UPDATED
Scientists say new strain of swine flu virus is spreading to humans in China

The virus should be “urgently” controlled to avoid another pandemic, scientists say in a new study.

A new strain of the H1N1 swine flu virus is spreading silently in workers on pig farms in China, according to a new study. 

–Alex Kraus/Bloomberg

By  Mike Ives,
The New York Times Company
July 1, 2020 

HONG KONG — A new strain of the H1N1 swine flu virus is spreading silently in workers on pig farms in China and should be “urgently” controlled to avoid another pandemic, a team of scientists says in a new study.

H1N1 is highly transmissible and spread around the world in 2009, killing about 285,000 people and morphing into seasonal flu.

The newer strain, known as G4 EA H1N1, has been common on China’s pig farms since 2016 and replicates efficiently in human airways, according to the study published Monday. So far, it has infected some people without causing disease, but health experts fear that could change without warning.

“G4 viruses have all the essential hallmarks of a candidate pandemic virus,” the study said, adding that controlling the spread in pigs and closely monitoring human populations “should be urgently implemented.”

The study, published online in the journal Proceedings of the National Academy of Sciences, is based on the surveillance of pigs in 10 Chinese provinces from 2011 to 2018. In the last three years of the study, researchers collected 338 blood samples from workers on 15 pig farms and 230 from people in nearby households.

The study found that 10.4% of the workers and 4.4% of the others tested positive for antibodies to G4 EA H1N1, and that workers between the ages of 18 and 35 tested positive at a higher rate: 20.5%.

Predicting risk is not a precise science, but close attention to the virus would be advisable, said Ian H. Brown, head of the virology department at Britain’s Animal and Plant Health Agency and one of two scientists who reviewed the paper before it was published.

“It may be that with further change in the virus it could become more aggressive in people much as SARS-CoV-2 has done,” Brown said in an email Tuesday, referring to the new coronavirus.

The study was sent for review in early December, weeks before the coronavirus outbreak in the Chinese city of Wuhan began making global headlines.

Li-Min Huang, director of the Division of ​Pediatric Infectious Disease​s at National Taiwan University Hospital, said that a crucial next step would be finding out whether any of the infected workers at the pig farms had contracted the virus from humans, as well as whether any had spread the virus to their families.

“It’s a very important study, and the virus looks quite dangerous,” Huang said. “We need to be worried about any disease with the potential to spread human to human.”

Eurasian variations of H1N1 have been circulating in pigs in Europe and Asia for decades, the study said, but the incidence of G4 viruses in farmed Chinese pigs with respiratory symptoms began rising sharply after 2014.

Recent evidence “indicates that G4 EA H1N1 virus is a growing problem in pig farms, and the widespread circulation of G4 viruses in pigs inevitably increases their exposure to humans,” it said.

Asked about the new strain at a U.S. Senate hearing Tuesday, Dr. Anthony Fauci, the nation’s top infectious disease expert, said that it was not an “immediate threat” but “something we need to keep our eye on the just the way we did with in 2009 with the emergence of the swine flu.”

The study was a collaboration among government agencies in China, including the Center for Disease Control and Prevention, as well as the World Health Organization, scientists from several universities in China and the University of Nottingham in Britain. Brown teaches at the University of Nottingham but was not involved in the research.

The H1N1 virus that caused a pandemic in 2009 had a relatively low fatality rate, estimated at 0.02%. By contrast, the fatality rate of the 1918 flu pandemic was about 2.5% of its victims. But that virus killed an estimated 50 million, perhaps more, because it infected so many people and spread at a time when medical care was cruder.

Determining the fatality rate of the new coronavirus is a key question for epidemiologists, but one they may not be able to answer until the pandemic has ended.

China downplays potential new swine flu pandemic
 01/07/2020 - 

Chinese authorities have played down the pandemic threat of a new swine flu strain discovered in pigs Noel Celis AFP/File

Beijing (AFP)

China on Wednesday played down the threat of a new swine flu strain with pandemic potential that researchers discovered in pigs, saying the study is "not representative".

The deadly COVID-19 pandemic, which has now infected more than 10 million people worldwide, first emerged in China and is thought to have originated in bats and jumped to humans through an unknown intermediary animal.

The new swine flu strain found in China, according to the study published Monday in the US science journal PNAS, had "all the essential hallmarks" to infect humans and raised fears over another potential pandemic.

But China's foreign ministry moved to downplay fears on Wednesday.

"The G4 virus mentioned in the relevant report is a subtype of the H1N1 virus," foreign ministry spokesman Zhao Lijian said in a routine briefing.

"Experts have concluded that the sample size of the report is small and not representative."

Zhao added that "relevant departments and experts" will continue to step up monitoring of the disease, send warnings and handle it in a timely manner.

The new G4 swine flu strain is genetically descended from the H1N1 strain that caused a pandemic in 2009, according to the study, which was authored by scientists at Chinese universities and the Chinese Center for Disease Control and Prevention.

G4 was observed to be highly infectious, they said, replicating in human cells and causing more serious symptoms in ferrets than other viruses.

Researchers took 30,000 nasal swabs from slaughterhouse pigs in 10 Chinese provinces, allowing them to isolate 179 swine flu viruses.

According to the study, 10.4 percent of pig slaughterhouse workers tested had already been infected.

So far, there has been no evidence of human-to-human transmission. China did not elaborate further on how many had been infected by G4.

"It is of concern that human infection of G4 virus will further human adaptation and increase the risk of a human pandemic," the researchers wrote, calling for urgent measures to monitor people working with pigs.

© 2020 AFP

Dr. Anthony Fauci says new virus in China has traits of 2009 swine flu and 1918 pandemic flu

WED, JUL 1 2020
Berkeley Lovelace Jr.@BERKELEYJR

KEY POINTS

White House coronavirus advisor Dr. Anthony Fauci said U.S. health officials are keeping an eye on a new strain of flu carried by pigs in China that has characteristics of the 2009 H1N1 virus and 1918 pandemic flu.

The virus, which scientists are calling “G4 EA H1N1,” has not yet been shown to infect humans but it is exhibiting “reassortment capabilities,” Fauci told the Senate Health, Education, Labor and Pensions Committee during a hearing Tuesday. 

The H1N1 swine flu emerged in Mexico in April 2009, infecting 60.8 million people in the U.S. and at least 700 million worldwide. An estimated 151,700 to 575,400 people died from the virus across the globe, according to the CDC.


Fauci: New virus in China has traits of 2009 swine flu and 1918 pandemic flu

White House coronavirus advisor Dr. Anthony Fauci said Tuesday that U.S. health officials are keeping an eye on a new strain of flu carried by pigs in China that has characteristics of the 2009 H1N1 virus and 1918 pandemic flu.

The virus, which scientists are calling “G4 EA H1N1,” has not yet been shown to infect humans but it is exhibiting “reassortment capabilities,” Fauci, director of the National Institute of Allergy and Infectious Diseases, told the Senate Health, Education, Labor and Pensions Committee during a hearing.

“In other words, when you get a brand new virus that turns out to be a pandemic virus it’s either due to mutations and/or the reassortment or exchanges of genes,” he told lawmakers. “And they’re seeing virus in swine, in pigs now, that have characteristics of the 2009 H1N1, of the original 1918, which many of our flu viruses have remnants of that in it, as well as segments from other hosts, like swine.”

The H1N1 swine flu and 1918 pandemic flu were both considered horrific viruses that spread across the globe.

The H1N1 swine flu emerged in Mexico in April 2009, infecting 60.8 million people in the United States alone and at least 700 million worldwide. An estimated 151,700 to 575,400 people died from the virus across the globe, according to the Centers for Disease Control and Prevention. It is now seen as one of a variety of seasonal flu viruses.

The 1918 flu, which Fauci has often compared to Covid-19, is estimated to have killed between 30 million and 50 million people, according to the CDC. More than 20 million people died in World War I, by comparison.

The new strain that is spreading in pig farms in China has been identified as having “all the essential hallmarks of a candidate pandemic virus,” scientists say.

Fauci said Tuesday there’s always “the possibility that you might have another swine flu-type outbreak as we had in 2009.”

“It’s something that still is in the stage of examination,” he said. It’s not “an immediate threat where you’re seeing infections, but it’s something we need to keep our eye on, just the way we did in 2009 with the emergence of the swine flu.”

Fauci’s comments came as the coronavirus continues to rapidly spread across the U.S., with the seven-day average of new cases growing by 5% or more in at least 40 states, including Arizona, Texas, Florida and Oklahoma, according to a CNBC analysis of data compiled by Johns Hopkins University.

Public health officials and physicians have criticized the Trump administration’s lack of coordinated response to the virus. In recent weeks, President Donald Trump has downplayed the virus, saying the U.S. is nearing the end of the pandemic, contrary to experts in his own administration.

Earlier this month, Fauci said Covid-19 turned out to be his “worst nightmare” come to life as the coronavirus continues to rapidly spread across the globe.

He said the virus is “very different” from other outbreaks such as Ebola and HIV. The virus jumped from an animal host and has a high degree of transmissibility and mortality, he said. It is historically one of the worst pandemics the world has ever experienced, he said, adding people have compared it to the 1918 flu.

First detected in Wuhan, China, about six months ago, the new coronavirus has already infected more than 10.4 million people across the globe, killing more than 500,000.

On Tuesday, Fauci told lawmakers that he is concerned about the rise in new cases in places such as Texas and Florida.

He said reopening schools in the fall season will depend on the dynamics of the outbreak and the particular location of the school in question.

Nebraska scientists closing in on long-lasting swine flu vaccine

Peer-Reviewed Publication

UNIVERSITY OF NEBRASKA-LINCOLN

 

IMAGE: A TEAM LED BY ERIC WEAVER, DIRECTOR OF THE NEBRASKA CENTER FOR VIROLOGY, HAS DEVELOPED A ROBUST VACCINE AGAINST A STRAIN OF SWINE INFLUENZA. FRAMED BY A MODEL OF NUCLEIC ACID PROTEINS, THE TEAM INCLUDES (FROM LEFT) WEAVER, MATT PEKAREK, A GRADUATE STUDENT IN THE WEAVER LAB; CEDRIC WOOLEDGE, A TECHNICIAN WITH THE INSTITUTIONAL ANIMAL CARE PROGRAM; DAVID STEFFEN, WITH THE NEBRASKA VETERINARY DIAGNOSTIC CENTER; AND NICHOLAS JEANJAQUET AND ERIKA PETRO-TURNQUIST, DOCTORAL STUDENTS IN THE WEAVER LAB. view more 

CREDIT: CRAIG CHANDLER|UNIVERSITY COMMUNICATION AND MARKETING|UNIVERSITY OF NEBRASKA-LINCOLN

A successful long-term experiment with live hogs indicates Nebraska scientists may be another step closer to achieving a safe, long-lasting and potentially universal vaccine against swine flu.

The results are not only important to the pork industry, they hold significant implications for human health. That’s because pigs act as “mixing vessels,” where various swine and bird influenza strains can reconfigure and become transmissible to humans. In fact, the 2009 swine flu pandemic, involving a variant of the H1N1 strain, first emerged in swine before infecting about a fourth of the global population in its first year, causing nearly 12,500 deaths in the United States and perhaps as many as 575,000 worldwide, according to the Centers for Disease Control and Prevention.

“Considering the significant role swine play in the evolution and transmission of potential pandemic strains of influenza and the substantial economic impact of swine flu viruses, it is imperative that efforts be made toward the development of more effective vaccination strategies in vulnerable pig populations,” said Erika Petro-Turnquist, a doctoral student and lead author of the study recently published in Frontiers in Immunology.

Petro-Turnquist is advised by Eric Weaver, associate professor and director of the Nebraska Center for Virology. Weaver’s laboratory is spearheading an effort that uses Epigraph, a data-based computer technique co-developed by Bette Korber and James Theiler of Los Alamos National Laboratory, to create a more broad-based vaccine against influenza, which is notoriously difficult to prevent because it mutates rapidly.

Pork producers currently try to manage swine flu by using commercially available vaccines derived from whole inactivated viruses and weakened live viruses. As of 2008, about half of the vaccines in use in the United States were custom-made for specific herds — an expensive, time-consuming and not very effective strategy because of the rapidity with which swine influenza evolves.

The Epigraph algorithm enables scientists to analyze countless amino acid sequences among hundreds of flu virus variants to create a vaccine “cocktail” of the three most common epitopes — the bits of viral protein that spark the immune system’s response. It could be a pathway to a universal flu vaccine, which the National Institutes of Health defines as a vaccine that is at least 75% effective, protects against multiple types of influenza viruses for at least one year and is suitable for all age groups.

“The first epitope looks like a normal influenza vaccine gene, the second one looks a little weird and third is more rare,” Weaver said. “We’re reversing the evolution and bringing these sequences that the immune system recognizes as pathogens back together. We’re computationally re-linking them and that’s where the power of this vaccine is coming from, that it provides such good protections against such a wide array of viruses.”

In another strategy to heighten effectiveness, the vaccine is delivered via adenovirus, a common virus that causes cold-like symptoms. Its use as a vector triggers additional immune response by mimicking a natural viral infection.

Two years ago, Weaver’s team published initial results in the journal Nature Communications, based on tests in mice and pigs. Those findings indicated the Epigraph-developed vaccine yielded immune response signatures and physiological protection against a much wider variety of strains than a widely used commercial vaccine and wildtype flu strains.

The follow-up study is apparently the first longitudinal study comparing the onset and duration of an adenovirus-vectored vaccine with that of a whole inactive virus vaccine. Petro-Turnquist and Weaver, along with Matthew Pekarek, Nicholas Jeanjaquet and Hiep Vu of the Department of Animal Science, Cedric Wooledge of the Office of Research and Economic Development and David Steffen of the Nebraska Veterinary Diagnostic Center, observed 15 Yorkshire cross-bred female pigs over a period of about six months, the typical lifespan of a market hog.

One group of five received the Epigraph vaccine, a second group of five received a commercial whole inactive virus vaccine, and a third group of five received a saline solution to serve as the control group. The pigs received their initial vaccination at three weeks of age and a booster shot three weeks later. Their antibody levels and T-cell responses were measured weekly for the first month and every 30 days thereafter. At six months of age, they were exposed to a strain of swine flu divergent from those directly represented in the vaccine.

The pigs that received the Epigraph vaccine showed more rapid and long-lasting antibody and T-cell responses to the vaccines. After exposure to the swine flu virus, the Epigraph-vaccinated hogs showed significantly better protection against the disease — less viral shedding, fewer symptoms of infection and stronger immune system responses.

“Those pigs weighed about five pounds when we vaccinated them and by the end of the study, six months later, they were over 400 pounds,” Weaver said. “It’s kind of amazing that this vaccine would maintain itself over that rate of growth. It continues to expand as the animal grows.”

Weaver’s team continues to pursue the research, with next steps including larger studies and possibly a commercial partnership to bring the vaccine to market.

“The more times we do these studies, the more confident we get that this vaccine will be successful in the field,” Weaver said.

---

JOURNAL

Frontiers in Immunology

DOI

10.3389/fimmu.2023.1143451 

METHOD OF RESEARCH

Experimental study

SUBJECT OF RESEARCH

Animals

ARTICLE TITLE

Adenoviral-vectored epigraph vaccine elicits robust, durable and protective immunity against H3 influenza A virus in swine

SWINE FLU REDUX

Duke-NUS scientists find new strains of influenza A virus in pigs, potentially posing a pandemic risk

Study addresses gaps in understanding of swine influenza A virus evolution and highlights need for early warning of disease emergence

Peer-Reviewed Publication

DUKE-NUS MEDICAL SCHOOL

Scientists from Duke-NUS Medical School and their collaborators have uncovered several previously unknown strains of swine flu viruses that have been circulating unnoticed in Cambodian pig populations over the past 15 years, potentially posing a pandemic risk. The strains include viruses that have been passed by humans to pigs, as well as some with genes originating from as far as North America.

The paper, published in the journal PNAS, makes the case for systematic surveillance to detect and warn of new strains of viruses early to prevent future pandemics.

The study, led by scientists Yvonne Su, Gavin Smith and Michael Zeller from the Emerging Infectious Diseases (EID) Programme, identified genetically diverse pools of influenza A viruses co-circulating in pigs. Pigs are a key intermediary in the emergence and potential spread of influenza viruses between animals and humans, the researchers noted, as they provide a suitable environment for the shuffling of gene segments between avian, swine and human hosts, ultimately giving rise to new viruses. With pork production dramatically increasing over the past 50 years, international trade and movement have further amplified the risks.

“The long-term evolution of different lineages has led to the establishment of genetically distinct viruses that have been continuously circulating in pig populations undetected for decades. Our study revealed the hidden and complex genomic landscape of swine flu virus evolution in Southeast Asia, marking the region as a hotspot for virus diversity and risk of new virus emergence,” said Associate Professor Yvonne Su from Duke-NUS, a senior and corresponding author of the study.

In the study, Assoc Prof Su and her colleagues from Duke-NUS collaborated with counterparts from various institutions, including the National Animal Health and Production Research Institute, Phnom Penh, and London School of Hygiene & Tropical Medicine. From March 2020 to July 2022, they conducted swine influenza surveillance in 18 pig slaughterhouses in Cambodia. They collected 4,089 nasal swabs from pigs in different districts of four provinces. Among these, 72 pigs—or around 2 per cent of the pigs—tested positive for influenza A virus.

The scientists identified nine distinct swine influenza A virus groups, at least seven of which had not been detected for between 2 to 15 years. Among these are multiple H3 lineages that had been passed by humans to pigs, circulating undetected for about 10 years; as well as the H1N1 subtype, which was predominant and likely derived from human origins dating back to the 2009 pandemic. Two seasonal viruses were detected in pigs from Kandal, Phnom Penh, and Takeo provinces, and likely originated from Thailand. The team also isolated a new swine European H1N2 variant (that originally came from birds) with North American genes in Cambodia. While they were the first to detect this variant, their genomic analysis suggests that it had been circulating in pigs in the region since 2014, highlighting the need for better surveillance.

Delving deeper into the movement of viruses across geographical borders, the scientists found that European swine flu viruses had been sporadically introduced into South Central China and Southeast Asia in the early 2000s. Genetic evidence indicated South Central China has served as the major source of European-like swine flu virus transmission in the region since around 2010, with the viruses subsequently spreading more widely across China and Southeast Asian countries such as Cambodia.  

“While swine influenza viruses typically cause mild symptoms in pigs, they pose a pandemic threat to humans, as the human population may lack immunity or have inadequate protection against new strains of swine influenza viruses. Therefore, systematic surveillance is crucial in early detection and warning of new subtypes or strains,” said Professor Gavin Smith, Director of the EID Programme and an author of the study.

Further studies are needed to understand the pandemic threat of the new viruses, including how they react with human viruses and how easily they can spread. To this end, the team is currently developing a platform that can identify major swine flu genetic subtypes. The screening will not be limited to swine and human subtypes but also include avian sequences. With the set up, they will be able to assess if pig and human populations have been infected with the influenza subtypes. 

Professor Patrick Tan, Senior Vice-Dean for Research at Duke-NUS, remarked: “Routine and sustained surveillance is indispensable in identifying new viruses so that their transmission risk can be assessed. It is therefore critical that more efficient and continuous surveillance methods are integrated with automated analytical tools to rapidly provide information on changes in human and animal pathogens. Such a system as the team at Duke-NUS is developing would improve animal health through selection of effective vaccines, and aid in human health by monitoring viruses with the potential for transmission.”

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JOURNAL

Proceedings of the National Academy of Sciences

DOI

10.1073/pnas.2301926120 

METHOD OF RESEARCH

Meta-analysis

SUBJECT OF RESEARCH

Animals

ARTICLE TITLE

The genomic landscape of swine influenza A viruses in Southeast Asia

Will this pandemic ever end? 

Here's what happened with the last ones

Jessica Roy
Thu, December 23, 2021

Volunteer nurses from the American Red Cross tend to influenza patients in the Oakland Municipal Auditorium in 1918. (Library of Congress via Associated Press)

This started as a story about what happens after a pandemic ends.

I pitched my editor on the idea in early May. Every adult in America could get a vaccine. COVID numbers started to fall. If the Roaring '20s came after the Spanish flu a century ago, did that mean we were on track for another Roaring '20s now? Would "Hot Vax Summer" give way to Decadent Gatsby Party Autumn?

I started to dig in. A number of compelling parallels emerged: America 100 years ago had staggering income inequality. A booming stock market. Racial uprisings. Anti-immigrant sentiment. A one-term president plagued by scandals after he left office. Plenty of material for a story.

Then the pandemic didn't end.

Vaccinations stalled. The Delta variant fueled new waves of infections, hospitalizations and deaths. By September, some states had more hospitalized COVID patients than they did during the winter surge. The economic outlook for this decade has gone from "champagne-soaked" to "room temperature." In late November, the World Health Organization announced a new "variant of concern": Omicron, which is currently on the cusp of pummeling California.

I called a meeting with my editor. I said I didn't think it was a good time to write a story in which the premise was "this pandemic is over, now what?"

The pandemic wasn't ending. Would it ever?

This is not humanity's first time staring down a seemingly unstoppable disease. Pandemics (a disease affecting a large number of people in multiple countries or regions around the world, per the World Health Organization), epidemics (a disease affecting people in a country or region) and outbreaks (a sudden occurrence of an infectious disease) have plagued us throughout history. Just in the past century, we've survived a few.

How did those end? And how might we get ourselves out of this one?

Spanish flu

This photo made available by the Library of Congress shows a demonstration at the Red Cross Emergency Ambulance Station in Washington during the 1918 Spanish flu pandemic. (Library of Congress via Associated Press)

How it started: Unclear, but probably not in Spain. It was a particularly deadly strain of H1N1 influenza and first took root in the U.S. in Kansas.

The disease was so virulent and killed so many young people that if you heard, "'This is just ordinary influenza by another name,' you knew that was a lie," said John Barry, the author of "The Great Influenza."

There was "zero partisanship" over the virus, Barry said.

If the flu did hit your town, it hit hard: A young person could wake up in the morning feeling well and be dead 24 hours later. Half the people who died of the flu in 1918 were in their 20s and 30s.

"It was a spooky time," said Georges Benjamin, executive director of the American Public Health Assn.

So how did we, as a species, beat the Spanish flu? We didn't. We survived it. It torched through individual communities until it ran out of people to infect. A third of the world's population was believed to have contracted the Spanish flu during that pandemic, and it had a case-fatality rate of as high as 10-20% globally and 2.5% in the United States. (Johns Hopkins University reports the COVID-19 case fatality rate in the U.S. is 1.6% as of Dec. 2021.) Roughly 675,000 people in America died out of a population of 103.2 million, a number recently surpassed by COVID-19 victims of a 2020 U.S. population of 329.5 million. Flu vaccines wouldn't be developed until the 1930s and wouldn't become widely available for another decade.

Ultimately, the virus went through a process called attenuation. Basically, it got less bad. We still have descendent strains of the Spanish flu floating around today. It's endemic, not a pandemic.

As a society, we accept a certain amount of death from known diseases. The normal seasonal flu usually kills less than 0.1% of people who contract it. Deaths have been between 12,000 and 52,000 people in the U.S. annually for the past decade.

The regular seasonal flu is both less contagious and less deadly than COVID-19. That people were washing hands, working from home and socially distancing in the winter 2020 flu season likely contributed to the fact that it was a comparably light flu season. Though business and school closures weren't enough to stave off the devastating winter surge of COVID, the measures were sufficient to keep the flu at bay. One strain may have been completely extinguished.

As places reopen and people feel more confident about socializing and traveling again, the flu could make a calamitous comeback. (By the way, have you gotten your flu shot yet?)

How it ended: Endemic

Polio

In this April 1955 file photo, first- and second-graders are inoculated against polio in Los Angeles. (Associated Press)

How it started: The first documented polio epidemic in the United States was in 1894. Outbreaks occurred throughout the first half of the 20th century, primarily killing children and leaving many more paralyzed.

Polio reached pandemic levels by the 1940s. There were more than 600,000 cases of polio in the United States in the 20th century, and nearly 60,000 deaths — a case fatality rate of 9.8%. In 1952 alone, there were 57,628 reported cases of polio resulting in 3,145 deaths.

"Polio was every mother's scourge," Benjamin said. "People were afraid to death of polio."

Polio was highly contagious: In a household with an infected adult or child, 90% to 100% of susceptible people would develop evidence in their blood of also having been infected. Polio is not spread through the air — transmission occurs from oral-oral infection (say, sharing a drinking glass), or by "what's nicely called hand-fecal," Paula Cannon, a virology professor at the USC Keck School of Medicine, told me. "People poop it out, and people get it on their hands and they make you a sandwich."

Polio, like COVID, could have devastating long-term effects even if you survived the initial infection. President Franklin Roosevelt was among the thousands of people who lived with permanent paralysis from polio. Others spent weeks, years, or the rest of their lives in iron lungs.

Precautions were taken during the polio pandemic. Schools and public pools closed. Then, in 1955, a miracle: a vaccine.

A two-dose course of the polio vaccine proved to be about 90% effective — similar to the effectiveness of our current COVID vaccines. Vaccine technology was still relatively new, and the polio vaccine was not without side effects. A small number of people who got that vaccine got polio from it. Another subset of recipients developed Guillain-Barre syndrome, a noncontagious autoimmune disorder that can cause paralysis or nerve damage. A botched batch killed some of the people who received it.

But there were no masses of polio anti-vaxxers. It was a "whole sense of the greater good, that this was the only way out of this terrible scourge," Cannon said. "You would have had to have been a psychopathic monster to not want to be part of the solution."

Benjamin said the polio vaccine campaign became a moment of national unity: "Jonas Salk and the folks that solved the polio problem were national heroes."

By 1979, polio was eradicated in the United States.

How it ended: Vaccination

Smallpox

How it started: The disease had been observed in the Eastern hemisphere dating to as early as 1157 BCE, and European colonizers first brought smallpox to North America's previously unexposed Native population in the early 1500s. A 2019 study suggested smallpox and other viruses introduced by colonizers killed as much as 90% of the indigenous population in some areas. Globally, smallpox is estimated to have killed more than 300 million people just in the 20th century. The case fatality rate of variola major, which caused the majority of smallpox infections, is around 30%.

Outbreaks continued in North America through the centuries after it arrived here, at one point infecting half the population of the city of Boston. We fought back by trying to infect people with a weakened version of it, long before vaccines existed. An enslaved man named Onesimus is believed to have introduced the concept of smallpox inoculation to North America in 1721 when he told slave owner Cotton Mather that he had undergone it in West Africa. Mather tried to convince Boston doctors to consider inoculating residents during that outbreak, to limited success. One doctor who inoculated 287 patients reported only 2% of them died of smallpox, compared to a 14.8% death rate among the general population.

In 1777, George Washington ordered troops who had not already had the disease to undergo a version of inoculation in which pus from a smallpox sore was introduced into an open cut. Most people who were inoculated developed a mild case of smallpox, then developed natural immunity. Some died, though at a far lower rate compared with other ways of contracting the disease. The practice of inoculation was controversial enough — some skeptics said it was not sufficiently tested, some argued it was doctors "playing God," others theorized that it was a conspiracy from slaves to trick white slave owners into killing themselves — that it was banned in several colonies.

Edward Jenner first demonstrated the effectiveness of his newly created smallpox vaccine in England in 1796. Vaccination spread throughout the world, and deaths from smallpox became rarer over time: In a century, smallpox went from being responsible for 1 in 13 deaths in London to about 1 in 100.

But while early vaccines reduced smallpox's power, it still existed: An outbreak hit New York City in 1947. It demonstrated that the vaccines were not 100% effective in everyone forever: 47-year-old Eugene Le Bar, the first fatality, had a smallpox vaccine scar. Israel Weinstein, the city's health commissioner, held a news conference urging all New Yorkers to get vaccinated against smallpox, whether for the first time or what we would now call a "booster shot."

The mayor and President Truman got vaccinated on camera. In less than one month, 6.35 million New Yorkers were vaccinated, in a city of 7.8 million. The final toll of the New York outbreak: 12 cases of smallpox, resulting in 2 deaths.

Our country's final outbreak affected 8 people in the Rio Grande Valley in 1949.

In 1959, the World Health Organization announced a plan to eradicate smallpox globally with vaccinations. The disease was declared eradicated in 1980.

Of all the diseases our species has tackled, "the only one we've ever been really successful to totally eradicating is smallpox," Benjamin said. The only remaining smallpox pathogens exist in laboratories.

How it ended: Vaccination

HIV/AIDS

How it started: In 1981, the CDC announced the first cases of what we would later call AIDS.

Roughly half of Americans who contracted HIV in the early 1980s died of an HIV/AIDS-related condition within two years. Deaths from HIV peaked in the 1990s, with roughly 50,000 in 1995, and have decreased steadily since then: As of 2019, roughly 1.2 million Americans are HIV-positive; there were 5,044 deaths attributed to HIV that year.

The Reagan administration did not take HIV seriously for years. Unlike COVID, which was quickly identified as a respiratory disease, HIV spread for years before scientists knew for sure how it was transmitted. Gay activists who encouraged their community to use condoms in the early 1980s were criticized as "sex-negative."

Today, we know how to prevent the spread of HIV, and treatments for it have progressed to the point where early intervention can make the virus completely undetectable.

"If you're HIV positive, the HIV pandemic never went away for you," said Cannon, who's spent much of her career studying the virus. She described it as a "great irony" that we identified the cause of COVID and developed a vaccine within a year, only to have people refuse it: "Anybody with HIV would tell you that the opposite is true for HIV, where despite decades now of research, we have not been able to come up with vaccines that work against this shapeshifter of a virus that is HIV, and people would be desperately pleased if there were vaccines."

Around 700,000 people in the U.S. have died of HIV-related illnesses in the 40 years since the disease appeared. In less than two years of the COVID-19 pandemic, we've surpassed 800,000 COVID deaths.

How it ended: Endemic

SARS

How it started: SARS first appeared in China in 2002 before making its way to the United States and 28 other countries.

Severe acute respiratory syndrome — quickly shortened to SARS in headlines and news coverage — is caused by a coronavirus named SARS-CoV, or SARS-associated coronavirus. COVID-19 is caused by a virus so similar that it's called SARS-CoV-2.

Globally, more than 8,000 people contracted SARS during the outbreak, and 916 died. (By comparison, there were 10 times more cases of COVID-19 than that registered globally by the end of February 2020.)

One hundred fifteen cases of SARS were suspected in the United States; only 8 people had laboratory-confirmed cases of the disease, and none of them died.

Like COVID-19, fatality rates from SARS were very low for young people — less than 1% for people under 25 — up to a more than 50% rate for people over 65. Overall, the case fatality rate was 11%.

Public anxiety was widespread, including in areas unaffected by SARS.

SARS and COVID-19 have a lot in common. But the diseases — and the way the government responded to them — weren't exactly the same, said Benjamin, who worked for the CDC during the SARS epidemic.

"There wasn't asymptomatic spread. Early on we had a functional test. We had a public health system that was in much better shape than it is today. All those things went wrong this time," he said. "And [COVID-19] turned out to be much more infectious, it turned out to have asymptomatic spread. ... [In 2020] you had a public health system which wasn't ready for prime time because it hadn't been invested in."

Conversely, he said, the response to SARS was robust and immediate. The WHO issued a global alert about an unknown and severe form of pneumonia in Asia on March 12, 2003. The CDC activated its Emergency Operations Center by March 14, and issued an alert for travelers entering the U.S. from Hong Kong and parts of China the next day. Pandemic planning and guidance went into effect by the end of that month.

"When [public health organizations] had the actual genetic sequence mapped out and then they made a test for it, they rapidly got that test out to state and local health departments, they began screening, doing surveillance, we contained it very quickly, we communicated effectively to the public, and it worked," he said.

In the case of SARS, the disease stopped spreading before a vaccine or cure could be created. Scientists knew another coronavirus could emerge that was more contagious. They laid the groundwork for developing the COVID-19 vaccines we have now.

How it ended: Died out after being controlled by public health measures

Swine flu

Passengers wait inside a subway station in Mexico City in 2009 after a government-ordered shutdown designed to contain the swine flu outbreak. (Brennan Linsley / Associated Press)

How it started: Both the Spanish flu and swine flu were caused by the same type of virus: influenza A H1N1.

Ultimately, according to the CDC, there were about 60.8 million cases of swine flu in the U.S. from April 2009 to April 2010, with 274,304 hospitalizations and 12,469 deaths — a case fatality rate of about 0.02%. So there were millions more cases of swine flu than there were of COVID-19 in the same time period, but a fraction of the fatalities. Eighty percent of swine flu deaths were in people younger than 65.

It was first detected in California on April 15, 2009, and the CDC and the Obama administration declared public health emergencies before the end of that month. As with COVID-19, hospital visits spiked. Hundreds of schools closed down temporarily. In Texas, a children's hospital set up tents in the parking lot to handle emergency room overflow; several hospitals in North Carolina banned children from visiting. Hospitals near Colorado Springs, Colo., reported a 30% increase in flu visits. Three-hundred-thousand doses of liquid Tamiflu for children were released from the national pandemic stockpile.

In the same month cases were first detected, the CDC started identifying the virus strain for a potential vaccine. The first flu shots with H1N1 protections went into arms in October 2009. WHO declared the swine flu pandemic over in August 2010. But like Spanish flu, swine flu never completely went away.

How it ended: Endemic

Ebola

How it started: From 2014 to 2016, 28,616 people in West Africa had Ebola, and 11,310 died — a 39.5% case fatality rate. Despite widespread fears about it spreading here — including close to 100 tweets from the man who would be president when the COVID-19 pandemic began — only two people contracted Ebola on U.S. soil, and neither died.

So how did we escape Ebola? Unlike COVID, Ebola isn't transmitted in the air, and there's no asymptomatic spread. It spreads through the bodily fluids of people actively experiencing symptoms, either directly or through bedding and other objects they've touched. If you haven't been within three feet of a person with Ebola, you have almost no risk of getting it.

Part of the problem in Africa, Benjamin said, was that families traditionally washed the bodies of the deceased, exposing themselves to infected fluids. And healthcare workers who treated patients without proper protective equipment or awareness of heightened safety procedures were at risk. Once adequate equipment was delivered to affected areas and precautions were taken by healthcare workers and families of the victims, the disease could be controlled. People needed to temporarily change their behavior to respond to the public health crisis, and they did.

While this particular outbreak ended in 2016, it's very possible we will see another Ebola event in the future. An Ebola vaccine was approved by the FDA in 2019.

How it ended: Subsided after being controlled by public health measures

How will COVID end?

More than 27,000 people had died of COVID-19 in Los Angeles County, and nearly 800,000 in the U.S., as of mid-December. Here, flags at the Griffith Observatory memorialize L.A.'s dead. (Luis Sinco / Los Angeles Times)

Big picture, "pandemics end because the disease is unable to transmit itself through people or other vectors that allow the transmission of the disease," Benjamin said.

The most likely outcome at this point is that COVID-19 is here to stay, he said: "I think most people now think that it will be endemic for a while." On Twitter, his colleagues in epidemiology and public health seem to agree.

COVID has a lot going for it, as far as viruses go: Unlike Ebola and SARS, it can be spread by people who don't realize they have it. Unlike smallpox, it can jump species, infecting animals and then potentially reinfecting us. Unlike polio, one person can unwittingly spread it to a room full of people, and not enough people are willing to get vaccinated at once to stop it in its tracks. It's less contagious than swine flu, and less deadly than Ebola, landing it in a sort of perverse sweet spot where it infects a lot of people but doesn't kill enough of them to run out of victims. For many people, it's mild enough that it convinces others they don't have to take the disease or precautions against it seriously. No one thought that about smallpox or Ebola.

In a conversation I had with Cannon for a different story in May 2020, she told me if someone were designing a virus with the maximum capacity to succeed, it would look a lot like this coronavirus.

"One of the really superpower things about this virus is its stealthiness," she told me then. "So you can feel fine, you can go hang out with friends and not obey the six-foot rule and the next morning you feel like death and you're like, 'oh crap.'" Back then, she contrasted it with the way we shut down SARS: "The reason we could stop it is everybody who had SARS, you were only infectious while you were sick. You woke up one day feeling like death and that was the day you were infectious. Infected people couldn't walk among us. ... With this coronavirus, they walk amongst us."

So what happens next? In some populations, enough people will get vaccinated to achieve something like herd immunity. In others, it will burn through the population until everyone's had it, and either achieves naturally gained immunity (which confers less long-term protection than vaccination) or dies. People still die from influenza and HIV in the United States; a disease becoming endemic isn't exactly a happy ending.

"We tolerate the tragedy a lot better when it's a disease that we've seen before," Benjamin said. "It is less scary to us."

Based on where we are now, "I don't think COVID-19 will ever go away," Cannon said.

We're still learning about the Omicron variant. Early reports out of South Africa suggest it may be a more contagious but milder version of the disease, though it's too early to say for sure. In a perfect world, COVID would go away entirely; with that possibility almost certainly off the table, an attenuated strain that displaces the Delta variant and turns COVID into an illness that rarely requires hospitalization is perhaps the best we can hope for at this point.

How it ends: A combination of vaccine- and naturally-gained immunity, attenuation, availability of rapid testing, and improvements in treatment for active cases could turn it into what skeptics wrongly called it to begin with: a bad cold or flu.

This story originally appeared in Los Angeles Times.

Fact check: Why is the 1918 influenza virus called 'Spanish flu'?

Matthew Brown, USA TODAY,
USA TODAY•March 23, 2020

The claim: The 1918 flu pandemic became known as the “Spanish flu” because wartime censors minimized reports of the illness while the Spanish press did not.

On March 20, the Facebook page Unbelievable Facts shared a graphic on the origins of the 1918 flu pandemic’s more common name, the “Spanish flu.”

According to the post, the pandemic earned the name “because during WWI, wartime censors minimized early reports of illness and mortality” in combating nations “but the papers were free to report the epidemic’s effects in neutral Spain, which created a false impression of Spain as being especially hard hit.”

Unbelievable Facts, which brands itself as “your source for the best bizarre, strange and extraordinary stories on the internet,” has more than 8.3 million followers on Facebook. The post in question has 6,100 reactions and about 1,300 shares on the site.
The origins of 1918 influenza and its spread

When it was discovered, the 1918 flu virus was spreading in a world at war. Because of the turmoil that World War I had wrought on societies around the globe, it’s difficult for scientists and historians today to piece together the exact origins of the virus.

The Centers for Disease Control and Prevention states there is no universal consensus as to the origins of the virus, though experts have theorized about origins as disparate as China, France, the United States and United Kingdom. Others have argued the virus was likely circulating in European armies for months – and potentially even years – before it was officially discovered. The CDC states that the first confirmed cases in the United States were military personnel in the spring of 1918.

“We don't know and will probably never know,” John M. Barry, the author of "The Great Influenza," a history of the 1918 flu, told USA TODAY. In his book, Barry advanced the theory that the virus began in rural Kansas, but “work since then has caused me to back away from that. The best evidence points to China. Other theories suggest France or Vietnam.”

Fact check: Coronavirus originated in China, not elsewhere, researchers and studies say

The comparatively mild effect the 1918 flu had on China has led some researchers to suspect that the virus or a related milder strain began there earlier, meaning the population had a higher level of immunity to the disease when it reached pandemic levels elsewhere. This research is disputed, however, notably because data from China’s Warlord Period is arguably less reliable.

The 1918 flu was an H1N1 virus with genes indicating it likely originated in birds. This makes it like the H1N1 strain that caused the swine flu pandemic of 2009. Unlike swine flu, however, the 1918 flu was far more damaging for the world; an estimated third of the world’s population was infected, with about 50 million people dying from the virus.

Unlike most influenza viruses, the 1918 flu was most lethal for people ages 20-40 and young children. Researchers don’t fully understand why this was the case, though the lack of a vaccine, poor sanitary conditions and no coordinated response nations likely contributed to the disastrous impact. The possibility of a similar virus having spread during the youth of 1918's older population may be why those 65 and older had a lower mortality rate than would be expected.
The role of governments in publicizing the flu's spread

A key factor that made both mitigating the virus and tracing its impact difficult today is that governments at the time downplayed the issue. Countries did not want to lower national morale or cause panic while also fighting what was then the largest and most costly war in history.

Public health officials in France, Germany, the United Kingdom and the United States all downplayed the spread of the virus, treating it as a normal influenza virus or cases of “simple pneumonia” found in the ranks of soldiers.

“The U.S. didn't formally censor,” Barry said, but the mainstream press and government institutions instead opted for a kind of “self-censorship.” This strategy ultimately proved more damaging, because when the gravity of the situation became unavoidable, governments had lost their credibility about the pandemic.

The pressures of the global conflict weren’t present in the Kingdom of Spain, which was neutral in World War I. As such, Spanish public officials and media more readily reported on the crisis as it spread throughout the country.

Additionally, King Alfonso XIII of Spain also fell gravely ill with the virus, heightening press coverage in the country and grabbing headlines elsewhere. There is no evidence, however, that the virus began in Spain, nor is there any indication that the virus was especially worse in Spain than anywhere else in Europe.
Our ruling: True

Though it is difficult to determine from the historical record where the 1918 flu virus originated and how it spread across the globe, the origins of its common name are not in doubt. The Spanish press, being those most likely to report on the virus and its spread, also gave the false impression at the time that the disease originated there.

The name “Spanish flu” has accompanied the 1918 pandemic ever since, largely because other countries were unwilling or uninterested in reporting on the outbreak within their own borders. We rate this claim TRUE, based on our research.
Our fact-check sources:


CDC History of 1918 Flu


The Great Influenza by John M. Barry


Did the 1918-19 Influenza Pandemic Originate in China?" by Christopher Langford


Chinese Warlord Era, Wikipedia


CDC History of 2009 H1N1 Flu


Pandemic versus Epidemic Influenza Mortality, The Journal of Infectious Diseases


The Flu That Wasn't Spanish, Government of the United Kingdom


Why Was It Called The 'Spanish Flu'?, History.com

This article originally appeared on USA TODAY: Fact check: How did the 1918 pandemic get the name 'Spanish flu'?

Have We Learned Nothing From the COVID-19 Pandemic? New Animal Epidemics Ignored

BY MARTHA ROSENBERG

 JANUARY 21, 2022
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You would think as COVID-19 has now killed 5.54 million, there would be greater vigilance about other brewing zoonotic epidemics. Yet even as 41 countries now have outbreaks of avian influenza, called HPAI or H5N1, including the US, there is little to no reporting on the threat in the US press. The attitude still seems to be “wait and see” as it was with COVID-19 though cases surfaced six months before any action was taken; have we learned nothing?

Since the new year, millions of birds have been killed in Israel, Spain, France (notable for its foie gras), the UK, the Netherlands, Hungary, Nigeria, India, Japan and other countries to stop the spread of avian influenza. Yet depopulating and “repopulating the global poultry stock” doesn’t work and just keeps “reloading the gun” of avian influenza say Dr. Michael Greger in his excellent book, “Bird Flu: A Virus of Our Own Hatching.”

While the HPAI/H5N1 “bird flu” virus does not easily transmit to humans, when it does it is often fatal. Moreover, since bird and swine viruses are both Type A influenzas, a bigger worry is reassortment as we saw with the 2009 H1N1 virus (called “swine flu” until pork industry pressure). This virus was an eerie mix of five swine and bird flu influenzas. The 1918 flu epidemic was also from a bird influenza virus.

Reporter Tom Philpott indicted the massive Smithfield Foods subsidiary Granjas Carroll de México, along the Mexican border, for hatching the 2009 virus –– though Smithfield strongly disagreed.

Concerns about influenza reassortments appear in the scientific literature. According to the journal Infection, Genetics and Evolution, “Nowadays, it is well-established that A(H1N1)pdm 2009 was the result of a genomic reorganization between two A(H1N1) swine viruses with at least four previously reassorted gene segments from avian, human and swine-adapted viruses…The H5N1 virus infecting humans was the result of a reassortment among a quail H9N2 strain with segment-4 (hemagglutinin, HA) from goose H5N1 and with segment-6 (neuraminidase, NA) from teal H6N1 viruses…These are excellent examples of how reassortment can impact the evolution of segmented viruses.”

In addition to bird flu mutations, scientists and public health officials also worry about the evolution of the Swine Acute Diarrhea Syndrome coronavirus or SADS-CoV which is very similar to COVID-19 and also endemic to China and linked to bats. While SADS-CoV does not appear to have reached US shores yet, it is related to porcine epidemic diarrhea virus (PEDV) which caused the death of millions of US pigs in 2013–2014.

Another disease that has overtaken most of the world while barely reported in the US is African Swine Fever (ASF) virus. It killed a quarter of the world’s pigs in 2019 and is now endemic in 50 countries including our neighbor Haiti. Unless you read the ag press you’ve probably never heard of it.

ASF has devastated China’s pork industry and may explain why China relies on the Smithfield Tar Heel, North Carolina slaughter plant, which it bought in 2013, for pork.

Few realize the gigantic slaughterhouse which kills as many as 35,000 pigs a day is owned by China’s WH Group. China bought the plant soon after thousands of pigs with circovirus were found floating in the Huangpu river. Congressional hearings were held but the sale went forward.

Has Pandemic Response Improved?

It is understandable that public health officials want to avoid “false alarms” when a pandemic does not develop –– especially after the apparent overreaction to a swine flu outbreak in the US in 1976 that did not materialize. Still, erring on the side of caution with COVID-19 and acting sooner would have saved millions.

Less noble are the motives of news outlets whose fast and processed food advertisers cause them to downplay and even ignore animal diseases that could cut into sales. Who, for example, ever saw piles of pig or poultry carcasses on the news when viruses that killed those animals relentlessly ripped through the US less than 10 years ago?

Thanks to slow-to-act public health organizations and Big Food-captured news outlets, zoonotic epidemics that could become pandemics are still ignored until they are knocking at our front door and it is too late. Has COVID-19 taught us nothing?

Martha Rosenberg is an investigative health reporter. She is the author of  Born With A Junk Food Deficiency: How Flaks, Quacks and Hacks Pimp The Public Health (Prometheus).