Misc. COVID-19 news

Winston

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OCTOBER 9, 2020
Do cloth masks work? Only if you machine wash them after use


A new publication from researchers at UNSW Sydney advises daily washing of cloth masks to reduce the likelihood of contamination and transmission of viruses like SARS-CoV-2.

Cloth masks must be washed daily at high temperatures to be protective against infection, a new analysis from the Kirby Institute at UNSW Sydney published in BMJ Open suggests.

“Both cloth masks and surgical masks should be considered ‘contaminated’ after use,” says Professor Raina MacIntyre, who conducted the study. “Unlike surgical masks, which are disposed of after use, cloth masks are re-used. While it can be tempting to use the same mask for multiple days in a row, or to give it a quick hand-wash or wipe-over, our research suggests that this increases the risk of contamination.


OCTOBER 18, 2020
Coronavirus survives on skin five times longer than flu: study


The coronavirus remains active on human skin for nine hours, Japanese researchers have found, in a discovery they said showed the need for frequent hand washing to combat the COVID-19 pandemic.

The pathogen that causes the flu survives on human skin for about 1.8 hours by comparison, said the study published this month in the Clinical Infectious Diseases journal.

"The nine-hour survival of SARS-CoV-2 (the virus strain that causes COVID-19) on human skin may increase the risk of contact transmission in comparison with IAV (influenza A virus), thus accelerating the pandemic," it said.

The research team tested skin collected from autopsy specimens, about one day after death.

Both the coronavirus and the flu virus are inactivated within 15 seconds by applying ethanol, which is used in hand sanitisers.


OCTOBER 16, 2020
Preliminary results find COVID-19 vaccine candidate based on inactivated SARS-CoV-2 virus is safe


A Chinese COVID-19 vaccine candidate based on the inactivated whole SARS-CoV-2 virus (BBIBP-CorV) is safe and elicits an antibody response, findings from a small early-phase randomised clinical trial published today in The Lancet Infectious Diseases journal have found.

A previous clinical trial reported similar results for a different vaccine that is also based on inactivated whole SARS-CoV-2 virus, but in that study the vaccine was only tested in people aged under 60 years.

The latest study included participants aged between 18 and 80 years, and found that antibody responses were induced in all recipients. Participants aged 60 and over were slower to respond, taking 42 days before antibodies were detected in all recipients compared with 28 days for participants aged 18-59. Antibody levels were also lower in those aged 60-80 years compared with those aged 18-59 (Mean neutralising antibody titre 42 days after receiving a 8μg vaccine dose was 228.7 for people aged 18-59, and 170.9 for those aged 60-80).

The trial was not designed to assess efficacy of the vaccine, so it is not possible to say whether the antibody responses induced by the vaccine, called BBIBP-CorV, are sufficient to protect from SARS-CoV-2 infection.

Professor Xiaoming Yang, one of the authors of the study, from the Beijing Institute of Biological Products Company Limited, Beijing, China, said: "Protecting older people is a key aim of a successful COVID-19 vaccine as this age group is at greater risk of severe illness from the disease. However, vaccines are sometimes less effective in this group because the immune system weakens with age. It is therefore encouraging to see that BBIBP-CorV induces antibody responses in people aged 60 and older, and we believe this justifies further investigation."

There are currently 42 vaccines for COVID-19 in clinical trials. These vary in type and include DNA plasmid vaccines, inactivated virus vaccines, adenovirus-vectored vaccines, RNA vaccines, protein subunit vaccines and virus-like particle vaccines. Some of these have already been shown to be safe and to elicit immune responses in early phase clinical trials.


A 12 Oct 2020 study published online in JAMA by authors from Virginia Commonwealth University School of Medicine and Yale School of Public Health:


From March to the end of July there were 1,336,561 deaths in the US, a 20% increase over the 1,111,031 expected deaths. Covid-19 was documented as the cause in 67% of the deaths, but the other deaths may also be related to the virus. A study of excess mortality during the early epidemic in March and April showed that 65% of excess deaths were due to covid-19 and other excess deaths were due to Alzheimer’s disease, diabetes, and heart disease in the five states with the most deaths.

Later excess deaths—from March to the end of July—that were attributed to causes other than covid-19 could reflect deaths from unrecognised or undocumented covid-19 infections or deaths from disruptions caused by the pandemic. Many people did not seek medical attention for apparently serious conditions such as myocardial infarction and strokes because they feared being infected with the covid-19 virus in hospitals.

The increase in deaths relative to expected values ranged from 22% in Rhode Island and Michigan to 65% in New York. The three northeastern states with the highest death rates, New York, New Jersey, and Massachusetts, accounted for 30% of US excess deaths but had the shortest epidemics, the authors wrote.


Case Series of Multisystem Inflammatory Syndrome in Adults Associated with SARS-CoV-2 Infection
United Kingdom and United States, March–August 2020
October 9, 2020



In a weekly report, the agency described the cases of 27 adults between the ages of 21 and 50. Most had extreme inflammation throughout their bodies and malfunction of organs such as the heart, liver and kidneys, but not the lungs. A third of the 27 patients tested negative for coronavirus infection but tested positive for antibodies, which indicated they had been infected in the past.

All but one of the MIS-A patients in the report belonged to racial or ethnic minority groups.

Their symptoms included:

Fever lasting 24 hours or more
Chest pain and irregular heartbeats
Evidence of heart dysfunction
Gastrointestinal symptoms
Rashes

The CDC said doctors should consider MIS-A in adults who are experiencing these symptoms. The agency said 10 patients in the report required intensive care. Three were intubated and three died.

In two young adults, their first symptoms were major strokes. Multisystem inflammatory syndrome in children (MIS-C) was first reported by the CDC in May.
 
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Winston

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Possibly the effects on the seasonal flu this year due to COVID-19 NPI (Non-Pharmaceutical Interventions - masks, hand washing, social distancing). Note I said, possibly, because there are other factors. Other countries show the same effect. A graphic I made from CDC graphs:

50510484477_378b81af24_h.jpg
 

Winston

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Could it be equally useful for cold and flu prevention?

NOVEMBER 19, 2020
Anti-COVID-19 nasal spray 'ready for use in humans'


A nasal spray that can provide effective protection against the COVID-19 virus has been developed by researchers at the University of Birmingham, using materials already cleared for use in humans.

A team in the university's Healthcare Technologies Institute formulated the spray using compounds already widely approved by regulatory bodies in the UK, Europe and the US. The materials are already widely used in medical devices, medicines and even food products.

This means that the normal complex procedures to take a new product to market are greatly simplified, so the spray could be commercially available very quickly.

A pre-print (not yet peer-reviewed) study describes cell culture experiments designed to test the ability of the solution to inhibit infection. They found cell-virus cultures inhibited the infection up to 48 hours after being treated with the solution and when diluted many times.

The spray is composed of two polysaccharide polymers. The first, an antiviral agent called carrageenan, is commonly used in foods as a thickening agent, while the second a solution called gellan, was selected for its ability to stick to cells inside the nose.

The gellan, is an important component because it has the ability to be sprayed into fine droplets inside the nasal cavity, where it can cover the surface evenly, and stay at the delivery site, rather than sliding downwards and out of the nose.

Lead author on the paper, Dr. Richard Moakes, said: "This spray is made from readily available products that are already being used in food products and medicines and we purposely built these conditions into our design process. It means that, with the right partners, we could start mass production within weeks."

The spray works in two primary ways. Firstly, it catches and coats the virus inside the nose, from where it can be eliminated via the usual routes—either nose-blowing or swallowing. Secondly, because the virus is encapsulated in the spray's viscous coating, it is prevented from being uptaken by the body. That means it will reduce the viral load in the body, but also even if virus particles are passed on to another person via a sneeze or cough, that person is less likely to be infected by active virus particles.

Co-author Professor Liam Grover, says: "Although our noses filter thousands of liters of air each day, there is not much protection from infection, and most airborne viruses are transmitted via the nasal passage. The spray we have formulated delivers that protection but can also prevent the virus being passed from person to person."



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Comment below that article:

You'll want the 25:75 ratio gellan gum (low acyl) to lamda Carrageenan at 1% w/v, see Figure 3. This is inexpensive to make, about US$ 10 per liter of spray even if you buy retail. [LOL... watch what it costs when it reaches the shelves... - W]
 

Winston

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Mysteries of COVID Smell Loss Finally Yield Some Answers
Explanations begin to arise at the molecular level for this vexing but commonplace symptom
November 18, 2020


Excerpts:

An estimated 80 percent of people with COVID-19 have smell disturbances, and many also have dysgeusia or ageusia (a disruption or loss of taste, respectively) or changes in chemesthesis (the ability to sense chemical irritants such as hot chilies). Smell loss is so common in people with the disease that some researchers have recommended its use as a diagnostic test because it may be a more reliable marker than fever or other symptoms.

One lingering mystery is how the novel coronavirus robs its victims of these senses. Early in the pandemic, physicians and researchers worried that COVID-related anosmia might signal that the virus makes its way into the brain through the nose, where it could do severe and lasting damage. A suspected route would be via the olfactory neurons that sense odors in the air and transmit these signals to the brain. But studies have shown that this is probably not the case, says Sandeep Robert Datta, a neuroscientist at Harvard Medical School. “My gestalt read of the data to date suggests that the primary source of insult is actually in the nose, in the nasal epithelium,” the skinlike layer of cells responsible for registering odors. “It looks like the virus attacks, predominantly, support cells and stem cells and not neurons directly,” Datta says. But that fact does not mean that neurons cannot be affected, he emphasizes.

Olfactory neurons do not have angiotensin-converting enzyme 2 (ACE2) receptors, which allow the virus entry to cells, on their surface. But sustentacular cells, which support olfactory neurons in important ways, are studded with the receptors. These cells maintain the delicate balance of salt ions in the mucus that neurons depend on to send signals to the brain. If that balance is disrupted, it could lead to a shutdown of neuronal signaling—and therefore of smell.

The sustentacular cells also provide the metabolic and physical support needed to sustain the fingerlike cilia on the olfactory neurons where receptors that detect odors are concentrated. “If you physically disrupt those cilia, you lose the ability to smell,” Datta says.

In a study in Brain, Behavior and Immunity, Nicolas Meunier, a neuroscientist at the Paris-Saclay University in France, infected the noses of golden Syrian hamsters with SARS-CoV-2. Just two days later, about half of the hamsters’ sustentacular cells were infected. But olfactory neurons were not infected even after two weeks. And strikingly, the olfactory epithelia were completely detached, which, Meunier says, resembled skin peeling after a sunburn. Although olfactory neurons were not infected, their cilia were entirely gone. “If you remove the cilia, you remove the olfactory receptors and the ability to detect odorants,” he says.

Disruption of the olfactory epithelium could explain the loss of smell. Yet it remains unclear whether the damage is done by the virus itself or invading immune cells, which Meunier observed after infection. Widespread reports of anosmia with COVID are not typical of other diseases caused by viruses. “We think it’s very specific to SARS-CoV-2,” Meunier says. In a previous study with other respiratory viruses at his lab, he found sustentacular cells infected only rarely, whereas with SARS-CoV-2, about half of cells contained the pathogen. With other viruses, smell is usually compromised by a stuffed-up nose, but COVID doesn’t usually cause nasal congestion. “This is very different,” Meunier says.

Researchers have found a few clues about the loss of smell, but they are less certain about how the virus causes a loss of taste. Taste receptor cells, which detect chemicals in the saliva and send signals to the brain, do not contain ACE2, so they probably do not get infected by SARS-CoV-2. But other support cells in the tongue carry the receptor, perhaps providing some indication of why taste goes away. (Although taste can seem to disappear with anosmia because odors are such a key component of flavor, many people with COVID truly develop ageusia and cannot detect even sweet or salty taste.)

The loss of chemical sensing—the burn of hot chilies or the refreshing sensation of mint—also remains unexplained and largely unexplored. These sensations are not tastes. Instead their detection is conveyed by pain-sensing nerves—some of which contain ACE2—throughout the body, including the mouth.

More clues to how the virus obliterates smell come from people recovering from anosmia. “The majority of patients lose smell like a light switch going off and recover it rapidly,” Datta says. “There’s a fraction of patients that have much more persistent anosmia and recover on longer time scales.” The olfactory epithelium regularly regenerates. “That’s the body’s way of protecting against the constant onslaught of toxins in the environment,” Meunier says.

Still, more than seven months after he first experienced anosmia, Kantor falls in the second group of patients: he has yet to detect any odors at all. “It’s hard because you don’t realize how much you relate to smell until you lose it,” he says. “If the house were on fire, I wouldn’t know it. It’s very concerning.” And then there is what anosmia does to the joy of eating. “Foods that used to be good now taste ‘meh,’” Kantor says.
 
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