Yet another COVID-19 strain has popped up — albeit in a surprising corner of the world.

Scientists in southern Finland have discovered the new variant, called Fin-769H, reported the country’s national news outlet Yle on Thursday.

The researchers noted that several mutations in the South African and U.K. virus versions are present within this one, but combined in a unique way.

“The variant was discovered in a patient last week, so details about the infectivity and potential resistance of this strain to vaccines are not yet known,” said Taru Meri, a researcher at Vita Laboratories.

The discovery of the mutant coronavirus in Finland perplexed some scientists due to the nation’s effective job in limiting deaths. The country of 5.5 million residents has reported only 725 disease fatalities, noted health tracker Johns Hopkins University.

Meri also pointed to the country’s relatively low current COVID-19 infection rates.

https://news.google.com/articl…=en-US&gl=US&ceid=US%3Aen

Yet another COVID-19 strain has popped up — albeit in a surprising corner of the world.

Scientists in southern Finland have discovered the new variant, called Fin-769H, reported the country’s national news outlet Yle on Thursday.

The researchers noted that several mutations in the South African and U.K. virus versions are present within this one, but combined in a unique way.

“The variant was discovered in a patient last week, so details about the infectivity and potential resistance of this strain to vaccines are not yet known,” said Taru Meri, a researcher at Vita Laboratories.

The discovery of the mutant coronavirus in Finland perplexed some scientists due to the nation’s effective job in limiting deaths. The country of 5.5 million residents has reported only 725 disease fatalities, noted health tracker Johns Hopkins University.

Meri also pointed to the country’s relatively low current COVID-19 infection rates.

Japan finds new Covid-19 strain, while immigration centre reports infections

The new variant has been found in 91 cases in the Kanto area of eastern Japan and in 2 cases at airports

https://news.google.com/articl…=en-US&gl=US&ceid=US%3Aen

Japan confirmed a new variant of Covid-19, and an infection cluster emerged at a Tokyo immigration facility, presenting new challenges as the country tries to overcome a third wave of the pandemic.

The new variant has been found in 91 cases in the Kanto area of eastern Japan and in 2 cases at airports, Chief Cabinet Secretary Katsunobu Kato told reporters on Friday.

The government is raising surveillance against mutant varieties as they may be more resistant to vaccines, which Japan started to distribute this week.

"It may be more contagious than conventional strains, and if it continues to spread domestically, it could lead to a rapid rise in cases," Kato said.

The new strain appears to have originated overseas but is different from other types that have been found sporadically in Japan, according to the National Institute of Infectious Diseases.

It has the E484K mutation on the spike protein of the virus that has been found in other variants, which may undermine the effectiveness of vaccines.

Japan has reported 151 cases of variants from Britain, South Africa and Brazil, according to the health ministry. The nation has had more than 400,000 cases of Covid-19 with 7,194 fatalities.

Meanwhile, 5 staff and 39 foreign detainees at a Tokyo immigration facility have tested positive for Covid-19.

All 130 detainees at the facility have been tested for the virus, according to a spokesperson for the Tokyo Regional Immigration Bureau. None of the cases is serious, and all infected detainees remain quarantined from others.

The representative declined to comment on the nationality of the infected detainees, citing privacy concerns.

Japan's detention system for immigration law violators and asylum seekers has been widely criticized for its medical standards, monitoring of detainees and response to emergencies.

"Many detainees are locked in a small, closed spaces," said Motoko Yamagishi, the head of a migrants-rights group. "It is regrettable that such a outbreak happened in the centre

Studies explore potential, concerning connection between COVID-19 and Alzheimer's disease

According to a recent study, the number of deaths attributable to Alzheimer’s and dementia during the pandemic has jumped by 12% in Minnesota alone.

https://news.google.com/articl…=en-US&gl=US&ceid=US%3Aen

Latest studies: jump in ALZ deaths, Alzheimer’s patients twice as likely to contract COVID

According to data from the Centers for Disease Control and Prevention (CDC), the number of deaths attributable to Alzheimer’s and dementia during the pandemic has jumped by 12% in Minnesota alone. Leaders with the Alzheimer’s Association, Minnesota-North Dakota note the reasons for the increase among the 99,000 Minnesotans living with Alzheimer’s may vary but could include: reduced access to physicians and health care during the pandemic, a disruption to daily routines and care provided by family members and other caregivers, and the simple toll of social isolation.

Meantime, a recent study by Case Western University – published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association – also found those with dementia have double the risk of contracting COVID-19 when compared to those without dementia. The study further noted that 20% of patients with dementia died when they contracted COVID, compared to just over 5% of people without dementia.

One big study: does getting COVID lead to dementia down the road?

But perhaps the most alarming study relates to whether a COVID infection could lead to developing dementia later in life.

“It seems like large organizations, like the Alzheimer’s Association, have the presence of mind, no pun intended, to start looking at cognitive consequences of this disease,” said Dr. Michael Rosenbloom, a behavioral neurologist and clinical director of the HealthPartners Center for Memory and Aging.

How many people get ‘long COVID’ – and who is most at risk?

Numerous studies over the past few months have shown that about 1 in 3 people with COVID-19 will have symptoms that last longer than the typical two weeks

.https://www.minnpost.com/other-nonprofit-media/2021/02/how-many-people-get-long-covid-and-who-is-most-at-risk/

Long COVID is similar to COVID-19

Many long-haulers experience the same symptoms they had during their initial fight with COVID-19, such as fatigue, cognitive impairment (or brain fog), difficulty breathing, headaches, difficulty exercising, depression, sleep difficulty and loss of the sense of taste or smell. In my experience, patients’ symptoms seem to be less severe than when they were initially sick.

Some long-haulers develop new symptoms as well. These can vary widely person to person, and there are reports of everything from hair loss to rapid heart rates to anxiety.

Despite persistent symptoms, SARS-CoV-2 – the virus itself – is not detectable in most long-haulers. And without an active infection, they can’t spread the virus to others.

Who are the long-haulers?

Patients who were hospitalized for COVID-19 are the most likely to have persistent long-term symptoms.

In a study published in July 2020, Italian researchers followed 147 patients who had been hospitalized for COVID-19 and found that 87% still had symptoms 60 days after they were discharged from the hospital. A more recent study, published in January, found that 76% of hospitalized COVID-19 patients in Wuhan, China, were still experiencing symptoms six months after first getting sick.

This Wuhan study was particularly interesting because the researchers used objective measures to evaluate the people reporting lingering symptoms. People in the study were still reporting persistent breathing problems six months after getting sick. When researchers performed CT scans to look at the patients’ lungs, many of the scans showed splotches called ground-glass opacities. These likely represent inflammation where SARS-CoV-2 had caused viral pneumonia. Additionally, the people in this study who had severe COVID-19 could not walk as fast as those whose illnesses were less severe – these lung problems reduced how much oxygen was moving from their lungs into their bloodstream. And remember, this was all measured six months after infection.

Other researchers have found similar objective health effects. One study found evidence of ongoing viral pneumonia three months after patients left the hospital. Another study of 100 German COVID-19 patients found that 60% had heart inflammation two to three months after initial infection. These German patients were relatively young and healthy – the average age was 49, and many had not needed hospitalization when they had COVID-19.

The sickest COVID-19 patients are not the only ones to suffer from long COVID. Patients who had a milder initial case that didn’t result in hospitalization can also have persistent symptoms.

According to a recent survey done by the Centers for Disease Control and Prevention, 35% of nonhospitalized patients who had mild COVID-19 cases did not return to baseline health 14 to 21 days after their symptoms started. And this wasn’t just in older people or people with underlying health conditions. Twenty percent of previously healthy 18-to-34-year-olds had ongoing symptoms. Overall, research shows as many as one-third of individuals who had COVID-19 and weren’t hospitalized will still be experiencing symptoms up to three months later.

To put these numbers in context, only 10% of people who get the flu are still sick after 14 days.

Long-term symptoms, long-term effects

The medical community still does not know just how long these symptoms will persist or why they occur.

According to recent research that has yet to be peer-reviewed, many long-haulers cannot return to work or do normal activities because of brain fog, pain or debilitating fatigue. Before my patient got sick, he would bike up a mountain in our Colorado town almost every day. It took him four months to recover to the point where he could climb it again.

The Increasing Need for Post COVID-19 Clinics

https://www.contagionlive.com/…for-post-covid-19-clinics

While most people who become ill with COVID-19 recover after a few days or weeks, an estimated 10% to 15% experience symptoms at least 4 weeks after the infection itself has resolved. So-called Long COVID, or Long-Haul COVID, is prevalent enough that clinics focusing on Covid’s aftermath are springing up around the U.S. and other nations. The Infectious Diseases Society of America (IDSA) held a press briefing during which experts discussed who they’re seeing at these clinics, why patients are having lingering symptoms, and the kinds of treatment they receive.

Technically, Long COVID is defined as the persistence of symptoms at least 4 weeks after the initial infection has resolved, according to Allison Navis, MD, assistant professor in the Division of Neuro-Infectious Diseases and neurology clinic director at New York’s Icahn School of Medicine at Mount Sinai. However, she noted that symptoms often continue for months; some patients have had symptoms for close to a year. These may be the same symptoms that plagued them during their infection or entirely new ones.

“Fatigue seems to be the most common thing,” Navis said. “It’s a little unclear as to what’s causing the fatigue because that can have many different etiologies. It can be cardiac, or pulmonary, and then for many others we’re not finding a specific cause.” Dyspnea and pulmonary issues are the second most common complaints. Chest pain is frequent, too, as are neurological changes and “brain fog.” Other symptoms include headaches, numbness and tingling, and manifestations of dysautonomia such as lightheadedness, dizziness, heart, palpitations, and gastrointestinal disturbances. Navis has also received reports of joint pain, rashes, and anosmia persistence.

A major focus at post COVID-19 clinics is figuring out whether symptoms are caused by COVID-19 itself or whether they’ve sprung up as part of a post viral syndrome. According to Navis, post viral problems can last up to a year or longer and then resolve.

At Mt. Sinai, Navis orders cognitive testing for all post COVID patients, and sometimes does imaging studies in older patients to look for vascular issues. For her patients with neuropathy, Navis checks for vitamin and hormone deficiencies. She might prescribe antidepressants or antiseizure medications, depending on the individual and any other problems they might be having. Treatment for most issues is supportive care, so managing depression, anxiety, and sleep disruptions is key. She acknowledged that it’s difficult to determine whether a symptom like depression is a direct result of COVID-19 or is secondary, but “[w]e still need to address the depression, because maybe that’s something we can do something about,” she said.

More good news come together as time goes by and more research is done...

Pfizer vaccine highly efficient already after 1st dose (Israel, Sheba Medical Center, 85% drop in infections 15...28 days after 1st jab), and does seem to remain stable also if not ultra-cooled (-15°C...-25°C is fine for 2 weeks!)...good news vs. unfortunately not so good news on public acceptance of the Astrazeneca vaccive (see switzerland, also in Germany quite some resistance since there are two other more efficient vaccines in the race and available already)..

https://www.ft.com/content/919…40-4389-bac9-04a48fdb0a36

https://www.thelancet.com/jour…-6736(21)00448-7/fulltext

India’s dramatic fall in virus cases leaves experts stumped

hittps://apnews.com/article/india-dramatic-fall-coronavirus-cases-199585f8d5cb023abe241c4c463d88ce

They have suggested many possible explanations for the sudden drop — seen in almost every region — including that some areas of the country may have reached herd immunity or that Indians may have some preexisting protection from the virus.

The Indian government has also partly attributed the dip in cases to mask-wearing, which is mandatory in public in India and violations draw hefty fines in some cities. But experts have noted the situation is more complicated since the decline is uniform even though mask compliance is flagging in some areas.

It’s more than just an intriguing puzzle; determining what’s behind the drop in infections could help authorities control the virus in the country, which has reported nearly 11 million cases and over 155,000 deaths. Some 2.4 million people have died worldwide.

“If we don’t know the reason, you could unknowingly be doing things that could lead to a flare-up,” said Dr. Shahid Jameel, who studies viruses at India’s Ashoka University.

India, like other countries, misses many infections, and there are questions about how it’s counting virus deaths. But the strain on the country’s hospitals has also declined in recent weeks, a further indication the virus’s spread is slowing. When recorded cases crossed 9 million in November, official figures showed nearly 90% of all critical care beds with ventilators in New Delhi were full. On Thursday, 16% of these beds were occupied.

That success can’t be attributed to vaccinations since India only began administering shots in January — but as more people get a vaccine, the outlook should look even better, though experts are also concerned about variants identified in many countries that appear to be more contagious and render some treatments and vaccines less effective.

Why are coronavirus cases suddenly dropping? Here are 4 key factors.

https://www.advisory.com/daily…1/02/17/coronavirus-cases

1. Increasing Covid-19 vaccination rates

2. Adherence to coronavirus countermeasures

3. The changing seasons

4. Undertesting for the novel coronavirus

A fourth, less optimistic reason why newly reported coronavirus cases may be declining in the United States is that the country could be undertesting for the virus, some experts say, as testing rates have decreased in recent weeks—and not necessarily because of a drop in demand.

For instance, a poll by conducted by STAT News and The Harris Poll between Feb. 5 and Feb. 7 found that 24% of the 2,043 respondents said they were unable to get a coronavirus test when they wanted one. The reasons respondents cited for not being able to access a test included not having a testing site near them and having to wait too long for a test.

Separately, a recent report by the health care consulting company Premier found that supplies for coronavirus tests, including pipette tips and micro pipettes, have seen significantly increased demand over the last year, leading to shortages of supplies necessary to complete the tests. According to the report, average daily usage of pipette tips in hospitals has increased by more than 50% since May 2020, and the number of outstanding orders for more pipette tips has tripled. Meanwhile, the average amount of time between an order for pipette tips being placed and the order being received has increased from a few days in fall 2020 to over 25 days in January.

In addition, Eleanor Murray, a professor of epidemiology at Boston University School of Public Health, in a tweet posted earlier this month wrote that she was concerned the U.S. health care system's increased focused on administering Covid-19 vaccines might be straining resources and making it more difficult for people to get tested for the novel coronavirus. In reference to the country's recent decline in newly reported coronavirus cases, she wrote, "I worry that it's at least partly an artifact of resources being moved from testing to vaccination."

According to The Atlantic's Covid Tracking Project, coronavirus testing rates in the United States have declined steadily from more than two million a day in mid-January to about 1.6 million a month later. "Demand for testing may have dropped because fewer people are sick or have been exposed to infected individuals, but also perhaps because testing isn't being promoted as heavily," the authors of the latest update to the project wrote.

Quote from JedRothwell

These companies are competitors. They do not help one another. They do not work together in a conspiracy.

Their directors are friends, dining at the same Rotary/free masons table and only want to order the best wine.

Quote from Fm1

The FDA’s own data show that a single shot of the BioNTech-Pfizer vaccine is 92.6 percent effective after two weeks, and a single Moderna jab is 92.1 percent effective, the researchers note in the New England Journal of Medicine.

Can ypou link the lastest confirmed data from a study?

Quote from Wyttenbach

Their directors are friends, dining at the same Rotary/free masons table and only want to order the best wine.

Can ypou link the lastest confirmed data from a study?

Title: Decreased SARS-CoV-2 viral load following vaccination

Matan Levine-Tiefenbrun 1,* , Idan Yelin 1,*,+ , Rachel Katz 2 , Esma Herzel 2 , Ziv Golan 3

, Licita

Schreiber 3 , Tamar Wolf 3 , Varda Nadler 3 , Amir Ben-Tov 2,4 , Jacob Kuint 2,4 , Sivan Gazit 2

, Tal

Patalon 2 , Gabriel Chodick 2,4 , Roy Kishony 1,5,+

1 Faculty of Biology, Technion - Israel Institute of Technology, Haifa, Israel

2 Maccabitech, Maccabi Health Services, Tel Aviv, Israel

3 Maccabi MEGA lab, Maccabi Healthcare Services, Rehovot, Israel

4 Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

5 Faculty of Computer Science, Technion - Israel Institute of Technology, Haifa, Israel

* These authors contributed equally to this work

+ corresponding authors. Email: [email protected] , [email protected] .

Abstract

Beyond their substantial protection of individual vaccinees, it is hoped that the COVID-19

vaccines would reduce viral load in breakthrough infections thereby further suppress onward

transmission. Here, analyzing positive SARS-CoV-2 test results following inoculation with the

BNT162b2 mRNA vaccine, we find that the viral load is reduced 4-fold for infections occurring

12-28 days after the first dose of vaccine. These reduced viral loads hint to lower

infectiousness, further contributing to vaccine impact on virus spread.

The recently authorized BNT162b2 COVID-19 mRNA vaccine is about 95% efficient in

preventing disease after 7 days from the second dose, and also provides some early protection

starting 12 days after the first dose 1,2

. As countries race to vaccinate a significant share of the

population within the coming months, the basic reproduction number of the virus is hoped to

decrease. This effect can be achieved by reducing the number of susceptible people, as well as

by reducing viral loads and thereby viral shedding of post-vaccination infections, turning them

less infectious 3–7 . However, the effect of vaccination on viral loads in COVID-19 post-vaccination

infections is yet unknown 8

.

It is made available under a CC-BY-NC 4.0 International license .

(which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.

medRxiv preprint doi: https://doi.org/10.1101/2021.02.06.21251283; this version posted February 8, 2021. The copyright holder for this preprint

NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice.

Quote from Fm1

A fourth, less optimistic reason why newly reported coronavirus cases may be declining in the United States is that the country could be undertesting for the virus, some experts say, as testing rates have decreased in recent weeks—and not necessarily because of a drop in demand.

In fact Germany does only 1/3 of the Swiss tests but this - more testing - will not give more corona deaths. It only helps to induce lock down terror!

The infection rate among age groups did go down at more or less the same speed --> no vaccine effects so far.

The oldest have in fact less cases than the trend, most likely because most vulnerable are already dead.

But every country is different.

Testing is a really big business and as the big daddy states pays the bill there will be no limit (at least here..)

I recommend testing only if you have undefined symptoms. With clear symptoms you should directly take ivermectin and not wait until you get the reason for your death on a 7 day old paper mailing.

Quote from Wyttenbach

...on a 7 day old paper mailing.

Is it the same situation in Switzerland like in Germany? I mean, one feels like being in the dark middle age with respect to any modern digital tools supporting this entire Covid mess (not talking about the more or less useless "Corona App" that nobody really uses to enter his positive test...or having support from the armed forces medical staff in the vaccination centers just for creating more paperwork....). There are countries like the Baltic states (e.g. Estonia, Latvia) where they manage almost everything digitally...

Global evidence suggests COVID-19 could be seasonal

https://www.scienceboard.net/i…b=def&pag=dis&ItemID=2055

January 28, 2021 -- As the world enters year two of the COVID-19 pandemic, new research suggests that seasonality, including temperature and location, could be a factor in the spread of infections with the SARS-CoV-2 virus, according to an analysis published in Evolutionary Bioinformatics on January 26.

Many viral infections are seasonal in nature, including the influenza virus, which makes an appearance every winter. In the early days of the COVID-19 pandemic, researchers and public health officials suggested that SARS-CoV-2 might behave like other endemic coronaviruses, peaking in the fall and winter seasons.

However, this claim was lacking scientific evidence, especially on the global scale. This question provided the impetus for researchers at the University of Illinois at Urbana-Champaign to conduct work that would fill this specific knowledge gap.

Taking into consideration all the similarities with influenza infection, the team investigated if COVID-19 infection is seasonal. They hypothesized that COVID-19 epidemiology and genetic makeup are affected by the seasonality phenomenon. For instance, they postulated that high temperatures and humidity would negatively affect viral transmission, as well as the resulting cases and death rates.

Does temperature and location affect COVID-19 disease?

First, the researchers downloaded relevant epidemiological data (disease incidence, mortality, recovery cases, active cases, testing rate, and hospitalization) from 221 countries, along with their latitude, longitude, and average temperature. They used Pearson correlation analyses to test if temperature and geographic location were associated with population-normalized data of incidence, mortality, recovery of patients, active cases, and testing rate in each country.

"One conclusion is that the disease may be seasonal, like the flu. This is very relevant to what we should expect from now on after the vaccine controls these first waves of COVID-19," said senior author Gustavo Caetano-Anollés, PhD, professor in the department of crop sciences, affiliate of the Carl R. Woese Institute for Genomic Biology at Illinois, in a statement.

"Indeed, our worldwide epidemiological analysis showed a statistically significant correlation between temperature and incidence, mortality, recovery cases, and active cases," noted Caetano-Anollés. "The same tendency was found with latitude, but not with longitude, as we expected."

Do viral mutations affect COVID-19 disease?

The team also sought to establish a link between temperature-location effects with genomic changes of SARS-CoV-2 to determine if temperature-related epidemiological effects are controlled by the virus in its interaction with the host. For this analysis, genomic change, and genomic change per unit time were computed from an alignment of 55, 453 SARS-CoV-2 genome sequences to determine if there were significant statistical correlations with temperatures and geographic coordinates of the various countries. Mutation accumulation and rates were calculated for the entire genome and for specific regions known for significant pathways of mutational change.

Mutational changes were based on results from a parallel study of 15,342 indexed virus genome sequences that revealed novel pathways of mutational change during the early stages of the COVID-19 pandemic. The analysis predicted mutational shift from spike and replication proteins to other regions of the proteome, including the nucleocapsid protein and the viroporin 3a protein. A lack of significant correlations indicates that mutational changes in the virus genomic makeup appear unrelated to the temperature modulation of the COVID-19 disease.

"Our results suggest the virus is changing at its own pace, and mutations are affected by factors other than temperature or latitude," said Caetano-Anollés. "We don't know exactly what those factors are, but we can now say seasonal effects are independent of the genetic makeup of the virus."

Host immune system and seasonality of COVID-19

The researchers noted that the host immune system could be in part responsible for the pattern of seasonality. While unconfirmed, some studies suggest that high environmental temperatures, host nutritional status, and vitamin D levels play a crucial role in the regulation of adaptive immune responses following respiratory viral infection, as is the case with influenza. The researchers recommend that the interaction of the environment and SARS-CoV-2 epidemiological data merits further investigation.

"We know the flu is seasonal, and that we get a break during the summer. That gives us a chance to build the flu vaccine for the following fall," explained Caetano-Anollés. "When we are still in the midst of a raging pandemic, that break is nonexistent. Perhaps learning how to boost our immune system could help combat the disease as we struggle to catch up with the ever-changing coronavirus

This study should help understand why reinfection will become the norm.

Evidence for adaptive evolution in the receptor-binding domain of seasonal coronaviruses OC43 and 229e

https://elifesciences.org/articles/64509

Abstract

Seasonal coronaviruses (OC43, 229E, NL63, and HKU1) are endemic to the human population, regularly infecting and reinfecting humans while typically causing asymptomatic to mild respiratory infections. It is not known to what extent reinfection by these viruses is due to waning immune memory or antigenic drift of the viruses. Here we address the influence of antigenic drift on immune evasion of seasonal coronaviruses. We provide evidence that at least two of these viruses, OC43 and 229E, are undergoing adaptive evolution in regions of the viral spike protein that are exposed to human humoral immunity. This suggests that reinfection may be due, in part, to positively selected genetic changes in these viruses that enable them to escape recognition by the immune system. It is possible that, as with seasonal influenza, these adaptive changes in antigenic regions of the virus would necessitate continual reformulation of a vaccine made against them

discussion

Using several corroborating methods, we provide evidence that the seasonal HCoVs OC43 and 229E undergo adaptive evolution in S1, the region of the spike protein exposed to human humoral immunity (Figures 3, 4, and 5). We additionally confirm that RdRp and S2 do not show signals of adaptive evolution. We observe that S1 accumulates between 0.3 (229E) and 0.5 (OC43) adaptive substitutions per year. We infer that these viruses accumulate adaptive substitutions at roughly half the rate of influenza A/H3N2 and at a similar rate to influenza B viruses (Figure 6). The most parsimonious explanation for the observation of substantial adaptive evolution in S1 is that antigenic drift is occurring in which mutations that escape from human population immunity are selectively favored in the viral population leading to repeated adaptive changes. However, it is formally possible that the adaptive evolution we detect is a result of selective pressures other than evasion of the adaptive immune system. Showing that this is truly antigenic evolution could involve a serological comparison of isolates that differ at S1 residues under positive selection.

In seasonal influenza and measles, the rates of adaptive evolution we estimate correlate well with relative rates of antigenic drift reported by other groups (Fulton et al., 2015; Bedford et al., 2014). The relative rates of adaptation we calculate also match the relative frequency of vaccine strain updates, as would be expected since vaccines must be updated to match antigenically evolving viruses. Since 2006, the A/H3N2 component of the seasonal influenza vaccine has been updated 10 times (11 different A/H3N2 strains), four different B/Vic strains and four different B/Yam strains have been included in the vaccine, and the measles vaccine strain has not changed (Global Influenza Surveillance and Response System [GISRS], https://www.who.int/influenza/vaccines/virus/en/). Using these numbers as guidance, our results suggest that a vaccine against OC43 or 229E might need to be updated as frequently as the B/Vic and B/Yam components of the influenza vaccine are.

We do not observe evidence of antigenic evolution in NL63 (Figure 3—figure supplement 1 and Figure 5—figure supplement 1). This likely represents a lack of marked adaptive evolution in S1. Our finding fits with a study of NL63 in Kenya, which identified multiple genotypes of NL63 and show that people regularly become reinfected with the same genotype of NL63 (Kiyuka et al., 2018). Additionally, Kiyuka et al. found that these genotypes circulate locally for a long period of time, suggesting a decent amount of viral diversity and a potential lack of evolution due to immune selection. Though our results cannot explain why OC43 and 229E likely evolve antigenically while NL63 does not, Kiyuka et al. observe that NL63 reinfections are sometimes enhanced by a previous infection and hypothesize that NL63 is actually under purifying selection at epitope sites (Kiyuka et al., 2018).

Though analysis of all HCoVs would benefit from more sequenced isolates, there is substantially less longitudinal sequencing data available for HKU1. Thus, despite finding no evidence of antigenic evolution in HKU1 (Figure 3—figure supplement 1 and Figure 5—figure supplement 1), it is possible that a more completely sampled time series of HKU1 genome sequences could alter the result for this virus (Figure 7—figure supplement 1).

Our conclusions of adaptive evolution in S1, arrived at through computational analyses of sequencing data, agree with studies that observe reinfection of subjects by heterologous isolates of 229E (Reed, 1984), sequential dominance of specific genotypes of OC43 (Lau et al., 2011; Zhang et al., 2015), and common reinfection by seasonal HCoVs from longitudinal serological data (Edridge et al., 2020). In this latter study, HCoV infections were identified from longitudinal serum samples by assaying for increases in antibodies against the nucleocapsid (N) protein of representative OC43, 229E, HKU1, and NL63 viruses. This study concluded that the average time between infections was 1.5–2.5 years, depending on the HCoV (Edridge et al., 2020). In comparison, influenza H3N2 reinfects people roughly every 5 years (Kucharski et al., 2015). Thus, frequent reinfection by seasonal HCoVs is likely due to a combination of factors and suggests waning immune memory, and/or incomplete immunity against reinfection, in addition to antigenic drift.

HCoVs are a diverse grouping split, phylogenetically, into two genera: NL63 and 229E are alphacoronaviruses, while OC43, HKU1, MERS, SARS, and SARS-CoV-2 are betacoronaviruses. The method of cell entry does not seem to correlate with genus. Coronaviruses bind to a remarkable range of host-cell receptors including peptidases, cell adhesion molecules, and sugars. Among the seasonal HCoVs, OC43 and HKU1 both bind 9-O-acetylsialic acid (Hulswit et al., 2019), while 229E binds human aminopeptidase N (hAPN) and NL63 binds angiotensin-converting enzyme 2 (ACE2) (Liu et al., 2020b). Despite a relatively large phylogenetic distance and divergent S1 structures, NL63 and SARS-CoV-1 and SARS-CoV-2 bind to the same host receptor using the same virus-binding motifs (VBMs) (Li, 2016). This VBM is located in the C-terminal domain of S1 (S1-CTD), which fits within the trend of S1-CTD receptor-binding in CoVs that bind protein receptors (Hofmann et al., 2006; Li, 2016). This is opposed to the trend among CoVs that bind sugar receptors, where receptor binding is located within the S1-NTD (Li, 2016). This localization roughly aligns with our observations that the majority of the repeatedly mutated sites occur toward the C-terminal end of 229E S1 and the N-terminal end of OC43 S1 (Figure 2).

Here we have provided support that at least two of the four seasonal HCoVs evolve adaptively in the region of spike that is known to interact with the humoral immune system. These two viruses span both genera of HCoVs, though due to the complexity of HCoV receptor binding and pathology mentioned above, it is not clear whether or not this suggests that other HCoVs, such as SARS-CoV-2, will also evolve adaptively in S1. This is important because, at the time of writing of this manuscript, many SARS-CoV-2 vaccines are in production and most of these exclusively include spike (Krammer, 2020). If SARS-CoV-2 evolves adaptively in S1 as the closely related HCoV OC43 does, it is possible that the SARS-CoV-2 vaccine would need to be frequently reformulated to match the circulating strains, as is done for seasonal influenza vaccines.

Israel vaccine study

Quote from zorud

Is it the same situation in Switzerland like in Germany?

No. Here you get the PCR result in less that 24 hours by e-mail. Doctors do quick tests onsite with a 15'' response time. The USA is worst due to very large labs, that do it the Harvard style = big is better....

Quote from Fm1

Israel vaccine study

2 week increase in cases now confirmed for the Pfizer vaccine! Efficiency after one dose is not yet clear (85..90% from current data) but collected under unrealistic lock down conditions. So this will go down certainly.

But for the health care system it is good news as 97% of all deaths are from people age > 65 at least here in Switzerland. So the vaccines will help for at least 1-2 years. So if you have comorbidity factors and are younger than 65 and older that 35 (only) then I would look for ivermectin or take a J&J or Sputnik jab.

Quote from Wyttenbach

2 week increase in cases now confirmed for the Pfizer vaccine! Efficiency after one dose is not yet clear (85..90% from current data) but collected under unrealistic lock down conditions. So this will go down certainly.

But for the health care system it is good news as 97% of all deaths are from people age > 65 at least here in Switzerland. So the vaccines will help for at least 1-2 years. So if you have comorbidity factors and are younger than 65 and older that 35 (only) then I would look for ivermectin or take a J&J or Sputnik jab.

At this point I'm not sure if any data can be trusted. The experts claim B117/ e484 is more infectious, up to 70% and up to 30% more deadly, yet both infections and deaths are dropping, maybe that would throw the vaccine results off. I think covid is seasonal and new vaccines will be needed each year like the flu

Johns Hopkins Doctor Thinks COVID Will Be Largely Gone By April, Half of U.S. Has Herd Immunity

https://news.google.com/articl…=en-US&gl=US&ceid=US%3Aen

Dr. Marty Makary, a surgeon and a professor at the Johns Hopkins School of Medicine and Bloomberg School of Public Health, believes that the coronavirus will be "mostly gone" by April

In an op-ed published by The Wall Street Journal on Friday, Makary argued that half of the U.S. has already reached herd immunity because there are more coronavirus cases in the country, possibly 6.5 times as many, than the 28 million that have been reported.

Combined with the 15 percent of Americans who have already begun receiving the vaccine, the doctor argued that normal life will return by the spring.