COVID Science
Excerpts from “In the meantime... Individual Health in the Early COVID Era”
Part 1: The Science
The Immune System
Humans have two branches of the immune system: the innate and adaptive systems. The innate immune system is evolutionarily older and is not as good as the adaptive at specifying and binding foreign invaders (also called antigens) such as viruses, but it serves as a warning mechanism to the adaptive. The innate system can capture some invading pathogens but we also use it as a signal caller for the adaptive immune system to kick in. The adaptive system works by creating antibodies very specific to each antigen. The innate system tells the adaptive system “hey, here’s an invader, create an antibody for it so we can destroy it.”
Without prior infection, it can take a long time for the adaptive system to create antibodies capable of handling a new infection. However, the adaptive immune system possesses B cells and T cells that act as memory cells from prior infections or vaccinations and the B cells can ramp up quickly to produce antibodies when a prior antigen is recognized (within a week or so). COVID has very unique abilities to escape the innate immune system. Studies have shown an ability of the virus to down-regulate interferon signaling of the adaptive system, among other mechanisms[1].
This makes it so it takes a long time before the adaptive immune system is signaled to kick in and start producing antigen specific antibodies if no prior infection or immunization has taken place. This is why the unimmunized face such an uphill battle with a primary COVID infection.
If you’ve had a vaccine, the adaptive immune system doesn’t actually require signaling by the innate system, but can turn on antibody production itself when antigens are recognized by the helper T cells that were generated by the vaccination. So, the vaccines make it so you can build an arsenal of antibodies relatively quickly, within a week or so, and they overcome COVID’s ability to escape the innate immune response.
What vaccines don’t do, however, is prevent you from experiencing peak viral load during the time that the adaptive system is forming its response. It’s COVID’s ability to escape the innate immune response in the unvaccinated that leads to a very long experience of peak viral load, so long in fact that the person can be hospitalized or so overcome that they die. Vaccines don’t prevent you from experiencing peak viral load, they simply make it so you rid that load much faster than an unvaccinated person. During this peak viral load, even in the vaccinated, the virus can still do enormous amounts of damage throughout the body to organs and vessels, along with dysregulation of many bodily systems. Research has shown that Long COVID is not prevented by vaccines.[2]
Most people who get COVID and are fully up on their immunizations and are not immunocompromised will most likely not be hospitalized or die. However, there are some other factors to consider. Anywhere between 10-30% of people will develop Long COVID after a primary infection. There are many different mechanisms currently understood as to what is occurring in the body. There is also an enormous amount we do not know. Long COVID is essentially lasting damage to the body.
Multiple Infections
Multiple research efforts have shown that repeat COVID infections tend to have a multiplicative effect, where subsequent infections cause greater damage than a first infection causes. It is believed that even if a primary infection leads to few immediate long term symptoms, there may be damage and dysregulations that become more pronounced on subsequent infections. The probability of having long term complications are significantly greater after multiple infections than after a primary.
One of the most comprehensive follow-up studies looking at the effects of reinfection was published in Nature Medicine in November of 2022 titled “Acute and postacute sequelae associated with SARS-CoV-2 reinfection” looked at reinfection effects in a population of over five million, concluding:
“compared to people with first infection, reinfection contributes additional risks of all-cause mortality, hospitalization, and adverse health outcomes in the pulmonary and several extrapulmonary organ systems (cardiovascular disorders, coagulation and hematologic disorders, diabetes, fatigue, gastrointestinal disorders, kidney disorders, mental health disorders, musculoskeletal disorders, and neurologic disorders); the risks were evident in those who were unvaccinated, had 1 shot, or 2 or more shots prior to the second infection; the risks were most pronounced in the acute phase, but persisted in the post-acute phase of reinfection, and most were still evident at 6 months after reinfection.”[3]
In a statement, the author emphasized:
“During the past few months, there’s been an air of invincibility among people who have had COVID-19 or their vaccinations and boosters, and especially among people who have had an infection and also received vaccines; some people started to referring to these individuals as having a sort of superimmunity to the virus,” said senior author Ziyad Al-Aly, MD, a clinical epidemiologist at the Washington University School of Medicine. “Without ambiguity, our research showed that getting an infection a second, third or fourth time contributes to additional health risks in the acute phase, meaning the first 30 days after infection, and in the months beyond, meaning the long COVID phase.”[4]
Their research found that people who were reinfected with COVID were twice as likely to die, three times as likely to be hospitalized, three times as likely to develop heart conditions, and 1.6 times as likely to develop brain issues versus people with only one infection[5]. The study found that the risk increases with each infection, so limiting getting a future one will reduce a compounding of health risk. If you’ve had three infections, it’s better to not get a fourth. If you’ve had four, avoid the fifth.
Effects on the Brain and Central Nervous System
Endothelial cells are critically important cells found throughout the human body. Specifically, they are found on the inner lining of blood vessels, including blood vessels in the brain, and they provide support structures to those vessels. They are relevant to COVID because endothelial cells contain ACE2 receptors, which are the receptors to which COVID binds.
When endothelial cells are attacked in brain blood vessels, the vascular structure of the vessels collapse, clots form, blood-brain barrier leakage occurs, and upon vascular collapse, cytotoxic hypoxia and regional cell death ensues[6]. This can occur in all COVID patients, including the immunized. A longitudinal MRI study in England published in the journal Nature has shown a material loss of Grey Matter in brains of COVID patients[7].
There are many other mechanisms by which COVID is thought to affect the brain, including by directly infecting and compromising Astrocytes, which are critical support cells for brain function. It’s also thought that dysregulation of the immune system by COVID can end up producing auto-antibodies that attack the brain[8].
Tau proteins are biomarkers of neurodegeneration that are found in the cerebrospinal fluid (CSF) of patients with neurodegenerative diseases including Parkinson’s and Alzheimer’s. Tau has been identified at elevated levels in recovering COVID patients[9]. It isn’t quite yet clear whether or not a permanent degeneration process has been kicked off or if this finding of elevated Tau will reduce over time. Massive increases in Parkinson’s cases were found to occur a decade after the 1918 flu pandemic. It was also found that the generation that went through the that pandemic had two to three times the likelihood of developing Parkinson’s than prior and later generations[10].
One mechanism by which viruses damage organ structures is by causing organ cells to fuse together, though not die. This produces large multicellular structures called syncytia. These structures have been found in lungs of COVID patients and researchers have recently shown how the COVID virus can cause the same syncytial effects in brain tissue. The virus accomplishes this by causing the infected host neuronal cell to express a structure called a fusogen on its surface, which triggers fusion with neighboring brain cells. This allows the virus to infect neighboring cells without having to be present extracellularly in large quantities and directly attack each cell it infects. It uses an infected cell to infect a neighboring cell.
The author of the study, Massimo Hilliard, a neuroscientist at the University of Queensland, explains that neurons typically fire independently, sending signals throughout the brain. However, the fused neurons fired 90% of the time as a single unit. He says this synchronous activity “is almost like a seizure.”[11] The author states in the published results:
“We show that SARS-CoV-2 infection induces fusion between neurons and between neurons and glia in mouse and human brain organoids. We reveal that this is caused by the viral fusogen, as it is fully mimicked by the expression of the SARS-CoV-2 spike (S) protein ... we demonstrate that neuronal fusion is a progressive event, leads to the formation of multicellular syncytia, and causes the spread of large molecules and organelles ... we show that fusion severely compromises neuronal activity. These results provide mechanistic insights into how SARS-CoV-2 and other viruses affect the nervous system, alter its function, and cause neuropathology.”[12]
In an interview, the second author on the study, Rosina Giordano-Santini, was asked if this was reversible. She answered that she didn’t see from a biological perspective why these merged neurons would naturally defuse and thought the process to be irreversible.
A U.K. study published in the Lancet in 2023 looked at cognitive impairment up to two years past an initial COVID infection and found “Cognitive deficits following SARS-CoV-2 infection were detectable nearly two years post infection, and largest for individuals with longer symptom durations, ongoing symptoms, and/or more severe infection.”[13]
Vascular System
An important compound in the body is Fibrinogen. It is part of the body’s complex clotting system. The clotting system is unique in that it requires a finely regulated positive feedback loop. Meaning, as clotting occurs, typically more clotting needs to occur to prevent bleeding out during an injury. Then, this process needs to be shut off or too many blood clots will form.
COVID has been shown to dysregulate the clotting system leading to a long term overproduction of Fibrinogen. This is important because excess Fibrinogen interacts with a protein called Amyloid (the same compound found in Alzheimer’s plaques), to form what are called Fibrin-Amyloid microclots. These microclots can be found in COVID patients long after the primary infection has left the body, indicating a long lasting or permanent clotting dysregulation. Some researchers believe these clots ending up in the brain and lungs are possible causes of brain fog and fatigue.[14] Fatigue has also been shown to be a possible result of long term dysregulation of metabolic processes within mitochondria, specifically within the lungs.
Other vascular issues found in COVID patients can stem from collagen breakdown. Collagen is the most abundant protein found in the body. Its unique structure provides for both strength and elasticity. This makes it perfect for providing structure to skin, bones, tendons and ligaments. It also provides the support structure for our vasculature and is a very important structural component of our large blood vessels that handle high pressure volume loads.
Vascular surgeons have recently published findings in the Journal of Vascular Surgery in an article titled “COVID-19 patients with abdominal aortic aneurysm may be at higher risk for sudden enlargement and rupture”. Their findings are corroborating earlier findings that Metalloproteinases are significantly elevated in COVID patients. These enzymes are known to metabolize the collagen and elastin infrastructure of large vessels that provide structural support and are therefore known biomarkers for aneurysm rupture.[15]
Diabetes
Sugar in the blood requires Insulin to be absorbed by cells throughout the body. Insufficient Insulin production leads to a condition called Type 1 Diabetes. The body not reacting or being sensitive to Insulin the blood is the characteristic of Type 2 Diabetes. Insulin is produced in the Pancreas by specialized cells called Beta cells. Impairment of Beta cells, typically by autoimmunity, leads to Type 1 Diabetes.
Researchers have shown several direct and indirect methods by which COVID can impair or destroy Beta cell insulin production.[16] A large cohort study looking at a population of over 30 million found that new onset Type 1 Diabetes risk is significantly increased following COVID infection.[17] Looking specifically at children, a study published in July 2023 showed incidence rates of Type 1 Diabetes at 14% higher than normal in the first year of the pandemic and 27% higher in the second year.[18] Development of Type 1 Diabetes puts these children at risk for a lifetime of related medical complications.
Even if a first infection doesn’t lead to full Diabetes, multiple infections can cause increasing damage to the Pancreas, where symptoms may start that first resemble pre-Diabetes and gradually progress with subsequent infections causing more damage.
Immune System Dysregulation and New Onset Autoimmune Diseases after COVID
Autoimmune diseases are generally caused by a dysregulation in the body’s ability to prevent the proliferation of self-targeting antibodies. The adaptive immune system has a process whereby it performs a kind of ‘quality assurance’ on newly created immune cells to ensure that they don’t target the body’s own cell signatures. When this process is disrupted, and various viruses have been shown to cause disruption of this process, immune cells that target the self are not selected out and can begin to target the body’s own organ systems.
COVID has been shown to trigger new onset autoimmune diseases after infection. A summary of two large cohort studies published in April, 2023 in Nature Reviews Rheumatology stated:
“The incidence of autoimmune conditions at 6 months follow-up was significantly higher in the COVID-19 cohort than in the non-COVID-19 group. The unique aspect of the autoimmune diseases after exposure to SARS-CoV-2, as compared with other previously known viral pathogens (such as coxsackie type 1, coronaviruses and Epstein–Barr virus), is the spectrum of conditions seen. In this COVID-19 cohort, an entire range of autoimmune conditions was noted, including rheumatoid arthritis, systemic lupus erythematosus and vasculitis as well as inflammatory bowel disease and type 1 diabetes mellitus.”[19]
Long-Term Disability
Beyond death rates, declaring a victory against COVID would also undoubtedly require an eradication of Long COVID and its debilitating effects. One place to look for how the U.S. stands on this front is in the raw disability numbers. It’s data that’s quite easy to obtain, published by the Federal Reserve Bank of St. Louis on behalf of the Bureau of Labor Statistics. The following graph shows a recent record of 34.15 million disabled adults, an increase of approximately 4 million from the average of 30 million before the pandemic.
Above: U.S. Bureau of Labor Statistics Disability Data as of July 2024.[20]
This chart, more than any, should be what’s most concerning to the general population. If you’re elderly, unvaccinated or immunocompromised, death is certainly your greatest concern. And we should be certainly doing something if only to help this part of our fellow population. But if you’re otherwise healthy and vaccinated, you can still get Long COVID, and you can end up on this chart.
Part 2: Public Health Messaging
Since the beginning of COVID, we’ve seen and continue to see countless articles and general messaging minimizing COVID, declaring that it’s no longer a threat. However, this is nothing new. In fact, it’s par for the course. It’s how most public health crises play out early on. We’ve seen this before.
“There is almost no danger of contracting AIDS through normal vaginal intercourse ... ”
The following was written in an article in Cosmopolitan magazine in 1988 by a New York City doctor, Robert E. Gould, M.D. :
“You are a healthy, vital American woman, and just when you’ve decided to have an active love life, everyone tells you that sex kills. You’re cautioned to hold onto chastity for dear life or face the deadly risk of contracting AIDS, the fatal disease. Meanwhile, all about you, policemen, firemen, law-court personnel, health-care workers are donning gloves, masks, outer-space wear - and even with the protective gear, they are afraid of being within spitting distance of a person with AIDS or suspected of carrying the virus. Where does all of this leave you? Is the hysteria justified? In my opinion, and from objective evidence, the answer is no: In all probability you won’t catch the virus by inhaling it, ingesting it, or, more to the point, having vaginal or oral sex.”
He continues ...
“And according to Dr. Harold Jaffe, chief AIDS epidemiologist at the Centers for Disease Control in Atlanta ‘Those who are suggesting that we are going to see an explosive spread of the virus into the heterosexual population have to explain why this is not happening.’ Why this isn’t happening, I believe, is that there is no danger of contracting AIDS through ordinary sexual intercourse, a conclusion I have reached by my own studies and after having gone over most of the published reports on AIDS, visited hospital wards, and talked with leading researchers in virology.”[21]
This was 1988. This was five years after it was announced that women could contract HIV through heterosexual intercourse. This was seven years after UCLA physician Michael Gottlieb reported the first cases of HIV/AIDS in Los Angeles. New genomic research shows that the disease was actually spreading throughout the 1970s. [22]
Let’s see what the CDC says now about heterosexual sex and the spread of HIV. On the CDC website, in the section titled “Can I get HIV through Vaginal Sex?”, the first line states: “You can get HIV if you have vaginal sex with someone who has HIV without using protection (like condoms or medicine to treat or prevent HIV).”[23]
It seems like CDC’s messaging on HIV has been made a lot more clear since 1988 when their chief AIDS epidemiologist, Dr. Harold Jaffe, was quoted in the Cosmopolitan article dismissing vaginal transmission of HIV. Further digging shows that the Jaffe quote used by Gould in Cosmopolitan actually came from a 1987 New York Times piece titled “AIDS Expert Sees No Sign of Heterosexual Outbreak”[24], which covered a panel session at the Third International Conference on AIDS. After posing his question as to why we haven’t seen this outbreak, James J. Goedert, of the National Cancer Institute, responded that the reason may be “that the infection may not have been present among American heterosexuals long enough for its maximum spread”. This wasn’t quoted in the Cosmopolitan article. Also in the Times article was a report by Dr. Nathan Clumeck and a team of researchers from Belgium who reported on a promiscuous engineer in Belgium who had infected at least 10 of his previous 19 known female partners before he died of the disease. This wasn’t quoted in the Cosmopolitan article either. Nor did it make the headline of the Times article. They chose instead “AIDS Expert Sees No Sign of Heterosexual Outbreak”.
And where are they now?
Robert E. Gould, M.D., the author of the Cosmopolitan article, died 25 years ago.
Harold Jaffe still serves as the CDC’s Associate Director for Science as of mid 2024.
We’re only four years into COVID. Expect more misinformation.
Above: Cosmopolitan Magazine, January 1988, “Reassuring News about AIDS, A Doctor Tells Why You May not Be at Risk” [25]
Messaging early in a disease can be quite unreliable. It can have ulterior motives. Its goal can be to placate and make everyone feel that “all is normal, nothing to see here”. Over time, the messaging changes. The disease starts to play itself out and affect society in ways that the early messaging can’t hold back. The reality eventually catches up. Eventually, a new society emerges that realizes that things are different now than in the past. That protection should be taken regardless of immediate risk magnitude due to high potential consequences. Behavior changes and the new society sees the old messaging as naively quaint and in some cases absurd. It becomes unclear why the original goal was to coddle the population like little children and make them feel that there was no new threat, rather than be honest about the truth of what is and what isn’t known. That perhaps some caution should be taken in light of what is and isn’t known. This change takes time. Sometimes, it takes a very long time. We need to shorten that time. You don’t prove that COVID is a problem by disproving people who say it isn’t. You follow the science. Science stands independent of opinion.
Part 3: The Future
“Preventing is more effortless than recovering, generally. Pretending looks more effortless but will have more distressing consequences, actually.”
- Hiroshi Yasuda
There is no reason to believe that this disease will simply disappear. There isn’t a reason to believe it will mutate into something materially weaker. Polio, HIV, Ebola, Dengue Fever, Bubonic Plague and many, many other viruses have been around for a long time. They have not mutated themselves out of existence or into weaker forms. With no global control, hotspots around the world will continually generate mutations. This virus has shown an ability not only to mutate quickly, but also re-combine prior strains. It mutates in an increasingly immunity evading manner.
Anthropologists believe a coronavirus in eastern asia in the past was only evaded by the evolution of the people in that region, currently marked by a set of common genes in their genome.[26] They believe a novel coronavirus or similar pathogen first appeared more than 20,000 years ago and induced an evolutionary selective pressure that left that population with a set of genes that produced proteins that interacted with the virus to better protect them. For the population in eastern asia that evolved out of their pandemic, massive amounts of death had to occur over a long period of time, with only those with the specific protective gene mutations surviving. The virus didn’t mutate itself out of existence. The human genome evolved. COVID isn’t just going away.
The way forward with COVID treatments will hopefully include the emergence of new and better therapies. Paxlovid works by down-regulating the enzyme that allows COVID to replicate. It can possibly reduce peak viral load, but it has also been associated with a rebound effect in some patients that sees COVID re-emerge after the drug is done being taken. Nonetheless, it’s better to take than not take.
While we can re-vaccinate each year, our bodies are more attuned to the original vaccine strain in a process called “Imprinting”, such that subsequent vaccinations tend to trigger simply more production of the original antibody and not significantly more of the new antibody (although studies do show it’s better to get the new vaccine than not). It is due to this concept of imprinting that they are no longer producing bivalent vaccines. The goal is to try to induce the immune system to produce specific new antibodies rather than more of the original.
This disease so far has disproportionately affected older people more than young. Younger people do indeed have more robust immune systems that help prevent hospitalization and death. However, they are still quite susceptible to the damage that is found with Long COVID. While they may possess better immune responses for now, they will spend a significantly greater proportion of their lives with COVID and enduring multiple infections than older generations. It would be wise to consider the effects of stacking infections for people of all ages.
Many people will try to make you feel bad or silly or small or like an outcast for wearing a mask. It makes them feel better about their own bad decision making. One should wear it with pride. A mask is a sign of intelligent life. It’s a sign that the wearer possesses an extreme logic of mind. Toughness is standing out in a crowd, not cowering within one. Toughness is an ability to adapt, not living in a fantasy based on wishful thinking. Choose your health and ignore the maskless commoners.
While those who choose not to protect their own health can do whatever they want, they are indeed part of a larger public health problem that puts enormous amounts of people at risk who didn’t ask to be marginalized by the society they’ve spent their lives contributing to. It puts at risk an entire generation of children who didn’t ask to be born at a time of a totally dismantled and non-existent public health system.
For those who wish to protect your own health, this requires a position of extreme individualism. You cannot and will not be able to count on any public health measures to help you out. You must mitigate the disease on your own to the extent you are capable. Wear a mask. Avoid groups that you aren’t sure are tested and clear of COVID. Most importantly, don’t succumb to the social pressures to change your stance in order to be accepted by others. Your giving in would undoubtedly make others feel better about their own bad decision making. But it won’t help you. COVID relies on you giving in to the social pressures and desires for a pre-2020 life. You have only one set of organs. Protect them. Don’t hand their fate over to the scientifically illiterate and uninformed masses who don’t care about you. In some future generations, there may be regular mandated testing tied into phone apps that allow access to venues, contact tracing, building code ventilation requirements and other measures. There may come a resurgence of public health in the fight against COVID and other diseases.
In the meantime …
[1] Chakraborty C, Sharma AR, Bhattacharya M, Lee SS. A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations. Front Immunol. 2022 Feb 9;13:801522. doi: 10.3389/fimmu.2022.801522. PMID: 35222380; PMCID: PMC8863680. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8863680/
[2] Al-Aly, Z., Bowe, B. & Xie, Y. Long COVID after breakthrough SARS-CoV-2 infection. Nat Med 28, 1461–1467 (2022). https://doi.org/10.1038/s41591-022-01840-0 https://www.nature.com/articles/s41591-022-01840-0
[3] Bowe, B., Xie, Y. & Al-Aly, Z. Acute and postacute sequelae associated with SARS-CoV-2 reinfection. Nat Med 28, 2398–2405 (2022). https://doi.org/10.1038/s41591-022-02051-3
[4] Repeat COVID-19 infections increase risk of organ failure, death
Researchers recommend masks, vaccines, vigilance to prevent reinfection
by Kristina Sauerwein•November 10, 2022
Washington University School of Medicine
https://medicine.wustl.edu/news/repeat-covid-19-infections-increase-risk-of-organ-failure-death/
[5] Getting COVID more than once might be even worse than we thought, Popular Science, Laura Baisas Nov 10, 2022 https://www.popsci.com/health/repeat-covid-19-infections-death-hospitalization/
[6] Wenzel, J., Lampe, J., Müller-Fielitz, H. et al. The SARS-CoV-2 main protease Mpro causes microvascular brain pathology by cleaving NEMO in brain endothelial cells. Nat Neurosci 24, 1522–1533 (2021). https://doi.org/10.1038/s41593-021-00926-1
[7] Douaud, G., Lee, S., Alfaro-Almagro, F. et al. SARS-CoV-2 is associated with changes in brain structure in UK Biobank. Nature 604, 697–707 (2022). https://doi.org/10.1038/s41586-022-04569-5
[8] Michael Marshall, COVID and the brain: researchers zero in on how damage occurs, Nature, Jul 7, 2021
[9] Sun B, Tang N, Peluso MJ, Iyer NS, Torres L, Donatelli JL, Munter SE, Nixon CC, Rutishauser RL, Rodriguez-Barraquer I, Greenhouse B, Kelly JD, Martin JN, Deeks SG, Henrich TJ, Pulliam L. Characterization and Biomarker Analyses of Post-COVID-19 Complications and Neurological Manifestations. Cells. 2021 Feb 13;10(2):386. doi: 10.3390/cells10020386. PMID: 33668514; PMCID: PMC7918597. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918597/
[10] How past pandemics may have caused Parkinson's, David Cox, BBC Future, Jan. 31 2022 https://www.bbc.com/future/article/20220127-could-covid-19-still-be-affecting-us-in-decades-to-come
[11] Claudia López Lloreda, Could fused neurons explain COVID-19’s ‘brain fog’?, Science, 7 Jun. 2023 https://www.science.org/content/article/could-fused-neurons-explain-covid-19-s-brain-fog
[12] Ramón Martínez-Mármol et al., SARS-CoV-2 infection and viral fusogens cause neuronal and glial fusion that compromises neuronal activity.Sci. Adv.9,eadg2248(2023).DOI:10.1126/sciadv.adg2248 https://www.science.org/doi/10.1126/sciadv.adg2248
[13] Nathan J. Cheetham, Rose Penfold, Valentina Giunchiglia, Vicky Bowyer, et al. The effects of COVID-19 on cognitive performance in a community-based cohort: a COVID symptom study biobank prospective cohort study. The Lancet. Open Access Published:July 21, 2023 DOI:https://doi.org/10.1016/j.eclinm.2023.102086
[14] Douglas B. Kell, Gert Jacobus Laubscher, Etheresia Pretorius; A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications. Biochem J 25 February 2022; 479 (4): 537–559. doi: https://doi.org/10.1042/BCJ20220016
[15] Bozzani A, Arici V, Franciscone M, Ticozzelli G, Sterpetti AV, Ragni F. COVID-19 patients with abdominal aortic aneurysm may be at higher risk for sudden enlargement and rupture. J Vasc Surg. 2022 Jan;75(1):387-388. doi: 10.1016/j.jvs.2021.10.003. Epub 2021 Nov 11. PMID: 34774979; PMCID: PMC8582098.
[16] Mine K, Nagafuchi S, Mori H, Takahashi H, Anzai K. SARS-CoV-2 Infection and Pancreatic β Cell Failure. Biology. 2022; 11(1):22. https://doi.org/10.3390/biology11010022
[17] The associations between COVID-19 diagnosis, type 1 diabetes, and the risk of diabetic ketoacidosis: A nationwide cohort from the US using the Cerner Real-World Data
Qeadan F, Tingey B, Egbert J, Pezzolesi MG, Burge MR, et al. (2022) The associations between COVID-19 diagnosis, type 1 diabetes, and the risk of diabetic ketoacidosis: A nationwide cohort from the US using the Cerner Real-World Data. PLOS ONE 17(4): e0266809. https://doi.org/10.1371/journal.pone.0266809
[18] D’Souza D, Empringham J, Pechlivanoglou P, Uleryk EM, Cohen E, Shulman R. Incidence of Diabetes in Children and Adolescents During the COVID-19 Pandemic: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2023;6(6):e2321281. doi:10.1001/jamanetworkopen.2023.21281
[19] Sharma, C., Bayry, J. High risk of autoimmune diseases after COVID-19. Nat Rev Rheumatol 19, 399–400 (2023). https://doi.org/10.1038/s41584-023-00964-y
[20] U.S. Bureau of Labor Statistics Disability Data as of July 2023, available on the St. Louis Federal Reserve FRED website: https://fred.stlouisfed.org/series/LNU00074597
[21] Reassuring News About AIDS: A Doctor Tells Why You Man Not Be At Risk. Robert E. Gould, M.D. Cosmopolitan Magazine, January, 1988.
[22] Worobey, M., Watts, T., McKay, R. et al. 1970s and ‘Patient 0’ HIV-1 genomes illuminate early HIV/AIDS history in North America. Nature 539, 98–101 (2016). https://doi.org/10.1038/nature19827
[23] CDC HIV Transmission Guidelines: https://www.cdc.gov/hiv/basics/hiv-transmission/ways-people-get-hiv.html
[24] AIDS Expert Sees No Sign of Heterosexual Outbreak. Lawrence K. Altman, New York Times, June 5, 1987
[25] Cosmopolitan Magazine, January 1988, “Reassuring News about AIDS, A Doctor Tells Why You May not Be at Risk”: [ https://pittasra.omeka.net/exhibits/show/asra2021/item/21 ]
[26] An ancient viral epidemic involving host coronavirus interacting genes more than 20,000 years ago in East Asia. Yassine Souilmi, M. Elise Lauterbur, Ray Tobler, Christian D. Huber, Angad S. Johar, David Enard bioRxiv 2020.11.16.385401; doi: https://doi.org/10.1101/2020.11.16.385401
Now published in Current Biology doi: 10.1016/j.cub.2021.05.067