JAMA just published their own review of the pathophysiology of the virus. I’ll highlight the important parts.
In later stages of infection,when viral replication accelerates, epithelial-endothelial barrier integrity is compromised. In addition to epithelial cells, SARS-CoV-2 infects pulmonary capillary endothelial cells, accentuating the inflammatory response and triggering an influx of monocytes and neutrophils. Autopsy studies have shown diffuse thickening of the alveolar wall with mononuclear cells and macrophages infiltrating airspaces in addition to endothelialitis.12 Interstitial mononuclear inflammatory infiltrates and edema develop and appear as ground-glass opacities on computed tomographic imaging. Pulmonary edema filling the alveolar spaces with hyaline membrane formation follows, compatible with early-phase acute respiratory distress syndrome (ARDS).12 Bradykinin-dependent lung angioedema may contribute to disease.13 Collectively, endothelial barrier disruption, dysfunctional alveolar-capillary oxygen transmission, and impaired oxygen diffusion capacity are characteristic features of COVID-19. In severe COVID-19, fulminant activation of coagulation and consumption of clotting factors occur.14,15 A report from Wuhan, China, indicated that 71% of 183 individuals who died of COVID-19 met criteria for diffuse intravascular coagulation.14 Inflamed lung tissues and pulmonary endothelial cells may result in microthrombi formation and contribute to the high incidence of thrombotic complications, such as deep venous thrombosis, pulmonary embolism, and thrombotic arterial complications (eg, limb ischemia, ischemic stroke, myocardial infarction) in critically ill patients.16 The development of viral sepsis, defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, may further contribute to multiorgan failure.
The most common symptoms in hospitalized patients are fever (up to 90% of patients), dry cough (60%-86%), shortness of breath (53%-80%), fatigue (38%), nausea/vomiting or diarrhea (15%-39%), and myalgia (15%-44%).18,44-47,49,50 Patients can also present with nonclassical symptoms, such as isolated gastrointestinal symptoms.18 Olfactory and/or gustatory dysfunctions have been reported in 64% to 80% of patients.51-53 Anosmia or ageusia may be the sole presenting symptom in approximately 3% of patients.53 Complications of COVID-19 include impaired function of the heart, brain, lung, liver, kidney, and coagulation system. COVID-19 can lead to myocarditis, cardiomyopathy, ventricular arrhythmias, and hemodynamic instability.20,54 Acute cerebrovascular disease and encephalitis are observed with severe illness (in up to 8% of patients).21,52 Venous and arterial thromboembolic events occur in 10% to 25% in hospitalized patients with COVID-19.19,22 In the ICU, venous and arterial thromboembolic events may occur in up to 31% to 59% of patients with COVID-19.16,22 Approximately 17% to 35% of hospitalized patients with COVID-19 are treated in an ICU, most commonly due to hypoxemic respiratory failure. Among patients in the ICU with COVID-19, 29% to 91% require invasive mechanical ventilation.47,49,55,56 In addition to respiratory failure, hospitalized patients may develop acute kidney injury (9%), liver dysfunction (19%), bleeding and coagulation dysfunction (10%-25%), and septic shock (6%).18,19,23,49,56 Approximately 2% to 5% of individuals with laboratory confirmed COVID-19 are younger than 18 years, with a median age of 11 years. Children with COVID-19 have milder symptoms that are predominantly limited to the upper respiratory tract, and rarely require hospitalization. It is unclear why children are less susceptible to COVID-19. Potential explanations include that children have less robust immune responses (ie, no cytokine storm), partial immunity from other viral exposures, and lower rates of exposure to SARS-CoV-2. Although most pediatric cases are mild,a small percentage (<7%) of children admitted to the hospital for COVID-19 develop severe disease requiring mechanical ventilation.57 A rare multisystem inflammatory syndrome similar to Kawasaki disease has recently been described in children in Europe and North America with SARS-CoV-2 infection.58,59 This multisystem inflammatory syndrome in children is uncommon (2 in 100 000 persons aged <21 years).60
It's pretty much exactly as I described it from the very beginning. COVID-19 affects all of the major vital organs and also causes strokes and other ischemic events because of how severe the coagulopathy is. 71% of the ICU patients with fatal outcomes had DIC. Diffuse intravascular coagulation is a fancy way of saying “your entire bloodstream is clots”.
Guidance from consensus group and others details on use across settings
www.medpagetoday.com
archived 22 Jul 2020 01:01:47 UTC
archive.is
Of COVID-19's hallmark symptoms, clotting may not rank high in the national consciousness. But it has made quite an impression in-hospital.
"I have never, ever, ever seen such high levels of D-dimer in any of the hundreds of other patients with venous thrombosis that I've seen over the past 15 years," said Behnood Bikdeli, MD, of NewYork-Presbyterian Hospital/Columbia University Irving Medical Center in New York City. "It's just mind-blowing."
Clinicians treating COVID-19 patients have described
pervasive clots in the lungs on autopsy, breakthrough clotting
clogging dialysis lines despite antithrombotic medication, and even
clots forming in real-time during mechanical thrombectomyfor ischemic stroke.
"At this point, even though our knowledge is limited, what we know is highly suggestive of a prothrombotic milieu -- an excess of thrombotic events in the setting of COVID-19, specifically severe COVID-19," said Bikdeli.
The neurotropic nature of the virus is quite firmly established by this point:
archived 17 Jul 2020 15:30:42 UTC
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The SARS-CoV-2 coronavirus attacks the
respiratory system, but there is growing evidence that it also affects the nervous system. Several studies based on thousands of Spanish patients show that most of these individuals developed at least one neurological problem. This manifested itself in a wide range of symptoms, ranging from headaches to comatose states. In a percentage of cases, neurological conditions were even the principal cause of death. Although these symptoms have been attributed to the
body’s excessive immune response to Covid-19, some research indicates that the virus is directly attacking the brain.
“The brain is characterized for being isolated from the bustle of the world. If there is a pathogen in the rest of the body, the blood-brain barrier stops it from entering,” explains Segura. This defense system allows oxygen-filled blood to reach the capillaries and even the neurons, but filters out toxins, bacteria and viruses that travel in the bloodstream. “The rupture of this barrier is an effect that we have not seen before,” he adds. For Segura, finding the endothelial cells (the thin layer of cells that line the interior surface of blood vessels) in the samples of analyzed blood tissue could indicate that the coronavirus has overcome the blood-brain barrier, and that the neurological problems have not been caused by weakness from the
immune system’s response to Covid-19.
According to Segura, the world is facing “a respiratory virus that is also neurotoxic.”
Coronavirus disease 2019 (COVID-19), a disease caused by the novel betacoronavirus (SARS-CoV-2), has become a global pandemic threat. The potential involvement of COVID-19 in central nervous system (CNS) has attracted considerable attention due to neurological manifestations presented throughout...
link.springer.com
Coronavirus disease 2019 (COVID-19), a disease caused by the novel betacoronavirus (SARS-CoV-2), has become a global pandemic threat. The potential involvement of COVID-19 in central nervous system (CNS) has attracted considerable attention due to neurological manifestations presented throughout the disease process. In addition, SARS-CoV-2 is structurally similar to SARS-CoV, and both bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter human cells. Thus, cells expressing ACE2, such as neurons and glial cells may act as targets and are thus vulnerable to SARS-CoV-2 infection. Here, we have reviewed the neurological characteristics of COVID-19 and summarized possible mechanisms of SARS-CoV-2 invasion of the CNS. COVID-19 patients have presented with a number of different neurological symptoms such as headache, dizziness, hyposmia, and hypogeusia during the course of illness. It has also been reported recently that some cases of COVID-19 have presented with concurrent acute cerebrovascular disease (acute ischemic stroke, cerebral venous sinus thrombosis, cerebral hemorrhage, subarachnoid hemorrhage), meningitis/encephalitis, acute necrotizing hemorrhagic encephalopathy, and acute Guillain–Barré syndrome. Furthermore, SARS-CoV-2 RNA detected in a cerebrospinal fluid specimen of a patient with COVID-19 have provided direct evidence to support the theory of neurotropic involvement of SARS-CoV-2. However, the underlying neurotropic mechanisms of SARS-CoV-2 are yet to be established. SARS-CoV-2 may affect CNS through two direct mechanisms (hematogenous dissemination or neuronal retrograde dissemination) or via indirect routes. The underlying mechanisms require further elucidation in the future.
You can't smell anything. Taste is botched. How depressing, right?Well, yes, that is right. But the real question is, why do you feel depressed when you
www.timesreporter.com
archived 21 Jul 2020 16:04:46 UTC
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You can’t smell anything. Taste is botched. How depressing, right?
Well, yes, that is right. But the real question is, why do you feel depressed when you have COVID-19 with smell loss? The answer could be that the disease caused by the novel coronavirus might be attacking your brain.
New research led by Dr. Ahmad Sedaghat, an ear, nose, throat specialist and internationally recognized expert in rhinology at the University of Cincinnati College of Medicine, indicates that COVID-19 may not only be knocking out the sense of smell for some but also using the olfactory tract as a way to get into the brain.
And once in the central nervous system, the illness might be causing the depression and anxiety that those with smell loss exhibit. No one will know that for sure until more research is done.
“It’s our hypothesis,” Sedaghat said last week.
The idea came to him after he and his team looked at the results of a phone study in which people with the disease were asked about feelings of depression and anxiety.
The patients reporting psychological distress were those with smell inhibition and problems associated with it.
Labored breathing? Days of high fever? These life-threatening symptoms weren’t linked with depression or anxiety.
“It is kind of absurd and ridiculous given how severe and how dire these symptoms are,” said Sedaghat, associate professor of otolaryngology and director of rhinology, allergy and anterior skull base surgery at Unversity of Cincinnati College of Medicine.
“I would’ve guessed that the symptoms that would be most associated with depressed mood and anxiety would be severe, dire symptoms: shortness of breath, coughing, fever,” Sedaghat said.
He called the results of the research “shocking.”
But then again, there’s been previous evidence that other coronaviruses, such as the severe acute respiratory syndrome (SARS) of the 2003 outbreak, have the potential to infect the brain. Mouse studies showed the virus can enter the brain when inoculated intranasally.
Sedaghat, who works with European specialists in his field, was among researchers who’d studied the COVID-19 symptom of smell loss during the early weeks when the novel coronavirus was hitting the United States. Europe had been experiencing more cases at first and identified the possible symptom, which has become commonly known.
Sedaghat noted that people were experiencing smell loss early in the disease. That meant it could be used as a screening tool, he said, to identify them as possible COVID-19 sufferers who should stay distanced from other people. The symptom is now commonly considered an indicator of the disease.
The latest phone questionnaire that Sedaghat headed is available online at The Laryngoscope. It looked at characteristics and symptoms of 114 patients actively infected with COVID-19 over six weeks at Kantonsspital Aarau in Aarau, Switzerland.
About 47% of respondents reported at least several days of depressed mood per week, with 21% reporting depressed mood nearly every day. Nearly 45% reported mild anxiety and 10.5%, severe anxiety.
Sedaghat said his research isn’t an end.
“This study raises more questions than produces answers,” he said. But he added, “It gives insight into what is going on with the disease.
COVID-19 sequelae are very similar to SARS. Chronic fatigue syndrome/myalgic encephalomyelitis, persistent lung fibrosis, and mental issues indicative of brain damage (brain fog, cognitive difficulties, depression, etc.).
There is a lot of evidence that
when a severe infection sweeps through the population, ME/CFS will often follow. The Institute of Medicine’s (NAM) 2015 report concluded that ME/CFS may be triggered by a number of acute viral infections, including herpesviruses such as EBV or HHV-6, enteroviruses, and echoviruses. A study on
Epstein-Barr virus, Q Fever, and Ross River virus showed that
~12% of subjects across the board met ME/CFS criteria at 6 months after clearing the infection; and another study of
people with mononucleosis (Epstein-Barr virus) produced identical numbers.
20% of patients with West Nile Virus (n=140)
met the criteria for CFS six months after tests first returned negative for West Nile. There are also a
handful of highly-publicized outbreaksleading to ME/CFS: some of the biggest ones include the Epstein-Barr Viral outbreaks in New York; the Lake Tahoe outbreak in Nevada; and the Royal Free Outbreak in London.
SARS-CoV-2 would not be the first coronavirus to result in documented ME/CFS. Studies have shown that long-lasting disabling symptoms commonly occur in people who contracted two other coronaviruses that cause
SARS and
Middle East Respiratory Syndrome (MERS). In
one study, 27% of SARS survivors were found to meet CFS criteria several years after developing SARS.
That a wide variety of different infectious organisms can lead to the same disease-state may seem surprising – but ME/CFS may be caused by the body’s unexpectedly uniform reaction to any number of assaults.
Dr. Ian Lipkin, the Director of the Center for Infection and Immunity and a coronavirus and ME/CFS expert, stated in an interview with #MEAction, “I wouldn’t suggest that coronavirus is the cause of ME; rather, innate immune mechanisms in response to a virus may cause it, meaning that many viruses can probably [initiate ME/CFS].”One study that he was a co-author of found that getting
H1N1 doubles a person’s risk of developing ME/CFS.
Doctors are starting to see many
emerging long-term effects of COVID-19 and in
Italy, neurologists have already created a separate neuro unit for COVID-19 patients, who are being treated for “stroke, delirium, epileptic seizures, and non-specific neurologic syndromes that look very much like encephalitis,”
according to Neurology Today. Professor Chris Ponting, Chair of Medical Bioinformatics at University of Edinburgh, explained to #MEAction that he would “expect that [of the] people who have COVID-19 symptoms quite severely… about 10% [would] have fatigue-like syndromes after 6 months, given current evidence.”
You do realize that the masks aren't a guarantee from catching the damn thing or giving it to people either, right? Virus particles are so small that they can easily escape the masks ... Especially when dumb people are using their cloth masks and not washing them (which is TOTALLY happening, let's be real here). The masks may even be detrimental to overcoming the pandemic, honestly: Imagine someone touching their dirty fucking mask without realizing how dirty it is and then they touch everything in the grocery store. Considering how the virus lingers on hard surfaces, I don't think I'm out of the realm of reality by expressing that the masks could cause more harm than good in a lot of cases.
Any kind of mask, no matter how piss-poor, even makeshift masks, will help trap droplets and aerosols inside. They can slash transmission, reducing the R0 below the exponential level. However, the key element here is that masking has to be practiced by basically everyone in order for it to be effective.
SARS-CoV-2 does not last very long on surfaces in the real world. The only tests that show it lasting days in detectable amounts are synthetic ones where tons and tons of virions were applied to a surface, far more than a person could exhale or cough onto something. IRL, the time between an infected person touching an object and the object being free of live, detectable virus is something on the order of about two hours maximum. Disinfecting surfaces and washing hands is a good practice, but it’s also a band-aid for the much larger problem of airborne transmission.
The 6-foot social distancing mandate is bullshit and has always been bullshit, because nobody can seem to decide whether or not the virus is airborne or droplet-borne only, and because the WHO has consistently downplayed airborne transmission. Well, guess what? SARS-CoV-2 is, in fact, airborne, it is readily aerosolized by an infected person so much as speaking, and it can linger in the air as an aerosol for hours.
Hundreds of scientists have written to the World Health Organization urging them to update their guidance pertaining to the risk of airborne spread of COVID-19. Health officials originally thought COVID-19 spread primarily through large respiratory droplets, but newer research suggests the virus...
www.healthline.com
archived 21 Jul 2020 16:56:12 UTC
archive.is
The 6-foot rule should be more like 15 feet, especially in enclosed spaces. You know how far away you can smell a freshly-cut onion or orange? That's aerosol distance. People should not be within five yards of each other in an enclosed, poorly-ventilated space.
Almost nobody is denying the existence of this virus, or what it can do to people (and what it has done to people). Statistically speaking, though, the odds are in most people's favor. People want to live their lives normally again, and they're not evil for wanting that.
Also, let's keep in mind that the narrative about the masks has been consistently inconsistent. Of course people are more reluctant and annoyed to wear them now. Can't say that I blame them at all.
A lot of these cloth masks are a bitch to breathe in as well. I know so many people who can't wear the damn things because they can't breathe in them. And if they got the medical grade masks, they'd be called assholes for taking the equipment from hospitals. You just can't win with this.
I never said people were evil for wanting a return to normalcy. The whole situation is tremendously fucked up, and yes, officials
did vacillate on the issue of masks and undermine their credibility as a result. It is unreasonable for people to be blamed for being skeptical about masks when our own officials told us that they don’t work for the sole reason of deceiving us and preventing a run on masks while there was a shortage. However, the science falls on the side of masking being effective. Vietnam—fucking Vietnam, of all places—managed to keep the virus under control. How? Universal masking and quick and effective contact tracing.
Vietnam has had no deaths, and only about 400 cases.
Initial viral load has a high effect on COVID-19 mortality. This is how COVID-19 can have relatively low lethality on average, but wipe out an entire family who are in close contact with each other.
www.cidrap.umn.edu
In-hospital mortality was 35.0% with a high viral load, 17.6% with a medium viral load, and 6.2% with a low viral load. The risk of intubation was also higher in patients with a high viral load, at 29.1%, compared with those with a medium (20.8%) or low viral load (14.9%), the authors found.
The effect on mortality is significant. A high initial viral load was correlated with a 35% rate of mortality for hospitalized patients, while a low initial load was correlated with a 6.2% rate of mortality. Even if the mask doesn’t prevent you from getting infected, if you do get sick, it could reduce the severity of the illness by reducing the initial dose of virus. A larger dose gives Corona-chan a bigger head start.
So 2 articles stuck out at me today
For the first time scientists found Aspergillus latus in a hospital and said the new hybrid fungi is more drug-resistant than its two parents
www.ibtimes.sg
And
Now im no scientician...but this seems to me like AIDS.
We heard rumors early on and i am noticing an alarming trend of stories regarding immune system decline. Some of these stories overseas are completely at odds with what our media is reporting.
Its almost like 2 seperate diseases?
It's not AIDS. It's not a retrovirus. It does, however, suppress the immune system.
Background: The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has posed great threat to human health. T cells play a critical role in antiviral immunity but their numbers and functional state in COVID-19 patients remain...
www.frontiersin.org
SARS-CoV-2 cuts down the body's T lymphocyte population and also inhibits the body's own interferon production, blunting the innate immune response and allowing the virus to replicate with impunity until the adaptive immune response can shut it out (at which point the immune system overreacts in a characteristically SARS-like way with a nasty cytokine storm). This leaves the body vulnerable to various types of secondary bacterial or fungal infections, of course.
On the plus side, there are some new treatments being developed that show great promise.
Synairgen has unveiled an inhaled form of interferon that is apparently very effective:
markets.businessinsider.com
A new vaccine is also being tested; an adenovirus vectored vaccine that induces an immune response to the spike of SARS-CoV-2. It's called ChAdOx1 (Chimpanzee Adenovirus vaccine, Oxford, 1):
Yes. It has Chad in the name.
Did a brief stint in academic science. Virtually everyone in the rank and file research trivialities in cash cow subjects like AIDS, cancer and addiction. Even before I started questioning "the Narrative" my thought was "We have thousands of full time researchers and doctors working on cures round the clock; why haven't we got cures yet?"
When I still listened to Joe Rogan I recalled he liked having doctors and scientists who were researching interventions not reliant on Big Pharma. My own aunt, though an MD and a psychiatrist has gotten all-in on alternative medicine.
There are treatments available that can be effective against COVID-19. It takes years to develop new bioactive compounds and test them for their efficacy as drugs. Many of the ones for COVID-19 are repurposed drugs that we already had. Let me run down the list.
- Mechanical ventilation/intubation. Necessary in many cases due to the severe hypoxemia, but may cause ventilator-induced lung injuries. 70 to 80% of patients who have required intubation have died.
- High-Flow Nasal Cannula. Lower impact than intubation and may deliver just enough oxygen.
- Heparin. Necessary to deal with all the clotting.
- Tissue Plasminogen Activator. Last resort if heparin fails. May cause severe hemorrhaging.
- IV Immunoglobulin. Effective at treating capillary leak and may prevent pulmonary angioedema, but not widely available in the amounts needed.
- Nitric oxide inhalation. Can have a beneficial therapeutic effect and replace lost NO signaling, dilating blood vessels and improving circulation in the lungs.
- Nitric oxide support. Cysteine, arginine, and citrulline supplementation may help counteract the virus’s interference with nitric oxide synthesis.
- Hyperbaric oxygen therapy. May improve nitric oxide production and endothelial health
- Vitamin C and D. May have beneficial antioxidant and anti-inflammatory effects.
- Methylprednisolone. Can reduce inflammation, but also has severe long-term side effects in doses relevant to SARS or COVID, such as osteonecrosis.
- Dexamethasone. Very effective at reducing inflammation and tamping the cytokine storm in COVID-19 patients.
- Budesonide. Inhaled steroid anecdotally reported as effective. Needs further investigation.
- Interferon. Very effective at reducing SARS-CoV-2 replication. Replaces the body’s own deficient interferon (COVID-19 suppresses interferon production). Even better when inhaled in nebulizer form.
- Kaletra. Quite effective HIV combo drug repurposed for COVID-19. Very hard on the organs.
- Hydroxychloroquine. Very modest effectiveness, mainly when given early in the disease course or as a prophylactic. Using it late has no benefit. Chloroquine is hard on the heart, retina, and inner ear.
- Remdesivir. Not very effective. Can cause kidney failure.
- Ivermectin. Effectiveness unclear.
- Camostat. Inhibits activation of SARS-CoV-2 S protein. Effectiveness unclear.
- Tocilizumab. Inhibits Interleukin-6 driven inflammation and reduces cytokine storm symptoms. Effective, but difficult to obtain.
- Meplazumab. Inhibits CD147 activity.
