individuals with compromised mitochondrial function, the virus might induce chronic inflammation and metabolic imbalance, driving long COVID symptoms. This state is characterized by mitochondrial dysfunction, ongoing inflammation, and a shift toward glycolysis. Restoring metabolic balance through interventions such as physical activity or with compounds that enhance mitochondrial function could be beneficial.

A New Way to Detect COVID-19?
MicroRNAs (miRNAs) are small non-coding RNAs with crucial roles in post-transcriptional gene regulation, and they have a significant impact on diseases such antiviral responses.29 A particular circulating miRNA, miR-2392, is linked to SARS-CoV-2 machinery when the host is infected. It contributes to suppressing mitochondrial gene expression, increasing inflammation, glycolysis, hypoxia, and COVID-19–associated symptoms. Additionally, miR-2392 is detected in blood and urine of patients with COVID-19, suggesting its potential use for minimally invasive COVID-19 detection. A miRNA-based antiviral therapeutic targeting miR-2392 reduces SARS-CoV-2 viability in hamsters, offering a potential avenue to mitigate COVID-19 infection in humans.

The immunological profiles of individuals with long COVID differ from those who recover quickly, with patients with long COVID showing a decrease in interferon gamma (IFN-γ) producing CD8+ cells 4 months after symptom onset.30 Cytotoxic lymphocytes, which impact viral clearance through IFN-γ release, seem affected. DNA methylation is a stable epigenetic marker with significant roles in normal biological processes and disease pathogenesis.31 Genomic and epigenetic studies have unveiled susceptibility genes for COVID-19, particularly ACE2, and demonstrated that methylation patterns can predict disease severity.32 Understanding the connection between epigenetic variation and infection involves analyzing how hosts respond to viral exposure, how viruses utilize the host’s epigenome to establish infection, and the inherent susceptibility differences between individuals.

When Will Biomarker Testing Be Available?
Since the spring, Evidence-Based Oncology has contacted multiple payer organizations—some more than once—seeking comment on the impact of long COVID and the potential availability of biomarker testing, following publication of Patel’s initial call to action on March 22.33 Patel’s comments appeared 2 months after a review article on long COVID, led by senior author Eric J. Topol, MD, concluded that “Diagnostic and treatment options are currently insufficient, and many clinical trials are urgently needed to rigorously test treatments that address hypothesized underlying biological mechanisms, including viral persistence, neuroinflammation, excessive blood clotting and autoimmunity.”9

Payer organizations contacted include Blue Cross and Blue Shield of Louisiana, Horizon Blue Cross Blue Shield of New Jersey, Anthem Blue Cross Blue Shield Indiana and Anthem Blue Cross Blue Shield New York, Centene, Humana, EmblemHealth, Priority Health, and Highmark. These organizations either did not respond to email or declined to comment.

“The lack of biomarker testing makes the disparities worse, and I think payers have an obligation to [put] some sort of process in place so that they can at least do their part of the work in addressing disparities,” Patel said. “By not saying what they plan to do is tantamount to denying patients the appropriate treatment options that are available based on scientific evidence.”

In discussing the lack of payer comment on biomarker testing for long COVID, Patel referenced the American Association for Cancer Research (AACR) Cancer Disparities Progress Report 2020, which highlights an urgent need for implementing guideline-concordant biomarker testing to reduce costs, improve patient outcomes, and address health care disparities.34

“I’m not surprised at the payers’ approach, but that’s the problem our country has,” Patel said. “It has itself a compartmentalized, fragmented system where the lobbyists let payers get away with whatever they want to get away with. This [AACR] article itself would undeniably mandate an inclusive approach,” Patel said.

According to Patel, it is imperative to shift our focus toward fact-based evidence generation, data collection, provider and payer education, intervention design, mass public education campaigns, and policy implementation. Although the exact pathophysiology of long COVID remains unclear, links have emerged among inflammation, altered immune responses, and long COVID manifestations. A proposed call to action that emerged from the conclave35 encompassed several aspects, such as:

• assessing the population health impact of long COVID and its relationship with cancer;
  
• evaluating the health care costs associated with long COVID and cancer;
  
• exploring the chronic comorbidities linked to long COVID;
  
• analyzing trends in new cancer cases among community cancer patients both pre- and post COVID;
  
• investigating the postpandemic ramifications on industry and payers resulting from long COVID;
  
• exploring the potential utility of the SARS-CoV-2 full spike protein as a biomarker for long COVID;
  
• uncovering the impact of COVID-19 infections on the epigenome of relevant tissues or blood and the development of epigenetic markers; and
  
• creating patient-derived organoid models from relevant tissues to better understand tumorigenesis.

Addressing these questions, Patel said, will provide insights into differences between vaccinated and unvaccinated patients, potential associations between long COVID and the emergence of rare cancers, the influence of biological factors on long COVID susceptibility, the persistence of SARS-CoV-2 in organs, the influence of host genetics and the microbiome, the potential for stage migration in cancer due to inflammation, the impact of severe inflammation on chronic end-organ damage, the establishment of common diagnostic criteria for long COVID, and the development of preventive and therapeutic strategies.

He also emphasized the need to explore strategies to prevent the reactivation of herpes family or other viruses due to COVID-induced immune dysfunction. To execute this call to action effectively, Patel proposed dividing it into 3 main themes, as follows:

• education, which includes educating health care providers, patients, payers, pharmaceutical companies, and the general public through awareness campaigns;
  
• research, which involves establishing a prospective real-world evidence registry for long COVID, identifying susceptibility factors, examining differences between vaccinated and nonvaccinated individuals, and investigating distinctions between patients with and without cancer; and
  
• intervention, with this category encompassing the development and implementation of therapeutic and health interventions as well as the provision of human services, support, and interventions.

For therapeutic interventions, Patel noted that research can include exploring anti-inflammatory approaches such as tumor necrosis factor-α inhibitors such as infliximab, kinase inhibitors such as imatinib, Janus kinase 2 inhibitors, Bruton tyrosine kinase inhibitors, anti-interleukin-6 treatments, and COVID-19–specific cytotoxic T lymphocytes for the treatment of acute-risk patients with COVID-19.

This comprehensive approach aims to address the multifaceted challenges posed by long COVID and provides a clear path forward for research, education, and intervention in response to this ongoing global health concern.

https://www.mdpi.com/2075-1729/13/10/2087 posted:

Abstract
An emergence of evidence suggests that severe COVID-19 is associated with an increased risk of developing breast and gastrointestinal cancers. The aim of this research was to assess the risk of heart tumors development in patients who have had COVID-19.

Methods: A comparative analysis of 173 heart tumors was conducted between 2016 and 2023. Immunohistochemical examination with antibodies against spike SARS-CoV-2 was performed on 21 heart tumors: 10 myxomas operated before 2020 (the control group), four cardiac myxomas, one proliferating myxoma, three papillary fibroelastomas, two myxofibrosarcomas, one chondrosarcoma resected in 2022–2023. Immunohistochemical analysis with antibodies against CD34 and CD68 was also conducted on the same 11 Post-COVID period heart tumors. Immunofluorescent examination with a cocktail of antibodies against spike SARS-CoV-2/CD34 and spike SARS-CoV-2/CD68 was performed in 2 cases out of 11 (proliferating myxoma and classic myxoma).

Results: A 1.5-fold increase in the number of heart tumors by 2023 was observed, with a statistically significant increase in the number of myxomas. There was no correlation with vaccination, and no significant differences were found between patients from 2016–2019 and 2021–2023 in terms of gender, age, and cardiac rhythm dis-orders. Morphological examination revealed the expression of spike SARS-CoV-2 in tumor cells, endothelial cells, and macrophages in 10 out of 11 heart tumors.

Conclusion: The detection of SARS-CoV-2 persistence in endothelium and macrophages as well as in tumor cells of benign and malignant cardiac neoplasms, the increase in the number of these tumors, especially cardiac myxomas, after the pandemic by 2023 may indicate a trend toward an increased risk of cardiac neoplasms in COVID-19 patients, which re-quires further research on this issue and a search for new evidence.

Skinnymansbeerbelly posted:

I mean, if, on a population level, the primary purpose of primary care doctors is to have someone regularly check blood pressure and make sure the population don't go all Scanners, aren't most people who don't have high blood pressure or some other trivially managed condition going to find their docs loving useless?

BusError posted:

Just got back from my local annual tabletop gaming convention. Quite a few more masks than I would have expected, and of those, a shockingly high number were N95s! I guess if any population is going to do their homework and have better than average risk/reward calculations, that's where I'd expect it. Bummer they weren't required, but my expectations are so far down in the sewer at this point that I'm happy when I see any effort at all.

RandomBlue posted:

I don't live in Florida, can I still use sesame care while traveling? Anyone know of a good place to get a pax prescription in the Orlando area?

RandomBlue posted:

My wife forced us to stop masking and go on this revenge travel trip to Florida, 7 days at Disney and universal studios plus 2 travel days. State
Started feeling like poo poo and tested. Two minutes in:

3.5 years COVID free until this poo poo.

We got the new booster the week it came out. Yeah i know it doesn't prevent infection.

Mola Yam posted:

what is the deal with the death drive to go to florida