There are three avenues to sars-cov-2 immunity: antibodies, memory B cells, and memory T cells. The (for some, discouraging) fact that Sars-CoV-2 antibodies disappear a few months after infection does not mean that immunity has also gone poof! The body remembers how to make new antibodies if needed. There is evidence of protective immunity in people up to four or eight months after mild or asymptomatic COVID-19.
It is possible to get COVID-19 twice, indicating that the immune response to the initial bout may be inadequate. But the immune response may be more robust the second time around. For most, COVID-19 immunity may last for years. SARS-CoV-2 genes may integrate with human DNA.
Here is lifetime of sars-cov-1 and sars-cov-1 virus on various surfaces. Can the virus survive 28 days on a smooth surface after (an evil and sick) someone sneezes on it? Maybe so. In another study, SARS-CoV-2 in the presence of a soil load persisted for up to 21 days on experimentally inoculated PPE, but lasted less than 1 day on cotton fabric. SARS-CoV-2 RNA was identified on a variety of surfaces in cabins of both symptomatic and asymptomatic infected cruise ship passengers up to 17 days after cabins were vacated. Mild heat may drastically reduce the viable lifetime of the SARS-CoV-2 virus.
Here is how one dies of covid-19 (a great video, though old – that doctor incorrectly states that COVID-19 does not spread via aerosols). Patients may experience relatively mild, flu-like symptoms for as long as a week before symptoms of ARDS begin, and its onset is usually sudden, without warning. A distinguishing feature of COVID-19 is the order in which symptoms first appear. Typically, patients will experience fever, cough, muscle pain and then nausea, and/or vomiting, and diarrhea. This is the order in which COVID-19 symptoms appear. The COVID-19 epidemic is real and deadly. You do not want to mess with this virus. Funerals are for the living.
Even apparently healthy people can shed Covid-19 virus. As little as 13% of people who get the coronavirus develop symptoms. As many as 50 % of people with COVID-19 aren’t aware they have the virus. Another study pegged the proportion at 1/3. In some, melatonin produced in the lung acts as a barrier against SARS-CoV-2, preventing the virus from entering the epithelium, activating the immune system and triggering the production of antibodies. In the young, it is 80%. Some can asymptomatically shed virus for weeks, such as this lady. Lack of recognition of asymptomatic sickies contributed to the explosive nature of the COVID-19 pandemic.
Temperature checks may be close to useless.
COVID-19 is much worse than the flue.
Here is what we know about how the SARS-CoV-2 virus infects humans.
COVID and the brain
COVID-19 can be a neurological threat for some patients. The neurological threat may be mostly due to excessive, lengthy brain inflammation via the nose, but even mild COVID-19 infections may have negative effects on the brain long term – no brain infection necessary.
SARS-CoV-2 infection is associated with a wide spectrum of neurological syndromes affecting the whole neuraxis, including the cerebral vasculature and, in some cases, responding to immunotherapies. Now we have pictures of COVID-19 brain damage. The high incidence of acute disseminated encephalomyelitis, particularly with haemorrhagic change, is striking. Brain fog in recovered patients my indicate PTSD. This complication was not related to the severity of the respiratory COVID-19 disease. But this study claims that neurological complications have been reported in 34.6 % patients with severe COVID-19 and include stroke, headache, and seizures. Some experience severe psychosis. A research review led by Oxford Brookes University has found a large proportion of COVID-19 survivors will be affected by neuropsychiatric and cognitive complications.
“We had expected that neurological and psychiatric symptoms would be more common in severe covid-19 cases, but instead we found that some symptoms appeared to be more common in mild cases,” said Jonathan Rogers at University College London, the lead author of this study. This microscopic video shows the coronavirus causing cell fusion and death in bat brain cells. It is entirely possible that this also happens in human brains, which may account for some of the cognitive deficits in COVID-19 survivors. SARS-CoV-2 spike protein S may spread, prion-like, in the human brain.
Using both mouse and human brain tissue, researchers at Yale School of Medicine have discovered that SARS-CoV-2 can directly infect the central nervous system and have begun to unravel some of the virus’s effects on brain cells. SARS-CoV-2 enters lung cells by binding to a protein called ACE2, but whether this protein is present on the surface of brain cells is unclear. The Yale team determined that the ACE2 receptor is, in fact, expressed by both astrocytes and neurons and that blocking this protein prevents the virus from human brain organoids.
Cognitive impairment as a result of severe COVID-19 is similar to that sustained between 50 and 70 years of age and is the equivalent to losing 10 IQ points, say a team of scientists from the University of Cambridge and Imperial College London. While even mild cases can lead to persistent cognitive symptoms, between a third and three-quarters of hospitalised patients report still suffering cognitive symptoms three to six months later.
Long COVID may be due to infection causes brain inflammation and even cell death, among other forms of brain injury. Prolonged inflammation after SARS-CoV-2 infections caused permanent damage to lungs and kidneys, affected the brain, and correlated with behavioral changes in hamsters.
SARS-CoV-2 can infect astrocytes, a type of cell that’s abundant in the brain and has many functions. “Astrocytes do quite a lot that supports normal brain function,” including providing nutrients to neurons to keep them working, says Arnold Kriegstein, a neurologist at the University of California, San Francisco. Infected astrocytes could explain some of the neurological symptoms associated with COVID-19, especially fatigue, depression and ‘brain fog’, which includes confusion and forgetfulness.
SARS-CoV-2 can also affect the brain by reducing blood flow to it — impairing neurons’ function and ultimately killing them. Out of the 919,731 individuals that tested for COVID-19 within the study, researchers found that the 43,375 people who tested positive had a 3.5 times increased risk of being diagnosed with Alzheimer’s disease, 2.6 times with Parkinson’s disease, 2.7 times with ischemic stroke and a 4.8 times increased with intracerebral hemorrhage (bleeding in the brain).
Stroke following the diagnosis of COVID-19 is a possible complication of COVID-19 that patients and clinicians should be aware of.
Megakaryocytes have been found in cortical capillaries in 33% of cases examined. Because the standard brain autopsy sections taken sampled at random only a minute portion of the cortical volume, finding these cells suggests the total burden could be considerable. By occluding flow through individual capillaries, these large cells could cause ischemic alteration in a distinct pattern, potentially resulting in an atypical form of neurologic impairment.
“We discovered that SARS-CoV-2 infection significantly altered Alzheimer’s markers implicated in brain inflammation and that certain viral entry factors are highly expressed in cells in the blood-brain barrier,” explained Dr. Cheng. “These findings indicate that the virus may impact several genes or pathways involved in neuroinflammation and brain microvascular injury, which could lead to Alzehimer’s disease-like cognitive impairment.” Patients hospitalized for COVID-19 had higher levels over the short term of blood proteins known to rise with neurological damage than non-COVID-19 patients diagnosed with Alzheimer’s disease.
COVID-19 can damage the blood-brain barrier.
A study of 81,337 participants showed that people who had recovered from COVID-19, including those no longer reporting symptoms, exhibited significant cognitive deficits versus controls when controlling for age, gender, education level, income, racial-ethnic group, pre-existing medical disorders, tiredness, depression and anxiety.
Hospitalized patients were more likely to have impairments in attention, executive functioning, category fluency), memory encoding, and memory recall than those in the outpatient group. Patients treated in the ED were more likely to have impaired category fluency and memory encoding than those treated in the outpatient setting.
Of course, severe lung damage is a common COVID-19 symptom via aberrant phosphorylation. We know that when you have the COVID infection you have trouble breathing and that’s because there’s infection in your lung, but an additional explanation is that the virus enters the respiratory centers of the brain and causes problems there as well. Severe lung inflammation and prolonged respiratory failure persist in COVID-19 even after the viral infection is no longer detectable. One-third of patients hospitalized with severe COVID-19 still have lung changes after a year.
SARS-CoV-2 infects and destroys the alveoli, the tiny sacs in the lungs that shuttle oxygen into the bloodstream. As the cellular barrier dividing these sacs from blood vessels break down, liquid from the vessels leaks in, blocking oxygen from getting to the blood. Other cells, including white blood cells, plug up the airway further.
30 to 80% of people with COVID-19 report loss of smell, known as anosmia. The likely targets of the SARS-CoV-2 virus are supporting cells in the nose that support growth of the nerve cells that allow us to smell. Researchers think that if the virus infects these support cells, they no longer provide nutrients and structural support to the olfactory neurons, leaving them damaged and unable to transmit smells from the nose to the brain.
Here is a list and a chart of long-term COVID-19 effects. Over 75% of patients admitted to hospital with COVID-19 have abnormal patient-reported outcome measures 3 months after symptom onset, with a third of patients reporting at least moderate impairment in major dimensions of quality of life. Over half of hospitalized COVID-19 patients in a new study are suffering long-term fatigue. Hospitalization appears to increase the chance of long COVID. In chronic fatigue syndrome we don’t know the cause, although it’s thought that infection can be a trigger. In long COVID we know people have had a specific infection, but we don’t know why symptoms linger. Dr. Fauci said that people with Covid-19 can continue to suffer from symptoms for up to nine months after the initial infection,This fellow used positive thinking to recover faster from long covid. Long COVID tends to affect older people more often. Hospitalized patients who have survived hospital discharge think ‘woohoo, I’m through the worst of it’. But actually, that’s not the end of the story by a long shot. Some long – COVID sufferers feel better after vaccination.
In this study, among COVID-19 survivors (mean [SD] age: 46.3 [19.8], 55.6% female), 57.00% had one or more long-COVID feature recorded during the whole 6-month period (i.e., including the acute phase), and 36.55% between 3 and 6 months.
Compared with the 2020 comparison group, COVID-19 patients were at increased risk of developing a range of conditions including respiratory failure (an extra 7.55 per 100 people), fatigue (an extra 5.66 per 100 people), high blood pressure (an extra 4.43 per 100 people), and mental health diagnoses (an extra 2.5 per 100 people) in the months after initial infection.
As much as 30 per cent of the health burden of covid-19 could be a result of lasting effects that need long-term care, rather than deaths. Another analysis pegs the long COVID ratio at 6%.The overall magnitude of these lingering effects, which can range from fatigue to cardiovascular disease, has been greatly underestimated, so the impact on younger people is greater than thought.
Long-COVID has been given a formal name; post-acute sequelae of SARS-CoV-2 infection, or PASC. (Sequelae is a fancy word for after effects.) There are two theories on long COVID: One is that the virus loiters for longer in some kind of reservoir, than you’d like, the other is that it does nasty things to the immune system like causing autoimmunity. Here are additional long-COVID risk factors.
Significant numbers of people who contract the disease report debilitating and varied symptoms weeks and months after recovering. The most commonly reported symptoms were fatigue, feeling unwell after physical or mental exertion and brain fog. Previous research showed that fatigue is the most common symptom among people with long covid, but the new survey also identified many other symptoms such as visual hallucinations, tremors, itchy skin, changes to the menstrual cycle, sexual dysfunction, heart palpitations, bladder control issues, shingles, memory loss, blurred vision, diarrhoea and tinnitus. Why this happens is a mystery.
Penis shrinkage and erectile dysfunction are possible side effects of COVID-19
“We’re really seeing a number of reports of people who report long-term fatigue, headaches, vertigo (and), interestingly enough, difficulties with cognition, hair loss, cardiac issues, and diminished cardiorespiratory fitness. And I think what we’re going to find out is that a large portion ― not all, but a large portion of that ― is likely to relate to the significant cellular-level damage that this virus can cause,” says Dr. Poland. Some of the possible long-term effects can affect even patients who are asymptomatic or have mild cases of COVID-19.
Blood clotting may be a root cause of long COVID syndrome.
SARS-CoV-2-infected cells trigger senescence-like cell-cycle arrest2,3 in neighboring uninfected cells in a paracrine manner via virus-induced cytokine production. The sustained infection-induced paracrine senescence described here may be involved in the long-term inflammation caused by SARS-CoV-2 infection.
COVID-19 may increase one’s chance of Parkinson’s Disease and also Alzheimer’s Disease. In the test tube, the SARS-CoV-2 N-protein interacts with a neuronal protein called α-synuclein and speeds the formation of amyloid fibrils, pathological protein bundles that have been implicated in Parkinson’s disease.
Type 1 and type 2 diabetes can follow a COVID-19 infection, even in kids younger than 18.
COVID and the heart
COVID-19 is also a cardiac threat: as much as 20% of people with mild or no COVID-19 symptoms experience heart damage. Even a mild case of COVID-19 can increase a person’s risk of cardiovascular problems for at least a year after diagnosis A small study suggests that 3/4 of recovered patients have lingering heart damage. One of the complications of COVID-19 is blood clots. Many patients who are hospitalized with COVID-19 have raised troponin levels during the critical illness phase, when the body mounts an exaggerated immune response to the infection. Damage includes inflammation of the heart muscle (myocarditis), scarring or death of heart tissue (infarction), restricted blood supply to the heart (ischaemia) and combinations of all three. COVID-19 can kill heart muscle cells, and interfere with contraction. Among patients with COVID-19, the incidence of myocarditis (like this young lady) is less than 5%. Many people who die of COVID-19 have the virus in their hearts.
An extra 2.7 vaccinated individuals in 100,000 were diagnosed with myocarditis compared to the unvaccinated population who hadn’t caught the disease. Most excess cases were among men aged 20 – 34. However, even if myocarditis was your only fear, it would still be advisable to get the vaccine anywhere COVID-19 is common. Among unvaccinated people who caught the disease the excess rate was 11 per 100,000 – four times as high.
For every 10 million people vaccinated with the AstraZeneca vaccine, the scientists found that those with COVID-19 are almost nine times more likely to experience thrombocytopenia than those who received one dose of the jab. The risk of blood clots in the veins was also 200 times lower than the risk following SARS-CoV-2 infection in the same group.
Three-quarters of people who died of COVID-19 harbored the SARS-CoV-2 virus in their hearts, according to the most detailed study of cardiac tissue to date. Those people were also more likely than patients without cardiac invasion to experience abnormal heart rhythms before they died.
The first large study to assess cardiovascular outcomes 1 year after SARS-CoV-2 infection has demonstrated that the virus’ impact is often lasting. In an analysis of more than 11 million U.S. veterans’ health records, researchers found the risk of 20 different heart and vessel maladies was substantially increased in veterans who had COVID-19 1 year earlier, compared with those who didn’t. The risk rose with severity of initial disease and extended to every outcome the team examined, including heart attacks, arrhythmias, strokes, cardiac arrest, and more. Even people who never went to the hospital had more cardiovascular disease than those who were never infected.
Autoimmune disorders can develop as a result of COVID-19 infection.
A cross-sectional survey of more than 1,000 Bangladeshi adult coronavirus patients over the course of one month showed that 48% of respondents were categorized as having moderate to severe depression.
COVID-19 has been linked with eye abnormalities like conjunctivitis, also known as pink eye, and retinopathy, a disease of the retina that can result in a loss of vision.
A less common COVID-19 symptom are rashes of various forms. Being able to identify the effects of COVID-19 on the skin may allow cases to be spotted earlier – or even picked up altogether in people who are otherwise asymptomatic. This could help limit transmission.
Cardiometabolic diseases including heart disease, obesity, hypertension and type 2 diabetes, are at the crest of an impending tsunami of chronic health conditions as a result of the SARS-CoV-2 pandemic that will affect society for decades.
In the United States children represent about 10% of all COVID-19 cases. Children get sick and die from COVID-19 far less often than adults do, though that does not mean they are immune. Maybe the reason children can neutralize the virus so fast is that their T cells are relatively naive. Because children’s T cells are mostly untrained, they might have a greater capacity to respond to new viruses. Children’s ability to neutralize the virus might also be linked to the fact that they have a strong innate immune response from birth. Also, children’s noses also contain fewer ACE2 receptors.
Risk of death in children is far lower than in adults, but some children have died of COVID-19. Children who are Hispanic, Black, or American Indian or Alaska native are at higher risk for severe disease and death. Research also suggests disproportionately higher rates of COVID-19 in Hispanic and non-Hispanic Black children than in non-Hispanic white children. Hispanic and non-Hispanic Black children also have had higher rates of hospitalization.
Children with underlying conditions, such as obesity, diabetes and asthma, are at higher risk of serious illness with COVID-19. Children who have congenital heart disease, genetic conditions or conditions affecting the nervous system or metabolism are also at higher risk of serious illness with COVID-19. Rarely, some children might also develop a serious condition that appears to be linked to COVID-19. Post-COVID Multisystem inflammatory syndrome can severely damage children’s hearts. The CDC advises parents or caregivers to contact a doctor right away if kids have fever, abdominal pain, vomiting, diarrhea, neck pain, rash, bloodshot eyes or extra tiredness.
Research also suggests disproportionately higher rates of COVID-19 in Hispanic and non-Hispanic Black children than in non-Hispanic white children. Hispanic and non-Hispanic Black children also have had higher rates of hospitalization. This is due, no doubt, to structural inequality in access to healthcare, as well as quality of life.
Changes in the concentration of antibodies against SARS-CoV-2 over time in children were found to be similar to adults up to three months after infection.
The B.1.1.7 variant does not result in an appreciably different clinical course to the original strain in children.
Compared with adults, children with nasopharyngeal swabs that tested positive for SARS-CoV-2 were less likely to grow virus in culture, and had higher cycle thresholds and lower viral concentrations, suggesting that children are not the main drivers of SARS-CoV-2 transmission.
Long-hauler syndrome can also affect the young. Post-COVID recovery programs offer hope to the so-called long-haul COVID patients, or long haulers. Because COVID’s “long-haul” condition is so new, health care providers are writing the script, as they go, for how best to treat people who have it. Like long Covid in adults, there is no way now to predict who might be vulnerable to later difficulties.
“You can get Covid at 18 months of age,” Audrey John, chief of pediatric infectious diseases at the Children’s Hospital of Philadelphia, pointed out. “Maybe you can’t tell us that you have a little brain fog. Maybe you can’t tell us that you just don’t feel great. But whether those kids grow like they’re supposed to, develop language like they’re supposed to, go on to be successful in school like they’re supposed to — we’re not going to learn for a long time.”
Severe outcomes in children were categorized as cardiac events, such as myocarditis, neurological issues, such as encephalitis, respiratory problems, such as pneumonia, infectious issues, such as sepsis, and death.
The South African Strain of SARS-CoV-2
The first two cases of B.1.351 (from South Africa) were reported in the U.S. on Thursday (Jan. 28) in South Carolina. This variant does appear to spread more easily, with studies finding that it is about 50% more transmissible than earlier strains of the coronavirus.
The E484K mutation in this strain may reduce the ability of antibodies from natural COVID-19 infection to neutralize the virus. In a study of 44 people in South Africa who were previously infected with COVID-19 earlier in the pandemic, more than 90% showed reduced immunity against the new variant when researchers tested their blood, and nearly half had no protection against it, according to USA Today.
Even more alarming is the finding that current COVID-19 vaccines may not work as well against this variant. BUT, “You could diminish the vaccine-induced antibody efficacy by a few fold and still be well within the protective range,” according to Dr. Anthony Fauci.
Estimates of the predicted coronavirus death toll have little meaning. Viral load may predict mortality, as may blood type, age, and gender. The lethality of COVID-19 may also depend on one’s genes, many of which have been poorly studied. even when one is otherwise young and of robust health. Genes involved include TYK2, DPP9, OAS, and IFNAR2. This may have a lot to do with the innate (vs. adaptive) immune system – see above. But there are risk factors that we can control (sort of): obesity, history of exercise, and good nutrition. COVID-19 could be about 10 times more deadly than the seasonal flu.
The CDC reports the leading underlying medical conditions related to coronavirus deaths were:
Influenza and pneumonia.
Vascular and unspecified dementia.
Intentional and unintentional injury, poisoning and other adverse events.
Being male is a COVID-19 hazard.
Also, of course, advanced age.
Those with blood type A are vulnerable.
Slow walkers are more likely to get severely sick and die from COVID-19.
Being obese is a COVID-19 hazard.
SARS-CoV-2 specific antibodies are only detectable for a few months in many people who have survived COVID-19 and may therefore only provide temporary protection against re-infection. A decline in antibodies is very normal. After the antibody response decreases over time, the body also has immune cells called memory B cells at the ready. If a person encounters SARS-CoV-2 again, these memory B cells could reactivate and produce SARS-CoV-2 antibodies to fight re-infection.
Infectiousness peaks around a day before symptom onset and declines within a week of symptom onset, and no late linked transmissions (after a patient has had symptoms for about a week) have been documented. In a paper that is the first large study to capture the extraordinary extent to which COVID-19 hinges on “superspreading,” in which a small percentage of the infected population passes the virus on to more people, researchers found that 71% of infected individuals did not infect any of their contacts, while a mere 8% of infected individuals accounted for 60% of new infections. Children and young adults were found to be potentially much more important to transmitting the virus—especially within households—than previous studies have identified, according to a paper by researchers from the United States and India. Children and young adults were much more likely to contract coronavirus from patients their own age, the study found.
There are genetic immune system vulnerabilities that cause one to suffer more when afflicted by COVID-19. The problem is the one does not know if these vulnerabilities are present until SARS-CoV-2 strikes. Then it is too late. None of us can be smug about this – not even kids. We are all vulnerable – some fatally so. This is why the elderly are so threatened by COVID-19.
The origin of SARS-CoV-2
An analysis of what we know about the earliest COVID-19 cases has strengthened the argument that the coronavirus pandemic began when animals at the Huanan market in Wuhan, China, passed the virus on to people. Among other things, it concludes that the first case was a woman who worked as a seafood vendor at the market, who became ill on 11 December 2019.
Dr. Fauci says that SARS-CoV-2 was not made in a lab. SARS-CoV-2 is unlikely to be a result of genetic engineering or a purposefully manipulated virus. Experts from WHO re-affirmed this fact. But direct bat-to-human transmission is unlikely, which shifts suspicion to laboratories. The head of the WHO said last month that he remained unconvinced by the investigation, especially because it was difficult for the investigators to access any raw data, and suggested that the lab leak hypothesis warranted further attention.
Did SARS-CoV-2 come from bats or other animals?
Bats, are still suspected as the natural reservoir of this, or a related, virus. In fact, the “mother” of all SARS-CoV-2 genomes has been traced to bats. A SARS-CoV-2 relative has been found lurking in frozen bats from Cambodia. SARS-CoV-2 did not need to change much to leap from bats to humans.
In some expert’s opinion, it is the global wildlife trade that brought this pandemic on. An intriguing study of serologic testing of U.S. blood donations identified SARS-CoV-2-reactive antibodies in December 2019-January 2020 – before such was identified in China. An Italian study found antibodies in samples dated as early as September 2019. Using molecular dating tools and epidemiological simulations, researchers at University of California San Diego School of Medicine, with colleagues at the University of Arizona and Illumina, Inc., estimate that the SARS-CoV-2 virus was likely circulating undetected for at most two months before the first human cases of COVID-19 were described in Wuhan, China in late-December 2019.
Here is an important, readable paper on the probable animal origin of SARS-CoV-2.
Scientists have found three viruses in bats in Laos that are more similar to SARS-CoV-2 than any known viruses. Researchers say that parts of their genetic code bolster claims that the virus behind COVID-19 has a natural origin — but their discovery also raises fears that there are numerous coronaviruses with the potential to infect people.
If confirmed by further analyses, the findings would add weight to the hypothesis that the pandemic originated in multiple markets in Wuhan, China, and make the hypothesis that SARS-CoV-2 escaped from a laboratory less likely.
Did SARS-CoV-2 crawl out of a lab?
It is possible, as stated here, that circulating COVID-19 originated as a failed attempt at a “live vaccine”.
We must take hypotheses about both natural and laboratory spillovers seriously until we have sufficient data. A proper investigation should be transparent, objective, data-driven, inclusive of broad expertise, subject to independent oversight, and responsibly managed to minimize the impact of conflicts of interest.
The way that virologists do in fact get spike proteins to bind to chosen targets, which is not by calculation but by splicing in spike protein genes from other viruses or by serial passage. With serial passage, each time the virus’s progeny are transferred to new cell cultures or animals, the more successful are selected until one emerges that makes a really tight bind to human cells. Natural selection has done all the heavy lifting. (This is a gain-of-function experiment: no need for genetic tinkering that would leave “footprints”. ) A top NIH official admitted that U.S. taxpayers funded gain-of-function research on bat coronaviruses in Wuhan. Now we have clarification: NIH-funded research was not gain-of-function aimed at enhancing the SARS-SoV-2 virus.
15 months after the SARS2 pandemic began, and after a presumably intensive search, Chinese researchers have failed to find either the original bat population, or the intermediate species to which SARS2 might have jumped, or any serological evidence that any Chinese population, including that of Wuhan, had ever been exposed to the virus prior to December 2019. Natural emergence remained a conjecture which, however plausible to begin with, had gained not a shred of supporting evidence in over a year.
Their work (in Wuhan) focused on enhancing the ability of bat viruses to attack humans so as to “examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs [coronaviruses].” In pursuit of this aim, in November 2015 they created a novel virus by taking the backbone of the SARS1 virus and replacing its spike protein with one from a bat virus (known as SHC014-CoV). This manufactured virus was able to infect the cells of the human airway, at least when tested against a lab culture of such cells. Here is why gain-of-function research is advocated.
(There is a) long history of viruses escaping from even the best run laboratories. The smallpox virus escaped three times from labs in England in the 1960’s and 1970’s, causing 80 cases and 3 deaths. Dangerous viruses have leaked out of labs almost every year since. Coming to more recent times, the SARS1 virus has proved a true escape artist, leaking from laboratories in Singapore, Taiwan, and no less than four times from the Chinese National Institute of Virology in Beijing. There is now evidence that researchers at the Wuhan virology lab allegedly fell ill with COVID-like symptoms in November 2019.
Now, China is not allowing any more WHO experts into the Wuhan lab, calling any continuing investigation “disrespectful“.
From its very first appearance, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 with late stage SARS1, which by then was well adapted to human cells, and found that the two viruses were similarly well adapted. “By the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV,” The Covid-19 pathogen has a genetic footprint that has never been observed in a natural coronavirus (?).
Dr. Hansen explains the above really well here.
A Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis but instead is laboratory derived.
Is the debate over SARS-CoV-2 origins worth having at this point?
The future of viral epidemics.
SARS-CoV-2 is constantly evolving, as viruses do. Common cold viruses may have first emerged as pandemic Corona viruses, but will not remain as a pandemic driver in future (one would hope). Due to the world-wide chronically low vaccination rates and the continued mutation of SARS-CoV-2, COVID-19 will, likely, never completely go away.
Industrial poultry farming may bring worse fatality than SARS-CoV-2. It is clear that the Hunan outbreak of COVID-19 was just a symptom of a sickness, not a cause of it. For two decades, evidence has been building of the link between how we encroach on, degrade and exploit the natural world and the risk of “zoonoses” – animal diseases that spill over into humans. “The same human activities that drive climate change and biodiversity loss also drive pandemic risk through their impacts on our environment. Changes in the way we use land; the expansion and intensification of agriculture; and unsustainable trade, production and consumption disrupt nature and increase contact between wildlife, livestock, pathogens and people. This is the path to pandemics.” About five new infectious diseases in people are identified every year, and 70 per cent of emerging diseases are caused by microbes of animal origin. Human, animal, plant and environmental health and well-being are all intrinsically connected and profoundly influenced by human activities. Using recent estimates of the rate of increase in disease emergence from zoonotic reservoirs associated with environmental change, we estimate that the yearly probability of occurrence of extreme epidemics can increase up to threefold in the coming decades.
Herbs from Traditional Chinese Medicine might be helpful vs. COVID-19.
Hydroxychloroquine is not helpful versus covid-19, proven again by a study of 667 patients, and again by 671 households. Hydroxychloroquinet can cause heart problems. FDA revokes emergency use ruling for hydroxychloroquine, the drug touted by Trump as a Covid-19 therapy. HQC can block the coronavirus from infecting kidney cells from the African green monkey. But it does not inhibit the virus in human lung cells – the primary site of infection for the SARS-CoV-2 virus. A WHO expert panel strongly advises against use of hydroxychloroquine to prevent COVID-19.
Ivermectin is not a wonder drug vs. COVID-19. We need more studies before moving forward on Ivermectin, though there have been some encouraging studies done in third-world countries, though India has now dropped the use of Ivermectin and Hydroxychloroquine (HCQ) drugs from their revised guidelines for the treatment of COVID-19. No wonder: dodgy science was behind published, now retracted, studies supporting ivermectin.
Among adults with mild COVID-19, a 5-day course of ivermectin, compared with placebo, did not significantly improve the time to resolution of symptoms. The findings do not support the use of ivermectin for treatment of mild COVID-19, although larger trials may be needed to understand the effects of ivermectin on other clinically relevant outcomes. A Merck analysis finds no scientific basis for a potential therapeutic effect against COVID-19 from pre-clinical studies, no meaningful evidence for clinical activity or clinical efficacy in patients with COVID-19 disease, and a concerning lack of safety data in the majority of studies. Another analysis in Salon came to the same conclusion.
The FDA says that you should never use ivermectin to treat or prevent COVID-19. Ivermectin has been at the center of scientific fraud. Ivermectin medicines are not authorized for use in COVID-19 in the EU, and European Medicines Agency has not received any application for such use. All of the positive studies of ivermectin were done in countries in which the population likely suffers from a high parasitic load. Eliminating a patient’s parasites can help them cope with COVID-19. The (highly respected) Cochrane analysis found not benefit of ivermectin vs. COVID-19.
Even at twice the dose normally given to people (for parasites), Ivermectin was ineffective vs. COVID-19.
Never use medications intended for animals on yourself. Ivermectin preparations for animals are very different from those approved for humans. You can also overdose on ivermectin, which can cause nausea, vomiting, diarrhea, hypotension (low blood pressure), allergic reactions (itching and hives), dizziness, ataxia (problems with balance), seizures, coma and even death.
Remdesivir is not helpful for faster recovery from COVID-19.
Evidence-based recommendations for the resumption of sports and exercise after COVID-19 are currently limited and continue to evolve . Guidance published in the Lancet Respiratory Medicine recommend prolonged rest after infection, 10 or more days from symptom onset plus 7 days from symptom resolution . These recommendations, however, do not address those with more severe disease manifestations. Strenuous exercise too soon after a viral infection that inflamed the heart can risk serious long-term heart damage. Here is sports guidance for young people. But exercise may may treat acute respiratory distress syndrome (ARDS).
Worldwide, scientists have not documented any instances of outdoor transmission unless people were in close conversation. Existing evidence supports the wide-held belief that risk of SARS-CoV-2 transmission is lower outdoors.
COVID-19 and pregnancy.
Misinformation is rampant. This glut of misinformation is a public health disaster. Especially damaging is vaccine misinformation. False information on the web is propagated mainly by a relatively small number of super-spreaders, often high-profile partisan media outlets, social-media influencers (like Joe Rogan) and political figures, such as Trump. Timing matters when correcting fake news. Coronavirus myths. Here is where to get your misinformation. Conspiracy theories are also damaging. Why some deny that COVID-19 is serious and deadly, even while dying from it.. Part of the problem is misinterpretation of statistics and testing results.
RT-qPCR: facts and fallacies.
Those adhering to COVID-19 conspiracy beliefs prospectively predicted a decreased likelihood of getting tested for corona; if tested, an increased likelihood of the test coming out positive; and, an increased likelihood of having violated corona regulations, deteriorated economic outcomes (job loss; reduced income), experiences of social rejection, and decreased overall well-being. Most of these effects generalized to a broader susceptibility to conspiracy theories (i.e. conspiracy mentality).
Recognising the acute threat of the infodemic and its potential to undermine hard fought gains against COVID-19, several international organizations (eg, WHO, the UN, UNICEF, UN Development Programme, UNAIDS, The United Nations Educational, Scientific and Cultural Organization, and the International Telecommunication Union) issued a joint statement calling on member states, platforms, researchers, and civil society to collaborate on strategies and tools to combat misinformation, while also recognising the need to respect freedom of expression.
Wow. Here is Dr. Fauci in 1984. Dr. Fauci recently won the first-ever presidential citation for exemplary leadership. He is a smart guy. He has been awarded the 2020 John Maddox Prize for standing up for science during the coronavirus pandemic. Here is his professional story.