Googling: “graves disease interferon” yields a number of directly related papers. 
A couple frinds and I were talking about medicines that are on the market that kill / cure diseases and I brought up interferon …My understanding is it pretty brutal but destroys Hep C which until the mid 2000s was thought to be incurable …
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Epidemiologist finds spike of coronavirus cases in those under age 40 -
Dr. Judith Malmgrem published a pre-print report showing nearly 40%
of coronavirus cases after peak in March were in those under 40-years-old.
(May 28, 2020):
A longitudinal cohort analysis of Washington State Department of Health COVID-19 confirmed case age distribution March 1 - April 19 2020 for proportional change over time using chi square tests for significance (N = 13,934).
Results: From March 1st to April 19, 2020 age distribution shifted with a 10% decline in cases age 60 years and older and a 20% increase in age 0-19/20-39 years (chi-square = 223.10, p <.001). Number of cases over the eight-week analysis period were 0-19 years n = 515, 20-39 years n = 4078, 40-59 years n =4788, 60-79 years n = 3221, 80+ years n = 1332.
0-19 years old: 3.696 %
20-39 years old: 29.267 %
40-59 years old: 34.362 %
60-79 years old: 23.116 %
80+ years old: 9.559 %
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With things reopening here in US, people seem to be trying to get “back to normal.” I am still hesitant and avoid going out but a few friends and family have stopped by for an occasional visit lately and now I can’t taste my food. I’m somewhat concerned and hoping it’s just vapor’s tongue.
I guess that’s what I get for trying to be polite and inviting them in… 
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(WIRED, June 1, 2020):
“Meet ACE2, the Enzyme at the Center of the Covid-19 Mystery”
ACE2, which stands for angiotensin-converting enzyme 2, is a protein that sits on the surface of many types of cells in the human body, including in the heart, gut, lungs, and inside the nose. It’s a key cog in a biochemical pathway that regulates blood pressure, wound healing, and inflammation. ACE2’s amino acids form a grooved pocket, allowing it to snag and chop up a destructive protein called angiotensin II, which drives up blood pressure and damages tissues. But angiotensin II isn’t the only thing that fits in ACE2’s pocket. So does the tip of the mace-like spike proteins that project from SARS-CoV-2, the coronavirus that causes Covid-19. Like a key turning in a latch, the virus gains entry to the cell through ACE2, then hijacks the cell’s protein-making machinery to make copies of itself. An infection begins. …
… they found that women and men produced similar amounts of ACE2 inside their lung cells. They also couldn’t find any differences between young adults and older ones. Aging didn’t change ACE2 one way or another.
But the smokers were a different story. When they looked at gene expression inside the lungs of smokers versus nonsmokers, they saw a huge spike in ACE2 coming from one particular kind of cell: secretory goblet cells. The job of these mucous-makers is to coat the inside of the respiratory tract, protecting it from any irritants you might breathe in (like say, tar, nicotine, or any of the other 250 harmful chemicals in cigarette smoke). The more people smoked, the more their goblet cells multiplied in an effort to trap these chemicals before they could damage surrounding tissue. Those expanding goblet cell army ranks fueled a surge in ACE2, as Sheltzer and his coauthors described in a study published in “Developmental Cell” in mid-May.
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The referenced research paper:
(Developmental Cell, May 16, 2020):
Highlights:
Lung ACE2 levels do not vary by age or sex,
but smokers exhibit upregulated ACE2
ACE2 is expressed in several lung cell types, including the secretory lineage
Chronic smoking triggers the expansion of ACE2+ secretory cells
ACE2 is also upregulated by viral infections and interferon exposure
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Summary:
The factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression. In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, we demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, our work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive feedback loops that increase ACE2 levels and facilitate viral dissemination.
(Dana G Smith, Medium, May 28, 2020):
… there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged. …
… “If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.
In a paper published in April in the scientific journal The Lancet , Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.
“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra. …
… A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus … did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.
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The paper referenced in article:
(The Lancet, April 20, 2020):
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(ACS Chemical Neuroscience, May 7, 2020):
The COVID-19 pandemic revealed that there is a loss of smell in many patients, including in infected but otherwise asymptomatic individuals. The underlying mechanisms for the olfactory symptoms are unclear. Using a mouse model … the cell surface protein ACE2 and the protease TMPRSS2 are expressed in sustentacular cells of the olfactory epithelium but not, or much less, in most olfactory receptor neurons. These data suggest that sustentacular cells are involved in SARS-CoV-2 virus entry and impairment of the sense of smell in COVID-19 patients. We also show that expression of the entry proteins increases in animals of old age. This may explain, if true also in humans, why individuals of older age are more susceptible to the SARS-CoV-2 infection. …
… Our results suggest that SARS-CoV-2 virus accumulates in sustentacular cells first and, by interfering with their metabolism, affects the function of olfactory receptor neurons. The damage to these cells caused by the virus may impair smell sensation as is often observed in COVID-19 patients. … An additional important finding of our work is that the murine OE contains a more intense accumulation of ACE2 protein than the respiratory epithelium. If this is true for the human OE, then the OE (and specifically the sustentacular cells) rather than the respiratory epithelium may be most susceptible to SARS-CoV-2 infection, and for this reason it may be the most relevant source of tissues to detect COVID-19 infection in early stages and in asymptomatic carriers.
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(Medical Xpress, June 2, 2020):
“Researchers map SARS-CoV-2 infection
in cells of nasal cavity, bronchia, lungs”
In a … study published in the journal “Cell”, scientists at the UNC School of Medicine and the UNC Gillings School of Global Public Health have characterized the specific ways in which SARS-CoV-2 - the coronavirus that causes COVID-19 - infects the nasal cavity to a great degree - replicating specific cell types - and infects and replicates progressively less well in cells lower down the respiratory tract, including the lungs.
The findings suggest the virus tends to become firmly established first in the nasal cavity, but in some cases the virus is aspirated into the lungs, where it may cause more serious disease, including potentially fatal pneumonia.
… In one set of laboratory experiments, the researchers used different isolates of SARS-CoV-2 to see how efficiently they could infect cultured cells from different parts of the human airway. They found a striking pattern of continuous variation, or gradient, from a relatively high infectivity of SARS-CoV-2 in cells lining the nasal passages, to less infectivity in cells lining the throat and bronchia, to relatively low infectivity in lung cells.
The scientists also found that ACE2 - the cell surface receptor that the virus uses to get into cells - was more abundant on nasal-lining cells and less abundant on the surface of lower airway cells. This difference could explain, at least in part, why upper airway nasal-lining cells were more susceptible to infection.
The referenced paper (May 20, 2020):
“SARS-CoV-2 Reverse Genetics Reveals a Variable Infection Gradient
in the Respiratory Tract”
(NEJM, May 28, 2020):
“Asymptomatic Transmission, the Achilles’ Heel of Current Strategies
to Control Covid-19”
… A key factor in the transmissibility of Covid-19 is the high level of SARS-CoV-2 shedding in the upper respiratory tract, 1 even among presymptomatic patients, which distinguishes it from SARS-CoV-1, where replication occurs mainly in the lower respiratory tract. 2 Viral loads with SARS-CoV-1, which are associated with symptom onset, peak a median of 5 days later than viral loads with SARS-CoV-2, which makes symptom-based detection of infection more effective in the case of SARS CoV-1. 3 With influenza, persons with asymptomatic disease generally have lower quantitative viral loads in secretions from the upper respiratory tract than from the lower respiratory tract and a shorter duration of viral shedding than persons with symptoms, 4 which decreases the risk of transmission from paucisymptomatic persons (i.e., those with few symptoms). …
… Asymptomatic transmission of SARS-CoV-2 is the Achilles’ heel of Covid-19 pandemic control through the public health strategies we have currently deployed. Symptom-based screening has utility, but epidemiologic evaluations of Covid-19 outbreaks within skilled nursing facilities such as the one described by Arons et al. strongly demonstrate that our current approaches are inadequate.
Sweden’s state epidemiologist Anders Tegnell now says they should have done more, too many died and if they had to do it again, they’d pick another strategy somewhere between what they did and what the rest of the world (I guess the neighboring countries?) did … He maintains that there is a way to handle it without a total lockdown.
Source in Danish: https://www.msn.com/da-dk/nyheder/udland/sveriges-statsepidemiolog-vi-burde-have-gjort-mere-mod-corona/ar-BB14Xetx
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(Science Magazine, June 2, 2020):
“Blood vessel attack could trigger coronavirus’ fatal ‘second phase’”
The key is direct and indirect damage to the endothelial cells that line the blood vessels, particularly in the lungs, explains Peter Carmeliet, a vascular biologist at the Belgian research institute VIB and co-author of a 21 May paper in Nature Reviews Immunology. By attacking those cells, COVID-19 infection causes vessels to leak and blood to clot. Those changes in turn spark inflammation throughout the body and fuel the acute respiratory distress syndrome (ARDS) responsible for most patient deaths. …
… This mechanism could explain why the disease pummels some patients who have obesity, diabetes, and cardiovascular conditions: The cells lining their blood vessels are already compromised. …
… In healthy individuals, endothelial cells help regulate blood pressure, prevent inflammation, and inhibit clotting, in part through the continual production of nitric oxide (NO); they also serve as gatekeepers for molecules passing in and out of the bloodstream. When injured, they send out a complex array of signals to immune cells and clotting factors, which rush to repair the site. …
… When SARS-CoV-2 enters the lungs, it invades cells in the air sacs that transfer oxygen to the blood. Surrounding those sacs are capillaries lined like bricks with endothelial cells. The virus directly invades some of those cells; others become “activated,” likely in response to signals from the invading virus and other damaged cells. Some infected cells likely commit suicide. “It’s not a quiet death where the cell just dies,” Mangalmurti says. “All the contents leak out.”
Carmeliet and colleagues suggest damage and other changes in the activated cells trigger vascular leakage, flooding the air sacs with fluid, a hallmark of ARDS. White blood cells swarm to the lungs and NO production likely plummets. Together with the activated endothelial cells, the immune cells release a host of signaling molecules, including interleukins, which raise local blood pressure and weaken cell junctions. Damage to endothelial cells exposes the membrane underneath them.
That exposed membrane in turn triggers uncontrolled clotting. The endothelial and immune cells add fuel to the fire, recruiting additional clotting factors and platelets, which help form clots. Those clots degrade into the key biomarker D-dimer, creating sky-high levels that alert clinicians to patients in trouble. Eventually, such clotting spreads throughout the body, blocking the blood supply within vital organs.
These chain reactions culminate in a final, destructive phase of inflammation. Like clotting, inflammation is an essential defense, sending a diverse army of cells and messenger molecules called cytokines to fight invaders and mop up the debris of battle. But in COVID-19, this reaction spirals out of control in a deadly cytokine storm and plunges patients’ bodies into shock.
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(Ars Technica, June 1, 2020):
… a US-based research team has done a detailed analysis of a large collection of viral genomes, and it finds that evolution pieced together the virus from multiple parts - most from bats, but with a key contribution from pangolins. …
… How do pieces of virus from different species end up being mashed together? The underlying biology is a uniquely viral twist on a common biological process: recombination. …
… the research team started with a collection of 43 different coronaviruses from a variety of species, including humans, bats, and the pangolin sequences known to be similar to SARS-CoV-2.
The basic genome analysis confirmed that SARS-CoV-2 is most closely related to a number of viruses that had been isolated from bats. But different areas of the virus were more or less related to different bat viruses. In other words, you’d see a long stretch of RNA that’s most similar to one virus from bats, but it would then switch suddenly to look most similar to a different bat virus. This sort of pattern is exactly what you’d expect from recombination, where the switch between two different molecules would cause a sudden change in the sequence at the point where the exchange took place. …
… there was a notable exception to this mixing of bat viruses: the spike protein that sits on the virus’s surface and latches on to human cells. Here, the researchers found exactly what the earlier studies had suggested: a key stretch of the spike protein, the one that determines which proteins on human cells it interacts with, came from a pangolin version of the virus through recombination. In other words, both of the ideas from earlier work were right. SARS-CoV-2 is most closely related to bat viruses and most closely related to pangolin viruses. It just depends on where in the genome you look. It’s looking likely that the pangolin sequence is essential for the virus’s ability to target humans. …
… rumors about this being an escaped weapons experiment make little sense in terms of what the genome sequences tell us about biology. …
… The authors find evidence that the viruses from different species may experience distinct selective pressure, which isn’t really surprising. But that also can produce difficult-to-predict results when those viruses hop to a new species - and the difficulty will rise if they then exchange information with other viruses native to that species.
Summing this up, there seem to be myriad coronaviruses out there (including plenty we don’t know about), and some species are serving as labs in which new genetic combinations are created. And, right now, we only have a very partial window into the sort of potential out there in species that have frequent contacts with humans. And some research cited by the authors suggests that humans have been exposed to at least some of these viruses (based on antibodies to them) - fortunately without a major outbreak occurring.
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I read that Darwin did not anticipate Horizontal Gene Transfer, and its seems that perhaps his considerations may also have not anticipated Genetic Recombination:
Recombination
Recombination involves the exchange of genetic material between two related viruses during coinfection of a host cell.
Recombination by Independent Assortment
Recombination by independent assortment can occur among viruses with segmented genomes. Genes that reside on different pieces of nucleic acid are randomly assorted. This can result in the generation of viruses with new antigenic determinants and new host ranges. Development of viruses with new antigenic determinants through independent assortment is called antigenic shift.
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Viruses are in a perpetual arm race with their hosts. Camouflage is a common strategy viruses use to escape to the immune system (either innate or adaptive) of their hosts. This generally translates in a propensity to develop replication strategies that are, at different extents, prone to the insertion of mutations in their genome. Accumulation of mutations is nevertheless limited by the need to maintain viability and its own genetic identity. Keeping subtle equilibrium between these two contrasting forces is vital for viruses, it often influences their pathogenic potential, and can be at the origin of outbreaks of infection of relevance for public health.
Recombination is an important source of genetic variability in viruses, particularly for viruses possessing an RNA genome. The remarkable power of recombination resides in its ability, in a single infectious cycle, to generate new combinations of mutations. This is important at two regards: one is that recombination does not generate new mutations but reshuffles pre-existing ones, whose compatibility with viral survival has already been established. This is expected to increase the probability of having a viable recombinant progeny.
On the other hand, the fact that, in general, several mutations are simultaneously introduced through the recombination process, is expected to favour the opposite outcome: that a high proportion of recombinant products will not be viable. Finally, recombination in concert with natural selection, can be responsible of combining advantageous mutations, as well as removing deleterious ones, by far the most abundant type of mutations found in nature.
For many viruses the generation of recombinant variants has been associated to important moments in the processes of adaptation, gain of pathogenic potential or increased spreading.
Source: https://www.mdpi.com/journal/viruses/special_issues/recomb-vir
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Viral Genome Evolution information:
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(The Lancet, June 1, 2020):
The findings of this systematic review of 172 studies (44 comparative studies; n=25697 patients) on COVID-19, SARS, and MERS provide the best available evidence that current policies of at least 1 m physical distancing are associated with a large reduction in infection, and distances of 2 m might be more effective. These data also suggest that wearing face masks protects people (both health care workers and the general public) against infection by these coronaviruses, and that eye protection could confer additional benefit. However, none of these interventions afforded complete protection from infection, and their optimum role might need risk assessment and several contextual considerations.
… In between study and within-study comparisons, we noted a larger effect of N95 or similar respirators compared with other masks. This finding is inconsistent with conclusions of a review of four randomised trials, in which low certainty of evidence for no larger effect was suggested. However, in that review, the CIs were wide so a meaningful protective effect could not be excluded. We harmonised these findings with Bayesian approaches, using indirect data from randomised trials to inform posterior estimates. Despite this step, our findings continued to support the ideas not only that masks in general are associated with a large reduction in risk of infection from SARS-CoV-2, SARS-CoV, and MERS-CoV but also that N95 or similar respirators might be associated with a larger degree of protection from viral infection than disposable medical masks or reusable multilayer (12–16-layer) cotton masks. Nevertheless, in view of the limitations of these data, we did not rate the certainty of effect as high. …
… The use of face masks was protective for both healthcare workers and people in the community exposed to infection, with both the frequentist and Bayesian analyses lending support to face mask use irrespective of setting. Our unadjusted analyses might, at first impression, suggest use of face masks in the community setting to be less effective than in the health-care setting, but after accounting for differential N95 respirator use between health-care and non-health-care settings, we did not detect any striking differences in effectiveness of face mask use between settings. …
… Physical distancing of at least 1 m is strongly associated with protection, but distances of up to 2 m might be more effective. Although direct evidence is
limited, the optimum use of face masks, in particular N95 or similar respirators in health-care settings and 12–16-layer cotton or surgical masks in the community, could depend on contextual factors.
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I don’t want to know…well, yes I do.
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What was the time lapse between the visits and the loss of smell/taste? And do you notice anything else? The incubation period is anywhere between 2-14 days with 5 days being the average.
While being seen by a gastroenterologist and director of the Liver Clinic at BIDMC I was offered to take part in a nationwide study involving both interferon and a new breakthrough drug that researchers were excited about. I accepted. There were 3 arms to the study and it was pretty much a “spin the wheel” to find out which arm you would be in. Of course, I wanted to be in the arm that only took interferon for 12 weeks along with the new drug. I was exceptionally lucky and got in on the last seat for the shortest duration of interferon. Long story short, with the new drug one patient was clear within 7 days. I was clear within 21 days. The traditional interferon course of treatment takes 11 months. I can not fathom that. Any of us were free to leave the study at any time but most of us stuck to it so the study could be successfully ended with accurate results. That’s why I was on interferon for 3 months. My arm was the 12 week one. Only one person left because the interferon was making her so ill.
I’m proud to have been a part of this nationwide successful study. The scientists were cracking open champagne even before the last participant was finished because of how quickly and successful the drug was working. Today interferon is no longer needed because of it.
The way the new drug works is that it disables the virus’s ability to reproduce itself. Btw, I forgot to mention. Before I knew I had it I lost a friend to hep c. He died of liver cancer and was a black man so declined the treatment. Interferon is useless against Hep C for Blacks and Asians. The new drug cures everyone.
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I signed up for a covid-19 tracer course on Coursera from John Hopkins (for free). I started today and have till June 7 to finish. With my certificate I can either volunteer or seek a paid position working from home.
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Amazing news!!! How long before this drug is available to the public? I know a couple people with hep C.
Visits were on the 23rd and tastlessness showed up on the 28th. Only other symptoms were lethargy and headaches. No cough or fever.
I know someone who works at Hornady MFG who had COVID and losing taste was his first symptom. He got really sick and thankfully has recovered.
Since I originally posted taste has come back but it’s not the same as before. Things still taste “blandish”. I haven’t tested since I don’t think that would be available to me unless more symptoms presented. But I’m still self isolating to be on the safe side.
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It’s been on the market for a few years now. I’m not sure what they named the drug but it may be Harvoni. I need to google fu. There are several others. Just do a search if curious.
Not everyone gets a cough or fever. It’s good that you’re isolating. Serious signs where you need to seek help asap would be trouble breathing or breathing fast. That means you’re not getting the oxygen you need. That would be critical. Can someone pick up an oximeter for you? They’re cheap and probably the most useful tool against covid. It will measure your oxygen levels before you notice anything yourself. Most people feel fine as their levels drop. That’s what gets you in danger. I’m not trying to be an alarmist, it’s just that there are only a couple rare diseases that cause the loss of smell and taste. It’s not common and that concerns me.
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