Keep it simple. Wear a Packers baseball hat with any glasses....prescription or otherwise, just to keep droplets out of the eyes.

Originally Posted by: KRK 

Sniffing Out Where Virus First Strikes in COVID-19
— More context for why COVID-19 patients might lose sense of smell
by Molly Walker, Associate Editor, MedPage Today August 19, 2020

https://www.medpagetoday.com/infectiousdisease/covid19/88148?xid=nl_mpt_DHE_2020-08-20&eun=g1398416d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=Daily%20Headlines%20Top%20Cat%20HeC%20%202020-08-20&utm_term=NL_Daily_DHE_dual-gmail-definition 

When examining how SARS-CoV-2 enters the body, one part of the nose may provide further insights into transmission, symptoms, and potential avenues of treatment for COVID-19, researchers suggested from a lab study of human tissue samples.

ACE2 receptor expression was 200- to 700-fold greater in the olfactory epithelium -- the center of smell detection -- relative to other areas of the nose and trachea, reported Andrew Lane, MD, of Johns Hopkins Outpatient Center in Baltimore, and colleagues. ACE2 is the primary portal through which the SARS-CoV-2 virus enters host cells.

These findings "suggest that active virus infection and replication occurs in the apical layer of nasal and olfactory mucosa," they wrote in the European Respiratory Journal.

"The olfactory epithelium is quite an easy part of the body for a virus to reach, it's not buried away deep in our body, and the very high levels of ACE2 that we found there might explain why it's so easy to catch COVID-19," co-author Mengfei Chen, PhD, also of Johns Hopkins, said in a statement.

The researchers noted prior research suggesting a link between ACE2 expression level and COVID-19 associated clinical traits, such as increased severity in young patients with obesity "linked to increased ACE2 expression in lung epithelial cells."

In addition, they highlighted one of the more unusual symptoms, and sometimes the only presenting symptom of COVID-19: anosmia, but without "concomitant nasal inflammatory symptoms."

"The loss of the sense of smell suggests the possibility of direct targeting by SARS-CoV-2 of the olfactory system," they wrote. "However, the cellular location of ACE2 protein in the olfactory epithelium has not been previously demonstrated."

Lane and colleagues examined tissue samples from the back of the nose of 23 patients (19 with chronic sinusitis, the others healthy controls) removed during endoscopic procedures, and biopsies from the trachea of seven patients. None of the participants had tested positive for COVID-19 or were suspected of infection; all were older than 30.

ACE2 was not detected on olfactory neurons, however.

Tobias Welte, MD, of Hannover University School of Medicine in Germany, who was not involved with the research, characterized this as a "clever study" that examines why COVID-19 patients may have loss of smell as their only symptom.

"It suggests that the part of our nose responsible for smelling could also be the place where the coronavirus gains a foothold in the body," said Welte, past president of the European Respiratory Society, in a statement. "This finding will need to be confirmed, but it offers possible new avenues for treating the infection."

Lane and colleagues noted that the differential expression of ACE2 in the "olfactory neuroepithelium and respiratory epithelium" could not only account for the spectrum of nasal-related symptoms, but could provide some insights into novel treatments.

"Whether nasal saline irrigation, a common treatment for sinonasal conditions, is beneficial or counterproductive in SARS-CoV-2 infection remains to be determined; however, consideration should be given to the delivery of topical anti-viral additives, such as detergent or povidone-iodine, directed at the nasal and nasopharyngeal viral reservoirs," they wrote.

Molly Walker is an associate editor, who covers infectious diseases for MedPage Today. She has a passion for evidence, data and public health. Follow

Euorpean Respiratory Journal Source Reference: Chen M, et al "Elevated ACE2 expression in the olfactory neuroepithelium: implications for anosmia and upper respiratory SARS-CoV-2 entry and replication" Eur Respir J 2020; DOI: 10.1183/13993003.01948-2020.

T-Cell Immunity Underestimated in Predictions for COVID-19 Herd Immunity: Study

BY MEILING LEE August 20, 2020 Updated: August 20, 2020

https://www.theepochtimes.com/t-cell-immunity-underestimated-in-predictions-for-covid-19-herd-immunity_3465083.html?ref=brief_News&utm_source=morningbriefnoe&utm_medium=email 

There has been a lot of discussion on herd immunity to COVID-19 lately as new studies suggest that people’s immune system has the ability to recognize the virus, explaining why certain individuals have only mild symptoms or none at all.
Herd immunity happens when a large number of people are immune to a disease—either from prior infection or vaccination—which acts to stop or slow down the spread, thus protecting the entire community, including those who have not had the illness.

Estimates for percentages needed for herd immunity has mainly focused on the role of antibodies of those who have recovered from COVID-19, although scientists are still unsure how long the antibodies protect against reinfection.

Studies are now also beginning to consider the contribution of T-cells to herd immunity for COVID-19.

T-Cell Immunity for COVID-19

COVID-19 Antibody Testing Collection Event at the Miami International Mall in Doral, Fla., on June 18, 2020. (Jason Koerner/Getty Images for BioReference Laboratories)

Director of the National Institutes of Health Dr. Francis Collins said in his blog post that studies on the immune response to SARS-CoV-2, the virus that causes the COVID-19 disease, have concentrated mostly on the body’s production of antibodies to determine if we will have immunity against the disease.

“But, in fact, immune cells known as memory T-cells also play an important role in the ability of our immune system to protect us against many viral infections, including—it now appears—COVID-19,” Collins said.

T-cells (along with B-cells) are a type of white blood cell that plays an essential part in the adaptive immune system by assisting the body in destroying and remembering antigens—foreign substances that invade the body. Although T-cells are produced in the bone marrow, they travel to the thymus, a small organ between the lungs directly behind the sternum in the chest, where they will mature into different types of T-cells with specific roles.

As people get older, the thymus shrinks, affecting the production and functionality of T-cells, and so adults 60 and older become more susceptible to infections. The elderly population has been the most affected in the pandemic, where at least 45 percent “of all COVID deaths are coming from 0.62 percent of the population—those in nursing homes and assisted living facilities,” Dr. Tom Reed, a double board-certified medical and surgical specialist, told a Facebook discussion hosted by Texas state Sen. Bob Hall.

A study published in Nature that Collins cites in his blog suggests that the immune system’s T-cells may offer protection against COVID-19 by “remembering past encounters with other human coronaviruses,” explaining why certain people can fight off the illness or experience only mild symptoms.

There are six coronaviruses besides SARS-CoV-2 that infect humans—four of them cause the common cold, while two caused the 2003 Severe Acute Respiratory Syndrome (SARS) outbreak and the 2012 Middle East Respiratory Syndrome (MERS) outbreak. These coronaviruses produced both memory T-cells and antibodies in infected individuals, but it was the memory T-cells that continued to confer immunity for over a decade, according to the study.

Multiple studies have been published since the Nature study confirming similar results.

The latest one to be published in Cell (pdf) shows a more promising role for T-cells in developing herd immunity against COVID-19.

Researchers found that “donors exhibited robust memory T-cell responses months after infection, even in the absence of detectable circulating antibodies specific for SARS-CoV-2, indicating a previously unanticipated degree of population-level immunity against COVID-19.”

Dr. Scott Atlas, President Donald Trump’s new advisor on the pandemic, said last month that emerging data showed that people who didn’t get infected have been found to have COVID-19 immunity. “This is probably due to this T-cell immunity, which is present, and is now shown to last for years,” he said.

Atlas, speaking during an appearance on Fox News, pointed to research from Singapore and from Sweden’s Karolinska Institute. Researchers from the institute stated that many people with mild or asymptomatic cases of COVID-19 demonstrate T-cell-mediated immunity to SARS-CoV-2.

Achieving Herd Immunity

It is generally thought that an estimated 60 to 70 percent of the population needs to become infected by SARS-CoV-2 before herd immunity is achieved. “However, several recent studies have suggested that depending on specific population factors (population density, propensity for travel, susceptibility, etc.), this number may be considerably lower in some sub-populations in particular places around the country,” Dr. Michael Devine, dual-board certified internist and geriatrician and co-founder of Devine Concierge Medicine, told The Epoch Times in an email.

But when asked if some states are already seeing herd immunity, Devine says he doesn’t believe that is the case just yet.
“In every measure we do have at present, the perceived proportion of the population who is believed to have acquired (by having been infected directly) or innate (naturally occurring or genetically predisposed) immunity falls vastly short of any model prediction that would infer herd immunity,” Devine said.

“The reduction in cases currently being enjoyed in some states is the byproduct of healthy population habits—social distancing, utilization of face coverings when in public, and maintaining good hand hygiene.”

Devine also said that limiting travel, the warmer weather, and people “spending more time outdoors, rather than being cooped up in close quarters” may be contributing to the lessening prevalence of the virus.

In a live Instagram session on Aug. 13, Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, said that sunlight kills the virus. “That’s one of the reasons why outside, in the sun, when you are interacting that, that is much better than being inside.”

Another important reason for people to be outdoors is to allow their skin to be exposed to direct sunlight for 15-30 minutes without being sunburnt, to activate the production of vitamin D—an important hormone that helps to fight off infections and regulate the immune system. Studies have found that vitamin D deficiency is associated with increased COVID-19 infection risk.

A study by the Georgetown University Medical Center in 2016 found that sunlight, specifically low-level blue light, also “energizes T cells that play a central role in human immunity” by making them move faster.

“T cells, whether they are helper or killer, need to move to do their work, which is to get to the site of an infection and orchestrate a response,” Gerard Ahern, PhD and lead researcher of the study said in a press release. “This study shows that sunlight directly activates key immune cells by increasing their movement.”

Areas of Possible Herd Immunity

States like Oregon, Washington, and Illinois—where large crowds of people are protesting and rioting frequently without social distancing and where some are not wearing masks—are not seeing a significant spike in new cases or deaths. The Washington Department of Health tweeted on Aug. 14 that the state’s “COVID-19 cases are plateauing” even in King County where the riots continue to take place.

Oregon reported its lowest daily COVID-19 cases on Aug. 17 of 189 and no new deaths, bringing the number of total cases to 23,451 and a death toll of 388.

In Illinois, while daily cases began to rise again towards the end of June with the increasing number of tests given, the fatality rates had begun to significantly decline at the same time.

And in Ventura County in California, a church protesting Gov. Gavin Newsom’s lockdown mandate has been offering indoor services for its congregants (of up to several thousand people) for the past two months without any virus outbreaks, according to NTD. While the church does focus on properly sanitizing before and after services, Pastor Rob McCoy of Godspeak Calvary Chapel leaves it up to church members if they want to wear masks and physical distancing. The pastor and his church members are facing legal consequences for attending an in-person church service after breaking a temporary restraining order to not hold indoor activities.

One possible explanation for lower deaths in these communities is that natural herd immunity has taken effect to some degree.

Zachary Steiber contributed to this story.

Even mild COVID-19 may produce long lasting immunity

A new study suggests that T cells might provide individuals who had a mild or asymptomatic case of COVID-19 with lasting immunity against future infection, even if their blood contains no neutralizing antibodies.

Research from Sweden suggests that people with mild or asymptomatic cases of COVID-19 may have immunity from future infection.

https://www.medicalnewstoday.com/articles/even-mild-covid-19-may-produce-long-lasting-immunity 

Most people who are exposed to SARS-CoV-2, the coronavirus that causes COVID-19, only experience mild symptoms or none at all.

However, the infection can still pass from them to other people, and the overall case fatality rate appears to be converging on 0.5–1.0%.

It is, therefore, important to establish whether individuals who have contracted the virus once can contract it again and become contagious, or whether they are immune to future infection.

“In the absence of a protective vaccine, it is critical to determine if exposed or infected people, especially those with asymptomatic or very mild forms of the disease who likely act inadvertently as the major transmitters, develop robust adaptive immune responses against SARS-CoV-2,” says Marcus Buggert, an immunologist at the Karolinska Institutet in Solna, Sweden.

Research suggests that not all individuals who have contracted SARS-CoV-2 in the past produce antibodies capable of neutralizing the virus, particularly if they only experienced a mild infection.

Studies have also found that immune cells known as memory B cells, which produce antibodies against previously encountered infections, tend to be short-lived after infection with the closely related coronavirus SARS-CoV, which causes severe acute respiratory syndrome (SARS).

In contrast, another type of immune cell called a memory T cell, which can recognize a previously encountered pathogen and initiate an immune response to it, may persist for years after the initial infection.

In a new study, memory T cells protected against SARS-CoV-2 infection, even in the absence of antibodies against the virus.
The new research features in the journal Cell.

Five categories of exposure

In the new research, Buggert and his colleagues investigated the immune status of 206 individuals in Sweden, where measures to control the spread of SARS-CoV-2 have been less strict than in other European countries.

Their participants fell into five categories:

As expected, the team found strong memory T-cell responses and high levels of antibodies specific to the virus in all 23 people who had recovered from severe COVID-19.

More surprisingly, 30 of the 31 people who recovered from a mild infection had memory T-cell responses to the virus, and 27 had antibodies against it.

Out of 28 family members exposed to an infected individual, 26 were able to mount T-cell responses to the virus, and 17 had antibodies against it.

Even after a very mild infection, memory T-cell responses were often detectable months later, sometimes even in the absence of SARS-CoV-2 antibodies.

“Our findings suggest that the reliance on antibody responses may underestimate the extent of population-level immunity against SARS-CoV-2,” says Buggert, the senior author of the study. “The obvious next step is to determine whether robust memory T-cell responses in the absence of detectable antibodies can protect against COVID-19 in the long term.”

“Our collective dataset shows that SARS-CoV-2 elicits robust, broad, and highly functional memory T-cell responses, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19.”
– The study authors

General coronavirus immunity
Remarkably, in 28% of those who had donated blood samples in 2019, before the current pandemic, the researchers detected T cells that reacted to SARS-CoV-2. The researchers believe that this reflects immunity induced by exposure to other coronaviruses that have protein sequences in common with SARS-CoV-2.

They speculate that these responses may provide some protection against the new coronavirus, though direct evidence for this is currently lacking.

The authors acknowledge that their study was limited by the small numbers in each group and lack of clinical follow-up. “It, therefore, remains to be determined if robust memory T-cell responses in the absence of detectable circulating antibodies can protect against severe forms of COVID-19,” they write.

Thus far, however, none of the individuals in their study who recovered from the infection have experienced further episodes of COVID-19.

In addition, the authors cite research showing that rhesus macaques infected with SARS-CoV-2 develop almost complete immunity against future infections with the virus.

There are also no confirmed cases of humans who have had COVID-19 contracting the infection again at a later date.

This makes it look like things might be getting gooder.
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Basically, if you're 44 years of age or younger, there's less than 1% chance of COVID-19 being the cause of your death. This is insane how strongly affects people in the second half of their life. My goodness.
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Originally Posted by: Zero2Cool