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Amy Elizabeth Freeze is a five-time Emmy winner for Outstanding Weather Announcer and Outstanding Host whose weight gain caused a lot of internet excitement. She was born in Utah and grew up in Indiana, USA.
Freeze is one of only a few women in the world to hold a broadcast meteorology certification from the American Meteorological Society.
Both the AMS and the National Weather Association have given it their seal of approval.
She is currently employed as a meteorologist at WABC-TV in New York City. Amy previously served as the senior meteorologist at WFLD in Chicago, Illinois for three years and eight months before joining WABC.
Amy Freeze Weight Gain Journey Explored
Amy Freeze gained a lot after getting pregnant – 70 pounds Many of your daily routines and behaviors may change as a result of pregnancy, including what you eat and how much exercise you get.
Most importantly, a woman’s body changes during pregnancy to ensure her unborn offspring receive adequate nutrition and other necessities.
These changes begin in early pregnancy and become more apparent as the pregnancy progresses.
Pregnant women gain more weight in the last months of their pregnancy than in the first few months.
This is not only related to the increased weight of the baby. Most weight gain is due to extra flu (water) in the body. This is needed for the baby’s circulation, placenta and amniotic flu.
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Before And After Photos Of Amy Freeze
Amy expected to lose weight a few months after having her baby, but things dn’t go as planned. She was out of shape and unhappy with herself. Gary Arbuckle, her spouse, was also overweight.
Then she came across a video titled “Body For Life” promoting a 12-week weight loss program with a $100,000 prize for the winner.
Participants had to prove “before and after” pictures. Amy and Gary both d and completed their daily exercises and incorporated them into nutritious meals.
They ate six meals a day and exercised three days a week, including cycling, swimming and running.
They also d strength training three days a week. After 12 weeks of intense training, the results began to show. Amy eventually lost 30 pounds.
How Many LBS D Amy Freeze Add?
Amy Freeze gained 70 pounds because of her pregnancy. In the past, medical rules were extremely strict and recommendations limited weight gain to a few kilos.
However, there is no universally accepted amount of weight gain for pregnant women. Women’s pre-pregnancy weight is now used to make recommendations.
Short, underweight women are more likely to gain weight than women who were overweight before pregnancy.
All In Binge Eating Recovery \u0026 Coping With Weight Gain – Katerina’s Story
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Amy Freeze Before And After Photographs. Amy had hoped to lose weight within a few months of giving birth to her child, but things dn’t go …
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Amy Freeze Weight Gain Journey Explored. Amy Freeze gained a lot of weight after becoming pregnant- 70 pounds. Many of your everyday …
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Treating PCOS with the DASH Diet Empower the Warrior from Within eBook Plano, Amy Amazon.com.au Kindle Store
First I want to say, I don’t have PCOS, or weight problems.
But I’m eating organic, Healthy, and I now know about PCOS, and it’s hard for me not to get a Cookbook.
If you have PCOS the first 56 pages are good information I think on PCOS.
Starting with the introduction,,
1 .. Part 1. Living with PCOS. Understanding PCOS. From page 1 to page 11.
2. Page 12. The controversy of birth control pills.
3. Page 15. To 24. (Do not see pages 13, 14!). The importance of a healthy lifestyle.
4. Page 25. On page 27, When your friends don’t understand.
5. Pages 28 to 29. One night on the town.
6. Pages 31 to 56. The Dash Diet.
7. Pages 61 to 140..Recipes.
Then there is, Conversions Measurement, index etc.
There are no photos in each recipe.
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The Deadliest Flu The Complete Story of the Discovery and Reconstruction of the 1918 Pandemic Virus
Blueprint Development
This is a picture of an influenza virus. Hemagglutinin (HA) is a surface protein of the virus that plays a role in allowing an influenza virus to enter and infect a healthy cell. Photo Credit: Dan Higgins, CDC. resize icon View Larger Close
The first effect of this discovery will first be described in a February 1999 paper in the Proceedings of the National Academy of Science (PNAS) journal entitled “Origin and evolution of the 1918” Spanish “influenza virus hemagglutinin gene,” by Ann Reid et al. al. 8 Hultin is recognized as a co-author. In the paper, the authors described their effort to sequence (i.e., characterize) the hemagglutinin “HA” gene of the 1918 virus.
The HA gene of an influenza virus determines the properties of proteins on the HA surface of the virus. These HA surface proteins allow an influenza virus to enter and infect a healthy cell of the respiratory tract. HA is also targeted by antibodies made by the immune system to fight infection. Modern flu vaccines work by targeting the unique HA of a flu virus (a fact that virologist Dr. Peter Palese, featured later in this article, helped pioneer).
In the 1999 study, the authors succeeded in sequencing the full-length HA gene sequence of the 1918 virus. To do this, the authors used virus RNA fragments obtained from the bodies of the previously described 21-year-old Fort Jackson service member, “Lucy” from the Brevik Mission, and a third person, a 30-year-old service man. member assigned to Camp Upton, New York. This man was admitted to the camp hospital with the flu on September 23, 1918, had a rapid clinical course of the disease, and died of acute respiratory failure on September 26, 1918.
Sequencing results suggested that the ancestor of the 1918 virus was infected by humans between 1900 and 1915. Reid and Taubenberger noted that the 1918 HA gene has a mammalian number compared to avian adaptations, and is more human -like or porous depending on the method of analysis. Phylogenetic analysis, used to group influenza viruses according to their evolutionary development and diversity, placed 1918 viruses’ HA in and around the root of the mammalian clade. This means that it is likely to be an ancestor or closely related to the earliest influenza viruses known to infect mammals. However, the authors believe that the virus likely acquired its HA from avian viruses, but they are not sure how long the virus can adapt to a mammalian host before emerging into pandemic.
According to the authors, the existing strain with which 1918 virus sequences are most closely related is “A/sw/Iowa/30,” the oldest classical swine influenza strain. The authors noticed that contemporary strains of the avian influenza virus were very different from the 1918 pandemic virus, and unfortunately, older avian strains from the 1918 pandemic period were not available for study. The authors also noticed that the 1918 virus’ HA1 had only four glycosylation sites, in contrast to modern human HA’s which accumulated up to five additional glycosylation sites through the process of antigenic drift. Antigenic drift refers to small changes in the genes of influenza viruses that continue to occur over time as the virus replicates itself. Antigenic drift is one reason why there is a flu season every year and also one reason why people can get the flu many times in their lives.
Glycosylation sites are believed to be necessary for the functioning of influenza viruses, and the inclusion of additional glycosylation sites is believed to be an adaptation of the virus to human hosts. Note also, the authors did not find any genetic modification in the 1918 virus ‘HA that would explain its extraordinary virulence.Unlike modern virulent strains of avian influenza, such as avian influenza viruses A (H5) and (H7), 1918 virus’ HA has no “cleavage site” mutation, which is a recognized genetic marker for virulence. , i.e., the severity or severity of a disease. The entry of amino acids into the HA cleavage site can allow an influenza virus to grow in tissues outside of its normal host cells. In the absence of such obvious markers, Drs. Reid and his fellow researchers likely that many genetic factors were responsible for the severity of the 1918 virus.
The microbiologist Dr. Peter Palese and his team created the plasmids used by Drs. Terrence Tumpey to recreate the 1918 pandemic virus. Palese has many achievements, including creating the first genetic maps of influenza A, B, and C viruses, as well as identifying the mechanism used by most current antiviral flu drugs. Image credit: Wikipedia (https://en.wikipedia.org/wiki/Peter_Palese) resize icon View Larger Close A follow-up paper published in June 2000, entitled “Characterization of the 1918“ Spanish ”Influenza Virus Neuraminidase Gene,” which described sequence of 1918 viruses’ neuraminidase (NA) gene.9 In an influenza virus, the neuraminidase gene is responsible for coding proteins on the NA surface of the virus (see previous virus picture for reference). Proteins on the NA surface of the influenza virus allow an influenza virus to escape an infected cell and infect other cells. Therefore, it plays an important role in the spread of influenza infection. The author noted that NA is also targeted by the immune system, and antibodies against NA do not prevent infection, but they significantly limit the ability of the virus to spread.
Remember, the authors were able to sequence the entire 1918 virus ‘NA code from a virus sample obtained from “Lucy”‘ s body. So here again, Hultin’s work proved to be very important. The authors found that the NA gene of the 1918 virus shared many sequences and structural characteristics across both mammalian and avian influenza virus strains. introduced to mammals shortly before the 1918 pandemic. Furthermore, the 1918 virus obtained from Lucy suggested that it was very similar to the ancestor of all subsequent pigs and humans isolated.9
Overall, phylogenetic analysis seems to indicate that the most recent source of the 1918 NA virus was naturally avian, but the authors could not determine the path from its avian origin to the last pandemic form of the virus. Regarding the genetic features of NA that may explain the severity of the 1918 virus, the researchers again could not find any single feature of the 1918 NA that contributed to the virulence of the virus.9 For example, in some modern influenza viruses, the loss of a glycosylation site in NA to amino acid 146 (in WSN/33) contributes to virulence and also results in virus attack on the nervous system in rats. However, this change was not found in the NA of the 1918 virus.
Following this study, a series of additional studies were published, each detailing findings from each of the remaining genes of the 1918 virus (influenza viruses have a total of 8 genes ). In 2001, a paper by Christopher Basler et al. published in the Proceedings of the National Academic of Science (PNAS) which described the sequence of 1918 virus ’nonstructural (NS) gene.10 A 2002 study in the Journal of Virology by Ann Reid et al. described the sequence of the virus matrix gene.11 Two years later, a 2004 Journal of Virology study described the sequence of 1918 viruses ’nucleoprotein (NP) genes.12 In 2005, polymerase genes of the virus was sorted by Taubenberger et al and described in an article in Nature.13 This last study culminated in the nearly decade-long process of sequencing the entire genome of the 1918 virus.
Since the entire genome of the 1918 virus has now been traced, the necessary information is in place to reproduce a live version of the 1918 virus. However, another intermediate step is needed to begin the reverse genetics process, which creates plasmids for each of the eight gene segments of the 1918 virus.This work was performed by a renowned microbiologist, Dr. Peter Palese and Dr. Adolfo Garcia-Tailor of Mount Sinai School of Medicine in New York City. A plasmid is a small circular DNA strand that can be enlarged (or reproduced) in the laboratory. A few years before that, Dr. helped. Palese to initiate the use of plasmids in reverse genetics to produce viable influenza viruses. The methods he developed allowed the relationships between the structure and function of viral genes to be studied, and these efforts paved the way for the methods used to reproduce the 1918 virus. . Once Dr. completes. Palese and his colleagues at Mount Sinai creating the plasmids, sent them to the CDC to begin the official reconstruction process.
The Reconstruction
The decision to reproduce the deadliest pandemic flu virus of the 20th century was made with great care and attention to safety. Senior government officials decided on CDC headquarters in Atlanta as the location of the reconstruction. The CDC conducted two levels of approval: first by the CDC’s Institutional Biosafety Committee and the second by the CDC’s Institutional Animal Care and Use Committee, before laboratory work began. The work will be carried out using strict biosafety and biosecurity precautions and facilities, including so-called Biosecurity Level 3 (BSL-3) practices and facilities with enhancements.
A photo by Dr. Terrence Tumpey working in improved BSL3 laboratory conditions.This includes (but is not limited to) use of a powered air purifying respirator (PAPR), double gloves, suit, and working inside a Class II biosafety cabinet (BSC). Now, Dr. Tumpey is the head of the Immunology and Pathogenesis Branch in the Influenza Division of the CDC. Photo credit: James Gathany – Public Health Image Library #7989. resize icon View Larger Close
For reference, there are four levels of biosafety that correspond to the level of risk posed by the research, with 1 having the lowest risk and 4 placing the greatest risk. Each level of biosecurity also corresponds to specific laboratory skills and techniques, personnel training requirements, laboratory equipment, and laboratory facilities appropriate for the operations being performed. The severity of these considerations – again from 1 as the lowest to 4 as the highest – is designed to protect the personnel performing the work, the environment and the community.
Each level of biosecurity includes considerations for so-called “primary” and “secondary” barriers. Examples of primary barriers include safety cabinets, isolation chambers, gloves and gowns, while secondary barriers include considerations such as facility construction and HEPA filtration of laboratory air. The specific criteria for each level of biosafety are detailed in the CDC/NIH publication Biosafety in Microbiological and Biomedical Laboratories.
A BSL3 laboratory with enhancements includes several primary and secondary barriers and other considerations. For example, all personnel must wear a powered air purifying respirator (PAPR), double gloves, scrubs, shoe covers and surgical gowns. They should also take a bath before leaving the laboratory. In addition, all work with viruses or animals must be carried out inside a certified Class II biosafety cabinet (BSC), and the air flow inside the laboratory is directly controlled and filtered so that it does not accidentally exit the laboratory. .
For the reconstruction of the 1918 virus, additional rules were created to manage the experiments to be conducted. For example, to prevent mix-ups and cross-contamination, working on the 1918 virus could not take place in conjunction with work on other influenza viruses.
As part of security and safety considerations, the CDC Director’s Office determined that only one person would be given permission, laboratory access, and the enormous responsibility of rebuilding the 1918 virus. That person was trained microbiologist Dr. Terrence Tumpey, who was approved for the project by then CDC director, Dr. Julie Gerberding.The reconstruction of the 1918 virus was also approved by the National Institute of Allergy and Infectious Disease (NIAID) within the National Institutes of Health (NIH), which partially funded the project.
Dr. Tumpey is a former microbiologist with the U.S. Department of Agriculture. at the Southeast Poultry Research Laboratory in Athens, Georgia. Earlier in his career, he applied for an American Society of Microbiology (ASM) postdoctoral fellowship with CDC microbiologist and flu expert Dr. Jacqueline Katz, who recently retired as Deputy Director of the CDC’s Influenza Division. This two -year fellowship in the CDC’s Influenza Division will mark the beginning of Dr.’s career. Tumpey at the CDC. He officially transferred work to the CDC for the purpose of studying the human health implications of influenza viruses, including the 1918 pandemic virus.
The 1918 virus is highly toxic. Figure a) shows mouse lung tissue infected with a seasonal human H1N1 flu virus. Figure c) shows the effect of the 1918 virus on mouse lung tissue. The 1918 virus recurs rapidly and causes severe disease in the lung tissues of rats. In 1918, the virus also caused severe lung disease of infected people. Photo credit: CDC, Science. resize icon View Larger Close
The work of Dr. Tumpey to reconstruct the complete 1918 virus began in the summer of 2005. To reduce the risk to colleagues and the public, he had to work on the virus alone and only after times when colleagues came out in the laboratory for that day and go home. A biometric fingerprint scan is required to access the BSL-3E laboratory, and the virus storage freezers are only accessible via an iris scan of his eyes. Dr. Tumpey had to take a prescribed prophylactic (preventative) daily dose of the influenza antiviral drug, oseltamivir, as an additional safety precaution to prevent him from becoming infected. If he became infected, he was told that he would be placed in quarantine and would not come into contact with the outside world. He understood and accepted this responsibility and its consequences.
Using reverse genetics, Drs. Tumpey the plasmids created by Dr.Palese for each of the eight gene segments of the 1918 virus and inserted them into human kidney cells. The plasmids then instructed the cells to reconstruct the RNA of the complete 1918 virus. For several weeks in July 2005, colleagues and colleagues asked Dr. Tumpey if he had the 1918 virus and if it appeared in cell-culture.
On the day the 1918 virus appeared in his cell-culture, Dr. knew. Tumpey that history has been made, and in fact, a historical virus has been brought back from extinction. He sent a playful email inspired by Neil Armstrong that day to colleagues and collaborators, saying “That’s a small step for humanity, a giant step for humanity.” Everyone knows what has been done. Dr. Tumpey became the first person to recreate the complete 1918 virus. The next step is to study it and unlock its deadly secrets.
Laboratory studies on the reconstructed 1918 virus began in August 2005. A report of this work, “Describing the Reconstructed 1918 Spanish Influenza Pandemic Virus”, was published in the October 7, 2005, issue of Science.14 To to examine the 1918 virus’ pathogenicity (i.e., the ability of the virus to cause disease and harm a host), animal studies involving rats were conducted. Mice were infected with the 1918 virus, and morbidity measurements (i.e., weight loss, virus replication, and 50% lethal dose titer) were collected and documented. For comparison, other mice were infected with different influenza viruses designed through reverse genetics to have different combinations of genes from the 1918 virus and contemporary human seasonal influenza A ( H1N1) viruses. These viruses are called “recombinant viruses.”
The completely reconstructed 1918 virus is remarkable in terms of its ability to replicate rapidly, i.e., make copies of itself and spread the infection to the lungs of infected rats.For example, four days after infection, the amount of 1918 virus found in the lung tissue of infected rats was 39,000 times higher than that made by one of the recombinant flu virus comparisons.14
The left image shows the replication of a seasonal human influenza virus called Tx/91 in cell culture. The picture on the right shows how when the polymerase (PB1) gene of this same virus is exchanged for the 1918 virus, the resulting ability of the virus to replicate (i.e., make copies of itself) greatly improves. Photo credit: Terrence Tumpey, CDC. resize icon View Larger Close
Furthermore, the 1918 virus is extremely lethal to rats. Some rats died within three days after infection with the 1918 virus, and the rats lost up to 13% of their body weight within two days after infection with the 1918 virus. The 1918 virus was at least 100 times more lethal than one of the other recombinant viruses tested.14 Experiments indicated that the 1918 virus ’HA gene played a large role in its severity. When the HA gene of the 1918 virus was replaced by a contemporary human seasonal influenza A (H1N1) flu virus known as “A/Texas/36/91” or Tx/91 for short, and combined with the remaining seven genes of the 1918 virus, the resulting recombinant virus notably did not kill infected rats and did not result in significant weight loss.14
Other experiments were conducted to determine if the 1918 virus infection could have spread to other vital parts of the rats ’bodies – such as the brain, heart, liver and spleen. Laboratory testing did not detect virus in these organs, suggesting that the 1918 virus did not cause systemic infection in its victims.
However, a well -documented side effect of the 1918 virus was rapid and severe lung damage. In 1918, victims of the pandemic virus experienced fluid -filled lungs, as well as severe pneumonia and inflammation of lung tissue. Within four days after infection, rats infected with the 1918 virus experienced similar lung complications, suggesting that this was a unique aspect of the severity of the 1918 virus.14
The effect of the 1918 virus on lung tissue was also studied using the human lung cell line (known as Calu-3 cells). The volume of 1918 flu virus was measured in cells at 12, 16 and 24 hours after infection and these results were compared with those produced by recombinant viruses with a combination of genes from 1918 virus mixed. of genes from contemporary human seasonal influenza viruses. Similar to experiments involving rats, the 1918 virus multiplied rapidly and spread within human lung cells. So the 1918 virus produced up to 50 times the amount of virus in human lung cells as one of the comparison viruses. These experiments suggested that in addition to HA, the polymerase genes of the 1918 virus played an important role in the transmission and virulence of the virus in human lung tissue.14A CDC scientific laboratory “licked” an egg of chicken to show the chicken embryo inside. Photo Credit: James Gathany – Public Health Image Library #10759. resize icon View Larger Close
Another set of experiments was conducted to better understand the possible avian origins of the 1918 virus. Earlier efforts in the sequence led by Drs. Taubenberger and Reid suggested that gene segments of the 1918 virus are more closely related to avian influenza A (H1N1) viruses than to H1N1 viruses found in other mammals. The researchers were interested to know if the 1918 virus would be lethal to fertilized chicken eggs, i.e., chicken eggs containing an embryo, similar to the modern highly pathogenic avian influenza virus.
To find an answer, 10-day-old fertilized chicken eggs were inoculated with the 1918 virus. The 1918 virus proved fatal for chicken egg embryos, similar to the effects caused by contemporary H1N1 bird flu viruses.14 Interestingly, comparison experiments using human seasonal influenza A (H1N1) viruses did not have such a destructive effect on chicken embryos. Furthermore, the recombinant flu viruses created by Dr. Tumpey containing two, five or seven genes of the 1918 virus also did not infect chicken embryos.14 Similar to the results of studies conducted on rats and human lung cells, the fertilized experiments in chicken eggs. indicated that the HA and polymerase genes of the 1918 virus are both likely to play roles in its virulence.
The work performed by Dr. Tumpey and his colleagues at the CDC provided new information about the traits that contributed to the poisoning of the 1918 virus. Dr. pointed out. Tumpey that the HA and PB1 virus genes of the virus play particularly important roles in its infection and severity. However, as his experiments involving recombinant influenza viruses with some but not all 1918 virus genes have shown, it is not any single component of the 1918 virus but rather the unique combination of all its genes put together have caused it to be extremely dangerous.
Tumpey and colleagues wrote that “the constellation of all eight genes together produces an extremely toxic virus.” 14 No other human flu virus has been tested as severely. That way, the 1918 virus is special – a uniquely lethal product of nature, evolution and the mixing of humans and animals. This will serve as a sign of nature’s ability to produce future pandemics with a variety of public health concerns and origins.
Learning from the Past
The crowded conditions and the movement of troops during World War I likely contributed to the spread of the 1918 virus around the world. (Photo credit: *100002 *) resize icon View Larger Close
Since 1918, the world has experienced three additional pandemics, in 1957, 1968, and most recently in 2009. These subsequent pandemics were less severe and resulted in lower mortality than the 1918 pandemic.2,3 , 4 The 1957 H2N2 pandemic and the 1968 H3N2 pandemic each resulted in an estimated 1 million global deaths, while the 2009 H1N1 pandemic resulted in fewer than 0.3 million deaths in its first year.3,4 This probably begs the question of whether a high severity pandemic on the scale of 1918 may have occurred in modern times.
Many experts think so. One particular virus has garnered international attention and concern: the avian influenza A (H7N9) virus from China. The H7N9 virus has so far caused 1,568 human infections in China with a case-fatality proportion of approximately 39% since 2013. However, it has not gained the ability to spread quickly and efficiently among humans. If this happened, experts believe it could result in a pandemic with a severity comparable to the pandemic of 1918. So far, it has only shown limited ability to spread among humans. Most human infections with this virus are the result of exposure to birds.
When considering the potential for a modern era of high pandemic severity, this is important; however, to reflect on the huge medical, scientific and social advances that have taken place since 1918, while recognizing that there are some ways that global preparations for the next pandemic still need improvement.
Apart from the properties of the virus itself, many additional factors contributed to the virulence of the 1918 pandemic. In 1918, the world was still engaged in the First World War. The movement and mobilization of troops put large numbers of people in close contact and the quarters were crowded. Health services are limited, and up to 30% of physicians in the U.S. was deployed to military service.3
In addition, medical technology and countermeasures at that time were limited or nonexistent. No diagnostic tests existed at the time that could diagnose for flu infection. In fact, doctors do not know that there are flu viruses.Many health experts at the time thought that the 1918 pandemic was caused by a bacterium called “Pfeiffer’s bacillus,” now known as Haemophilus influenzae.
Flu vaccines did not exist at that time, and even antibiotics had not been developed. For example, penicillin was not discovered until 1928. Also, no antiviral drugs were available for influenza. Critical care measures, such as intensive care support and mechanical ventilation were also not available in 1918.4 Without these medical measures and treatment capabilities, physicians were left with few options. treatment other than supportive care.3
In terms of national, state and local pandemic planning, no integrated pandemic plans existed in 1918. Some cities were able to implement community mitigation measures, such as closing schools, banning public gatherings, and issuing isolation or quarantine orders, but the federal government had no centralized role in assisting in planning or initiating these interventions during the 1918 pandemic.3
Today, great advances have been made in the fields of health technology, disease monitoring, medical care, medicines and drugs, vaccines and pandemic planning. Flu vaccines are now made and updated annually, and annual vaccinations are recommended for all 6 months of age and older. Antiviral drugs now exist that treat the flu, and in case the virus is exposed, they can also be used for prophylaxis (prevention). Importantly, many different antibiotics are now available to treat secondary bacterial infection.
Diagnostic tests for diagnosing the flu are now available and they are improving over time. Current rapid tests for the flu, also known as RIDTs, give results within 15 minutes and have sensitivities ranging from 50-70%. Recently, new “rapid molecular assays” have become available that are more timely and more accurate than RIDTs. Similar to the importance of these advances in diagnostic tests are the improvements made to laboratory testing capacity within the United States and around the world.
The World Health Organization’s (WHO) Global Influenza Surveillance and Response System (GISRS) is a global influenza surveillance network that monitors changes in seasonal influenza viruses and also monitors the emergence of new viruses (i.e., new to humans) influenza viruses, many of which originated in animal populations. Through animal-human interactions and environmental exposures, these viruses can cause human infections. The CDC in Atlanta is one of WHO’s six Collaborating Centers for Reference and Research on Influenza (joining others in Australia, China, Japan and the United Kingdom). WHO collaborating centers collect influenza viruses obtained from respiratory specimens from patients around the world, and they are supported by 143 National Influenza Centers in 114 WHO member countries.3
Expanding laboratory testing and influenza surveillance capacity around the world has been an important focus of pandemic preparedness efforts. In 2004, the CDC began an international monitoring capacity building initiative requiring a 5-year period of financial support to improve laboratory diagnostic tests and monitoring influenza like illness (ILI) and severe acute respiratory infection. (SARI) in 39 partner countries.
In 2008, the CDC established the International Reagent Resource (IRR), which provides reagents to laboratories around the world to identify seasonal influenza A and B viruses, as well as new influenza A viruses. during the 2009 H1N1 pandemic, IRR distributed a new CDC -developed 2009 H1N1 PCR assay to domestic public health laboratories and laboratories around the world less than 2 weeks after the 2009 H1N1 virus was first detected. This has greatly enhanced the ability of the global flu surveillance community to monitor the spread of the virus.3As part of the WHO’s International Health Regulations (IHR), countries must notify WHO within 24 hours of any case of human infection caused by the novel influenza A virus subtype. This requirement is designed to help quickly identify emerging viruses with pandemic potential.
Since 2010, the CDC has used its Influenza Risk Assessment Tool (IRAT) to evaluate and score emerging novel influenza A viruses and other viruses of potential public health concern.The score provided by IRAT answers two questions: 1) What is the risk that a virus novel in humans could result in continued human -to -human transmission? and: 2) What is the potential for the virus to have a significant impact on public health if it were to be able to spread efficiently from person to person? The results from the IRAT have helped public health experts target pandemic preparedness resources against the greatest disease threats and to prioritize the selection of vaccine virus candidates and the development of pre -pandemic vaccines against emerging viruses with the greatest potential to cause severe pandemic.
When vaccines are made before a pandemic, they are stored in the Strategic National Stockpile, along with facemasks, antiviral drugs and other materials available in case of pandemic.
All of these resources, tools, technologies, programs and activities are great tools for pandemic planning, and pandemic planning itself has improved significantly since 1918. In the United States, the Department of Health and Human Services (HHS) maintains a national Pandemic Influenza Plan, and this plan was updated in 2017. The World Health Organization (WHO) has published instructions for countries to use in developing their own national plans on pandemic, as well as a checklist for pandemic flu risk and impact management.3
Planners also have access to other materials. For example, in 2014, the CDC published a pandemic framework with six intervals that were within a pandemic curve. Each interval helps prioritize data collection, government resources and interventions, and other important activities during a pandemic. In addition, CDC experts have developed a Pandemic Severity Assessment Framework that uses data to assign severity and transmissibility scores to pandemics. The tool is useful for planning purposes and for determining appropriate mitigation based on the severity of a pandemic. In addition, guidelines for non -pharmaceutical interventions, such as school closures and large social gatherings, were established and revised, for use during a pandemic.
Although all of these plans, resources, products, and improvements show that significant progress has been made since 1918, gaps remain, and a severe pandemic could still devastate populations in worldwide. In 1918, the world population was 1.8 billion people. One hundred years later, the world population grew to 7.6 billion people in 2018.3 As the human population increased, so did the population of pigs and chickens as a way to feed them. The expanded number of these hosts provides more opportunities for new flu viruses from birds and pigs to spread, thrive and infect humans. The global movement of people and goods has also increased, allowing the latest threat of disease to become an international plane flight away. Due to the mobility and expansion of human populations, even once exotic pathogens, such as Ebola, which previously only affected people living in remote African jungle villages, have now found their way into urban areas. , which caused large outbreaks.
If a severe pandemic, such as the one that occurred in 1918 happened today, it would likely still overwhelm the health care infrastructure, both in the United States and around the world. Hospitals and doctors ’offices find it difficult to meet demand from the number of patients in need of care.Such an event would require a significant increase in the manufacture, distribution and provision of life-saving medicines, products and medical equipment, such as mechanical ventilators. Businesses and schools will be difficult to operate, and even basic services such as garbage collection and garbage disposal could be affected.
The best defense against the flu continues to be a flu vaccine, but even today, flu vaccines face many challenges. One challenge is that flu vaccines are often moderately effective, even when well matched to circulating viruses. But perhaps the biggest challenge is the time it takes to produce a new vaccine against an emerging pandemic threat. Generally, it takes about 20 weeks to select and make a new vaccine.
During the 2009 H1N1 pandemic, the first doses of the pandemic vaccine did not become available until 26 weeks after the decision to make a monovalent vaccine.3 As a result, most vaccinations in the United States occurred after the peak of 2009 H1N1 disease. The HHS Pandemic Influenza Plan aims to reduce the timeframe to produce a pandemic flu vaccine from 20 weeks to 12 weeks, but implementing it is difficult.
One possible solution is to create greater protection and longer -lasting vaccines. The creation of a “universal vaccine” continues to elude the world’s leading scientists, but in the future, it may become a reality. In the meantime, health officials are trying to make the most of new and current flu vaccine technologies. , such as cell -based and recombinant vaccines, which do not rely on the supply of chicken eggs, like traditional vaccines, and have the potential to do so. faster.
Another vaccine issue is the insufficient global capacity for mass production of influenza vaccines. The capacity of the global pandemic flu vaccine was estimated at 6.4 billion doses in 2015, but it would not be enough to cover at least half of the world’s population, if two doses of the pandemic vaccine were needed for protection.3
Other challenges at the global level include pandemic monitoring, infrastructure and planning capacity. The majority of counties reporting to WHO still do not have a national pandemic plan, and critical and clinical care capacity, particularly in low-income countries, continues to be inadequate to the demands of an extreme pandemic.3 In 2005, milestones were created. in the revised International Health Regulations (IHR) for countries to improve their response capacity for public health emergencies, but in 2016, only one-third of countries complied.3
All of these issues show that more work needs to be done, here in the United States and around the world, to prepare for the next pandemic. On May 7, 2018, the Rollins School of Public Health at Emory University in partnership with the U.S. Centers for Disease Control and Prevention, hosted a one-day symposium on the 100-year anniversary of the 1918 influenza pandemic. The event will involve experts from government and academia discussing current pandemic threats and the future of pandemic preparedness, flu prevention and control. U.S. flu experts and global meeting attendees agreed that we still face major challenges to prepare for the coming flu pandemics, but part of the solution is recognizing these challenges and working with the rest of the world to address the them.
For more information on the 1918 pandemic, see the CDC’s 1918 (H1N1 virus) website. For more information about influenza pandemics, see Pandemic Influenza.
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