In response to the MEP’s question, if the Pfizer mRNA vaccine had ever been tested before its release to the general public on its ability to prevent Covid transmission, Ms. Small responded by admitting it hadn’t. If the comment is accurate, we must determine how this disclosure impacts trust in scientific exchange and public health.

“Regarding the question around did we know about stopping immunization before it entered the market…No., We have to really move at the speed of science to really understand what is taking place in the market.”

Small then continued to justify her answer and you can watch her full response above by forwarding the video to the timestamp of 15.31.

Roos then immediately took to social media at the conclusion of the hearing, questioning on what basis governments within the EU had justified Covid vaccine passports if the vaccine was unable to affect the transmissibility of the virus. The main reason that people were vaccinating to protect each other was based on a fiction.

From a medical perspective, this admission matters tremendously. If the vaccines offered little to no communal benefit of protection against the transmission of the virus, the justification for, for instance, vaccinating school children is questionable. The known risks of the vaccines and listed SAEs far outweigh the benefits to this population.

By extension, the same logic can be applied to young and healthy adults not at risk from any comorbidities. It would appear that the argument offered by Governments and Health bodies for the public to act in the interests of protecting their fellow citizens was nothing less than disingenuous. A fabrication designed to coerce public compliance, exposing yet another fundamental flaw in the global management of the Covid pandemic.

The need for these products in the high-risk population is clear. Covid can kill and it is critical that public health institutions enjoy the trust of the public for the health system to function effectively. Otherwise, communication breaks down, creating chaos. To discover more truths and fictions relating to mRNA vaccines, read this piece.

The post Pfizer Confirms mRNA Vaccine Never Tested for Preventing COVID Transmission appeared first on Medika Life.

Like McGuyver, the Covid virus can find its way through air ducts and tight spaces, infecting people in adjacent rooms, as hotels used for quarantining people have discovered. The poliovirus is capable of a similar feat and it has to do with the size of the airborne particles. They’re small, really small, and can stay aloft for hours in the right conditions.

It turns out that one of our best defenses against infection from airborne particles is a very simple one. Fresh air and its ability to vent through a building or vehicle or any confined space. Clear the contaminated air and replace it with untainted air, preferably good old-fashioned outdoor fresh air. Our societies, however, have other plans.

I’ve been sweating out the pandemic in the Philippines, quite literally. The country is poor and the government has been understandably paranoid about the virus gaining a foothold here in the tropical climate. With a population of over 120 million, most in rural locations spread over more than 700 islands, the consequences would be devastating.

The result has been an extended and ongoing Extended General Quarantine across the islands. Children here haven’t seen the inside of a classroom since March of 2020. Masks and face shields are mandated, you cannot leave home without them and to add another layer of well-intentioned protection, plastic has been introduced almost everywhere.

Every building, every public transport vehicle, and every shop or bank features screens constructed out of thick plastic, separating either staff or members of the public from each other. The result is the creation of isolated small hotboxes surrounded by a plastic shield that proves impenetrable to even a determined hurricane.

The normal circulation of air stands no chance.

The result is obvious. Have an infected person breathing in these spaces and the virus has multiple targets to focus on. It’s a little like shooting stranded ducks in a gallery. Without a free flow of fresh air to expel it, the SARS-CoV2 virus can take its time selecting new hosts.

All of this matters, as one of our most effective tools to combatting transmission, maybe the simplest of all. Cracking a window. In fact, there’s now a valid reason to open all of them, particularly in close-quarter environments like classrooms.

This is one of the reasons densely populated cities like Manila (the Philippines capital) are suffering under the brunt of the Delta variant whilst the rural areas in the country remain mostly untouched by the pandemic. The ability of fresh air to move freely.

If your weather permits and even if it really doesnt, make sure you have windows open. The introduction of fresh outdoor air is most definitely one of our most potent weapons in the fight to reduce transmission. Air conditioners don’t offer any protection. Recycled air is often simply recycling the virus as most air filtration units are not designed to catch particles as small as the SARS-CoV virus.

This is true in most buildings, and even in hospitals. Equipment designed to filter out such small particles remains very expensive and has never previously been considered a priority. Poor air quality and circulation is a notorious cause of illness in large buildings, we even have a name for it, sick building syndrome.

Add the virus to the mix and you can see why opening a window, although not environmentally friendly in an air-conditioned environment, may be your best health move.

The post Blocking Airflow During a Pandemic Helps the Covid Virus Spread. Open Your Windows appeared first on Medika Life.

It is indeed a compelling theory, and I commented on this research when it was released before being peer-reviewed. That piece generated a lot of buzz, and so did this article by Drs. Ghandi and Rutherford. In response, several scientists wrote to the New England Journal of Medicine to respond to the article, and the Journal published those correspondences along with Dr. Ghandi’s response.

In the first letter, scientists from Columbia, New York, and Virginia wrote,

There is insufficient evidence to support the claim that masks reduce the infectious dose of SARS-CoV-2 and the severity of Covid-19, much less that their use can induce protective immunity. Substantial knowledge gaps must be addressed before claims are made about the efficacy of face masks in reducing morbidity or eliciting immune responses.

Masks are used primarily to reduce SARS-CoV-2 transmission rather than reduce the dose of infectious particles or mitigate the severity of Covid-19. The suggestion that masks offer an alternative to vaccination without evidence that the benefits outweigh the great risks implicitly encourages reckless behavior.

The second letter was a lot longer, written by scientists from New Orleans and Minneapolis:

Gandhi and Rutherford’s theory regarding the potential for variolation by means of facial masking is not consistent with the emerging science of transmission of SARS-CoV-2. This virus does not appear to follow a classic dose–response relationship (i.e., the lower a viral inoculum exposure, the less severe the disease). Experimental infection studies involving healthy adult macaques have shown that severe clinical disease rarely occurs after respiratory infection in SARS-CoV-2, which would be the expected pathophysiological consequence if the dose–response assumption were valid (1). Viral replication is related to dose, but disease severity is not. The epidemiology indicates that the occurrence of severe Covid-19 is associated with preexisting conditions and other risk factors, such as age, sex, and pregnancy status (2).

They made good points, and so I was very interested in seeing what Drs. Ghandi and Rutherford had to say in response:

We agree that well-described host characteristics, including age and coexisting conditions, influence disease severity. However, more evidence is accruing to support the idea that the viral inoculum of SARS-CoV-2 (lowered by means of masking or social distancing) is associated with disease severity (1–4). Direct experimentation in humans to support this theory is not feasible, but studies in animals have shown the association; in addition to the hamster model, which we cited in our Perspective article, a new model in ferrets shows the same dose–response relationship (3). The association between viral inoculum and disease severity may be related to an overwhelmed innate immune response and has been seen in other viral infections in which the host immune response contributes prominently to viral pathogenesis, such as in SARS-CoV-2, measles, influenza, and dengue.

The use of the term “variolation” refers to the fact that strong T-cell immunity to SARS-CoV-2 appears to be generated with asymptomatic or mild infection, as shown in multiple recent studies; the duration of that immunity is unknown, and we stress the need for a safe and effective vaccine. We did not mean to imply in our Perspective article that people should be deliberately infected with SARS-CoV-2. In fact, as practicing infectious disease physicians, we counsel very strongly against deliberate infection, given the case fatality rate and the complicated interplay between host and pathogen. However, because vaccine trials are also examining strategies for reducing the severity of infection, we are interested in any public health strategy (including masking or social distancing) (4) that could reduce disease severity.

Although the evidence regarding reduced transmission and acquisition of infection with the wearing of cloth masks was originally mixed, there is increasing evidence both from physical sciences and from epidemiologic investigations that cloth masks (if worn properly) reduce both transmission and acquisition (5). The data have evolved on cloth and surgical masks, leading the state of California, for instance, to change its public health messaging to “masks protect you and others.” We hope our article encourages investigators to conduct further studies of the relationship between viral inoculum and disease severity with SARS-CoV-2. Although proving this hypothesis by means of experiments in humans will never be feasible, further studies in animals and observational studies will strengthen the evidence base.

These letters to the editor in medical journals are a great window into the discussions between scientists, and they don’t make the news headlines or press releases. That’s why I shared them in this piece.

Now, notice, none of the scientists — not one — claimed that masks should not be worn or that masks are not effective, unlike the “expert” the White House has enlisted. They simply took issue with the claims of Drs. Ghandi and Rutherford as lacking scientific evidence. And their response to the letters made me even more comfortable with the theory that masks can indeed act as crude vaccines.

Also notice that Drs. Ghandi and Rutherford did not say that masks are the be-all and end-all. They also agree that a vaccine is essential to ending this pandemic once and for all. While we await the trials to be completed to ensure the vaccines’ safety and efficacy, however, everyone needs to be wearing a mask. That’s what the science says. We need to listen to the science.

The post Inside a Debate Between Scientists on Facial Masking for Covid-19 appeared first on Medika Life.

When the coronavirus pandemic first hit, Obgyns around the world wanted to know if mothers could pass SARS-CoV-2 to their babies, a process called vertical transmission.

The vertical transmission of Covid-19 was an unthinkable nightmare putting humanity’s next generation of babies at risk. 

Fortunately, data surveillance so far indicates in-utero coronavirus infections are very rare. According to the American College of Obgyn (ACOG) July practice advisory, “the data are reassuring that vertical transmission appears to be uncommon.”

Why are fetal coronavirus infections rare?

New NIH research may explain why pregnant women with SARS-CoV-2 pass the infection to their baby infrequently. Examining the placental response to the virus demonstrates the difference.

Research shows the placenta may be missing what the virus needs to enter the fetal circulation: the door and the key.

The placenta protects the baby from infection

The placenta is the organ inside the uterus that keeps the baby alive. Maternal blood circulates through this internal filtration system. The growing baby receives oxygen and nutrients from the mother, and the placenta removes carbon dioxide and waste products. 

The placenta is also the defense system against invading infections like bacteria and viruses. Placental immune system cells called trophoblasts are the first line of defense against any invading organisms. 

Most infectious invaders do not make it across the placental defense system. Trophoblasts stop them in their tracks. But babies are at risk of a group of maternal pathogens called TORCH infections.

These diseases have developed ways to bypass trophoblasts. They cross the maternal-fetal barrier and cause illness in the baby. The TORCH infections are:

1. Toxoplasmosis
2. Other (like ZIKA)
3. Rubella
4. Cytomegalovirus
5. Herpes

How does the placenta protect against Covid-19? 

For SARS-Cov-2 to enter the placenta it needs to find an entry point and use its spike protein to enter cells. The human placenta may be missing both the door and the key the virus needs to find its way inside the fetal circulation.

The door is the ACE2 receptor. SARS-CoV-2 enters cells through the ACE2 receptor located all over our bodies. These receptors are in our nose, lungs, heart, blood vessels, kidneys, liver, and gastrointestinal tract. 

The placenta has very few ACE2 receptors. It lacks receptors because the human placenta is missing the molecules needed to create it. Without the entry portal, SARS-CoV-2 is unable to bypass the placental defense system and cause infection. 

Because the placenta has a low-level ACE2 receptor expression, SARS-CoV-2 can not find the door to enter cells to cross over from mom to baby. 

But the placenta does have a small level of ACE2 receptors. Even with a small number of receptors, coronavirus could still infect a fetus. Fortunately, the virus needs something more than just an entry point. The ACE2 receptor door is deadbolted and locked. SARS-CoV-2 needs a key to open it.

Researchers demonstrate the placenta is also missing the key the virus needs to unlock the door when it locates an ACE2 receptor. 

The placenta tissues lack the mRNA needed to produce an enzyme called TMPRSS2. This enzyme primes the SARS-CoV-2 spike protein allowing it to enter cells. The TMPRSS2 is the key and without this enzyme, the virus is unable to enter. 

Both the ACE2 receptor and TMPRSS2 are present in the placenta but only in tiny amounts. The low levels likely indicate SARS-CoV-2 can’t find the door and is missing the key to enter into the fetal circulation. 

Many questions remain regarding the risk of pregnancy and Covid-19. This research on the protective effects of the placenta is encouraging. At the same time, fetal infection can occur in rare cases. 

In Dallas, Texas, Parkland Hospital reported one of the first verified cases of intrauterine Covid-19 infections in The Pediatric Infectious Disease Journal on July 10, 2020.

As research continues, let’s hope the placenta keeps protecting babies from harm. 

The post The Placenta Protects Babies From Covid-19; Here’s How appeared first on Medika Life.

DATE OF ISSUE: Aug. 28, 2020

WASHINGTON /PRNewswire/ — New research suggests that children can shed SARS-CoV-2, the virus that causes COVID-19, even if they never develop symptoms or for long after symptoms have cleared. But many questions remain about the significance of the pediatric population as vectors for this sometimes deadly disease, according to an invited commentary by Children’s National Hospital doctors that accompanies this new study published online Aug. 28, 2020 in JAMA Pediatrics. The commissioned editorial, written by Roberta L. DeBiasi, M.D., M.S., chief of the Division of Infectious Diseases, and Meghan Delaney, D.O., M.P.H., chief of the Division of Pathology and Lab Medicine, provides important insight on the role children might play in the spread of COVID-19 as communities continue to develop public health strategies to reign in this disease.

The study that sparked this commentary focused on 91 pediatric patients followed at 22 hospitals throughout South Korea. “Unlike in the American health system, those who test positive for COVID-19 in South Korea stay at the hospital until they clear their infections even if they aren’t symptomatic,” explains Dr. DeBiasi.

The patients here were identified for testing through contact tracing or developing symptoms. About 22% never developed symptoms, 20% were initially asymptomatic but developed symptoms later, and 58% were symptomatic at their initial test. Over the course of the study, the hospitals where these children stayed continued to test them every three days on average, providing a picture of how long viral shedding continues over time.

The study’s findings show that the duration of symptoms varied widely, from three days to nearly three weeks. There was also a significant spread in how long children continued to shed virus and could be potentially infectious. While the virus was detectable for an average of about two-and-a-half weeks in the entire group, a significant portion of the children — about a fifth of the asymptomatic patients and about half of the symptomatic ones — were still shedding virus at the three week mark.

Drs. DeBiasi and Delaney write in their commentary that the study makes several important points that add to the knowledge base about COVID-19 in children. One of these is the large number of asymptomatic patients — about a fifth of the group followed in this study. Another is that children, a group widely thought to develop mostly mild disease that quickly passes, can retain symptoms for weeks. A third and important point, they say, is the duration of viral shedding. Even asymptomatic children continued to shed virus for a long time after initial testing, making them potential key vectors.

However, the commentary authors say, despite these important findings, the study raises several questions. One concerns the link between testing and transmission. A qualitative “positive” or “negative” on testing platforms may not necessarily reflect infectivity, with some positives reflecting bits of genetic material that may not be able to make someone sick or negatives reflecting low levels of virus that may still be infectious.

Testing reliability may be further limited by the testers themselves, with sampling along different portions of the respiratory tract or even by different staff members leading to different laboratory results. It’s also unknown whether asymptomatic individuals are shedding different quantities of virus than those with symptoms, a drawback of the qualitative testing performed by most labs. Further, testing only for active virus instead of antibodies ignores the vast number of individuals who may have had and cleared an asymptomatic or mild infection, an important factor for understanding herd immunity.

Lastly, Drs. DeBiasi and Delaney point out, the study only tested for viral shedding from the respiratory tract even though multiple studies have detected the virus in other bodily fluids, including stool. It’s unknown what role these other sources might play in the spread of this disease.

Drs. DeBiasi and Delaney note that each of these findings and additional questions could affect public health efforts continually being developed and refined to bring COVID-19 under control in the U.S. and around the world. Children’s National has added their own research to these efforts, with ongoing studies to assess how SARS-CoV-2 infections proceed in children, including how antibodies develop both at the individual and population level.

“Each of these pieces of information that we, our collaborators and other scientists around the world are working to gather,” says Dr. DeBiasi, “is critical for developing policies that will slow the rate of viral transmission in our community.”

About Children’s National Hospital
Children’s National Hospital, based in Washington, D.C., celebrates 150 years of pediatric care, research and commitment to community. Volunteers opened the hospital in 1870 with 12 beds for children displaced after the Civil War. Today, 150 years stronger, it is among the nation’s top 10 children’s hospitals. It is ranked No. 1 for newborn care for the fourth straight year and ranked in all specialties evaluated by U.S. News & World Report. Children’s National is transforming pediatric medicine for all children. In 2020, construction will be complete on the Children’s National Research & Innovation Campus, the first in the nation dedicated to pediatric research. Children’s National has been designated twice as a Magnet®  hospital, demonstrating the highest standards of nursing and patient care delivery.

This pediatric academic health system offers expert care through a convenient, community-based primary care network and specialty outpatient centers in the D.C., metropolitan area, including the Maryland and Northern Virginia suburbs. Children’s National is home to the Children’s National Research Institute and Sheikh Zayed Institute for Pediatric Surgical Innovation and is the nation’s seventh-highest NIH-funded children’s hospital. It is recognized for its expertise and innovation in pediatric care and as a strong voice for children through advocacy at the local, regional and national levels.

For more information, follow us on Facebook, Instagram and Twitter.

SOURCE Children’s National Hospital

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