A Comprehensive Review and Update on Avian Influenza (Bird Flu) in the U.S.

I have been writing about avian influenza since April 1^st a year ago in a large number of blog posts.

To understand why I have written so much about this virus and why it remains a concern to me, let’s first review information I have previously provided and then let’s discuss an update and why there is growing concern.

Many of my long-term followers of the blog will recall that Dr. Epperly and I wrote a book entitled: Preparing for the Next Global Outbreak: Lessons from the Schoolhouse to the White House https://press.jhu.edu/books/title/12896/preparing-next-global-outbreak that was published by the Johns Hopkins University Press and released in April of 2023. In that book, we point out why we are at risk of future pandemics, why we need to prepare for them, and the lessons learned (117 of them, specifically) that should influence our preparedness and future responses to a pandemic. I also explained that pandemics are not 100-year events as commonly believed among the public, and why it would not be surprising for us to have another pandemic as soon as a decade from our last (recall that COVID-19 was declared a pandemic in March of 2020.)

Part of pandemic preparedness is surveillance of viruses with pandemic potential. (By the way, a pandemic does not have to be caused by a virus, and prior pandemics have been caused by bacteria, however, advances in science and medicine and the difference in transmission modes among viruses, bacteria, and fungi make viruses the strongest candidates for causing future pandemics.)

When I pick viruses for my list of those with the greatest pandemic potential, the criteria I use are:

1^st level selection:  Viruses with airborne transmission, i.e., the virus is emitted from the mouth and nose of the infected person in small enough particles that it can be carried large distances in an area with common ventilation (e.g., a home, classrooms, an airplane, public spaces) and can hang suspended in the air for some period of time. (examples are SARS-CoV-2, influenza viruses, and the measles virus).

2^nd level selection: Of those viruses with airborne transmission, then I rank highest on the list those viruses that have the suspected or demonstrated ability for sustained human-to-human transmission and those that are novel viruses or known viruses with novel mutations, recombinations or reassortments for which there is expected to be little population-level immunity. (A novel virus is one that has not previously circulated in the current human population, and as a consequence, there is no or little existing immunity in humans and all or most all people would be considered susceptible to infection.)

(Levels 1 and 2 select for viruses with pandemic potential, then level 3 selects for the likely severity of the pandemic were it to materialize, which means not only would the virus be considered to have pandemic potential, but the pandemic would likely cause severe disease manifesting as the need for medical care and potentially hospitalization, be disruptive to society and its normal functioning, and have the potential for overwhelming our health care system.)

3^rd level selection: Then, of those viruses that satisfy the first and second levels of selection, I rank those viruses with any of the following traits higher up the priority list, and even higher up the list based upon the number of these traits that they have:

1. Relatively high levels of morbidity (illness, but not death) and mortality (death) across all age groups, or at least many age groups;
2. Significant presymptomatic or asymptomatic spread of infectious virus;
3. School-aged children able to transmit the virus efficiently;
4. High infectious load of virus (the amount of virus in the nose and throat) in infected persons;
5. Low infectious dose required for transmission (the amount of virus that you must breathe in to become infected);
6. The virus is not particularly vulnerable to environmental factors (temperature, humidity, UV light) and is able to remain infectious in the air and on surfaces for an extended period of time;
7. No existing test or the only available tests are high complexity tests that can only be conducted in certain specialized laboratories (meaning that we will have trouble knowing the full extent of transmission of the virus in real time and we will not have the ability to quickly screen persons to determine whether they are infected with the virus);
8. Widespread zoonotic and reverse zoonotic spread (the virus can transmit among humans, to our pets and farm animals, and back to humans);
9. Non-durable immunity from infection and vaccination (meaning that reinfections will further increase the amount of disease transmission and illness, and the potential exists, as with COVID-19, that repeated infections will lead to long-term health conseequences);
10. No existing vaccine that is effective or that could quickly be modified to be effective in preventing severe disease;
11. No known existing medications with antiviral effect against the virus;
12. High degree of viral fitness and rapid evolution to increase transmissibility; and
13. Significant levels of infection among health care workers and nosocomial spread (this refers to patients infecting other patients and health care staff allowing for continued transmission chains among the most vulnerable people and the work force needed to care for patients) in health care facilities.

Using my criteria, avian influenza viruses and novel coronaviruses certainly have to be at the top of the list.

HPAI A(H5N1), an influenza A virus [HPAI is the abbreviation for “highly pathogenic avian influenza.” When referring to an avian influenza virus as being highly pathogenic we are indicating that it is a virus that causes death to all or the vast majority of birds (often chickens) that it infects as opposed to low pathogenic avian influenza viruses (LPAI) that do not typically cause severe illness or death in birds].  

Let me take a moment and explain some of the nomenclature I am using. The A in “A(H5N1)” is an abbreviation for an influenza A virus (as opposed to influenza B, C or D viruses. A (other than the avian influenza viruses) and B viruses circulate across the globe in humans and generally cause seasonal epidemics annually. Influenza C generally causes very mild illness, and therefore, is not seen as a public health threat, nor is its activity tracked. Influenza D viruses circulate primarily in cattle, and we have not identified spillovers into humans.). The H5 refers to hemagglutinin subtype 5). The influenza virus has an envelope (not all viruses do), and hemagglutinin is the major protein found within the envelope. It is both involved as a site for binding to cells to cause infection, but also a target for neutralizing antibodies. There are 18 antigenically distinct (meaning that our immune responses to one form of hemagglutinin may provide little, if any, cross-reactive protection against another) subtypes of hemagglutinin protein – (H1 – H18).

The designation N1 refers to the fact that the other major protein of the virus is neuraminidase type 1. The neuraminidase is another envelope protein that plays a number of roles in the transmissibility of the virus, the infectivity of the virus and in the release of viral progeny once reproduced in an infected cell. There are 11 antigenically distinct subtypes of neuraminidase proteins – (N1 – N11).

A(H5N1) viruses are avian influenza viruses adapted to infect and transmit among birds because the cell receptor the virus attaches to that allows the virus to enter the cells of birds and replicate has an α-2,3 sialic acid sugar attached to the protein receptor whereas human influenza viruses utilize receptors on the cells of the human lung with α-2,6 sialic acid sugars that allows them to infect humans and transmit forward from humans.

The first identified outbreak of H5N1 was among poultry in Scotland in 1959. The first known transmission of this virus to a human was in 1997 in Hong Kong. In that year, a total of 18 persons were infected, and six of them died- i.e., a case fatality rate of 33%.

The predecessor virus to the one now spreading in North America has circulated in birds since at least 1996 (the first infection of the H5N1 virus that we are currently dealing with was detected in 1996 in China in a domestic goose) when it caused an epidemic among birds. The good news was that from 1997 until 2024, only a total of 902 sporadic human A(H5N1) cases had been reported from 23 countries, caused by different HPAI A(H5N1) virus clades.

Avian influenza viruses are of the N5 or N7 type. There are three avian influenza types that have been responsible for large disease outbreaks- H5N1, H5N8 and H7N9. Of these three, H5N1 is considered to be the most pathogenic and severe.

The first recognized transmission of the virus to non-human mammals was in 2021 to foxes. However, from late 2021 on, there have been concerning spread of the virus to an ever-expanding range of animal species and increasing numbers of infections within those species. Unfortunately, the wider geographic range of infections and the involvement of new species create opportunities for the emergence of new and potentially more dangerous variants of the virus. Further, the easy transmission observed between certain mammalian species, such as Spanish minks and Peruvian sea lions, raises concern about the potential for the virus to establish reservoirs in different animal populations and pose ongoing risks to both animal and human health.

Influenza A viruses are carried by wild birds in their intestinal tract and can be shed by these birds through various means, such as saliva, feces and nasal secretions. Transmission of HPAI H5N1 resulting in human infection primarily occurs through direct contact with infected birds. 

The introduction of H5N1 into North America was not known to have occurred until late 2021, and this resulted from migratory birds. The bad news is that with ongoing transmission in animals, the virus does evolve and there is always the chance that it could mutate or reassort in a manner that would increase transmission to humans. In fact, the reference to different HPAI A(H5N1) virus clades is a reference to significant genetic changes to the virus warranting assignment to a new clade (for influenza viruses, we call these clades, but you can think of them as strains). The other bad news is that from 1997 to 2024, there is a cumulative case fatality rate of greater than 50% in humans.

In the last century, there have been four occasions when influenza viruses with genes that originated from swine (pig) or avian (bird) reservoirs entered the human population with wide-spread, efficient and sustained human-to-human transmission causing pandemics [1918 Spanish flu A(H1N1), 1957 Asian flu A(H2N2), 1968 Hong Kong flu A(H3N2), and 2009 swine flu A (H1N1)]. (Recall that I mentioned above that there is a common belief that pandemics are 100-year events, but obviously, this is not the case, and here I am only listing pandemics caused by influenza viruses.)

Thus far, while the H5N1 virus has infected humans, it has not shown the ability for efficient human-to-human transmission, and unless and until that happens, it will not produce a pandemic. Most of the infections have been in people with close contact with infected animals, and we have not seen much forward transmission, even to family members.

Then, why all the concern? The concern is that the virus is spreading globally, even to remote areas (including Antarctica), with an alarming expanded range of hosts, including occasional spillovers to humans, all of these events increasing the potential for mutations or reassortments that would all the virus to efficiently transmit to and among humans.

Waterfowl are natural hosts for low pathogenic influenza viruses. These wild and migratory birds then move to new locations and carry the virus with them. They congregate with domesticated ducks and geese to which they can transmit the viruses. Influenza viruses mutate frequently and while the virus started out as a low pathogenic virus (promoting its spread by these migratory birds that are not too sick to relocate geographically and find new domestic birds to transmit the virus to), there is the potential for the virus to evolve to a highly pathogenic form of virus that can result in loss of many domestic birds (some involved in our food chain) as it is transmitted among these birds and then potentially back again to migratory birds that can carry the virus to new areas of the state, country or world further infecting more domestic poultry before these birds die as appears to be happening with this current H5N1 epizootic.

What has been alarming during the past two years is that this particular HPAI A(H5N1) has been increasingly identified in mammals that generally have not been impacted by previous avian influenza viruses and we have seen the evidence that this particular virus can be highly pathogenic in many of these species of animals, as well, including ocean animals.

Human transmission of avian influenza viruses has historically been rare, as opposed to swine influenza viruses, which are much more suited for human transmission (while avian influenza viruses utilize only the α-2, 3 sialic acid receptors, swine have both α- 2, 3 and α- 2, 6 sialic acid receptors (the latter being the receptor type in the human lower airways), but still relatively uncommon (for example, we had three documented cases in 2023 (two in Michigan and one in Montana – all from direct exposure to pigs at fairs).

Swine flu is endemic to pigs. But pigs can be the intersection between birds (poultry on farms or even wild birds that transiently stop on land shared with pigs, or in the case of HPAI, where the bird carcasses remain following their death) and humans (farmers, visitors at fairs, live markets, etc.) and pigs can serve as a “mixing bowl” for human, swine and avian viruses when co-infected with both types of virus.  “Mixing bowl” is a reference to the fact that coinfections of pigs with these different strains of influenza virus can result in the influenza viruses swapping segments of their genetic material, a process referred to as reassortment, in which the resulting virus has an increased ability to transmit from the pig to humans, and the most worrisome case being when the resulting reassorted virus also has the ability to transmit efficiently from humans to other humans. In fact, this is exactly what happened with the influenza A virus that caused the 2009 pandemic [A(H1N1)pdm09]. Genetic sequencing of this virus revealed that the eight gene segments of the virus were from a mix of avian, human and swine origins.

We have been experiencing an epizootic (an epidemic in animals) of avian influenza in dairy cattle in the U.S. for more than a year now, and we still have demonstrated little ability to contain the spread of this virus. The earliest detected cases were in Texas. This is also where we had the first detected spillover into a dairy worker.

We know where this virus came from: it’s a reassortment between Eurasian highly pathogenic avian influenza and low pathogenic North American avian influenza strains that were circulating naturally in wild birds.

While we have known for some time that cows could be infected with influenza D viruses, we previously had not observed avian influenza virus infections of cattle to any significant degree. And while we knew experimentally that virus could infect the mammary tissue of cows, mastitis was the common and prevailing manifestation of avian influenza infection in cattle, resulting in very high levels of virus in the milk of infected cows. An additional concern arose when it was reported by at least one laboratory that cow utters have both α- 2, 3 and α- 2, 6 sialic acid receptors giving rise to the theoretical risk that cows’ utters could serve as “mixing bowls” for different influenza viruses in addition to pigs.

Further, farmers started reporting deaths of domestic and peridomestic (wild animals that surround and come into frequent contact with domestic animals) on their farms, particularly grackles and pigeons and outdoor domestic cats who we believe contracted infection from drinking infected raw milk from the cows. Disturbingly, the cats known to be infected showed rapid and drastic neurological deterioration and death in the majority of cases.

We have now identified at least 70 human infections, with 1 reported death. However, more concerning are cases of bird flu of a different clade that are in migratory birds and have spilled over to humans. Most recently (April 8, 2025), a previously healthy, 3-year-old Mexican girl died from respiratory manifestations (respiratory failure) after a month’s long illness of avian influenza from a clade (D.1.1 transmitted by wild birds, compared to the B.1.1 and B.1.3 clades that have been transmitted by cows) of virus that is related to the case of a man in Louisiana who died from bird flu in January of this year (he was an older man and did have underlying medical conditions) from this clade of the virus. A person in Wyoming and a poultry worker in Ohio also were infected with this clade and experienced severe disease requiring hospitalization. A 13-year-old girl was also infected with this same clade and hospitalized in Canada with very severe disease requiring extraordinary care for a protracted period of time in the intensive care unit to save her life. Though these deaths are tragic, it might not be as concerning had these occurred in persons who had prolonged and close contact with cattle or poultry. However, most had no obvious source of contact with animals or exposure to account for their disease.

A case report in the New England Journal of Medicine provided us with important details about this first known transmission of H5N1 from a dairy cow to a human.

In late March of 2024, the farm worker developed redness and discomfort in his right eye. The worker denied having any fever, chills, cough, shortness of breath or loss or distortion of vision.

The worker denied any contact with dead or diseased birds or poultry. He did report close contact with cows, including cows that were showing signs of possible infection with avian influenza manifested by lethargy, fever, decreased appetite, dehydration, and/or decreased milk production. He did routinely wear gloves, but no other PPE including masks or eye protection.

On physical examination, the patient did not appear severely ill. His lungs were clear.

His eye examination revealed the following:

We are looking at the patient facing us, so the eye on the left side of this photo is actually his right eye, and the eye to our right is actually his left eye. Looking at his left eye, he has conjunctivitis (inflammation of the conjunctiva, which is the superficial lining of the eye and eye lids). We can see that it is red and injected, meaning that we see the blood vessels much more prominently than in someone with a normal-appearing eye. His right eye demonstrates a subconjunctival hemorrhage, in other words, there is bleeding directly under the conjunctiva. We can tell that there is a hemorrhage (bleeding) because the redness is confluent and obscures the blood vessels, whereas in his left eye, we can see the blood vessels much more clearly.

The examiner swabbed the patient’s nose and right eye to test for influenza virus. The test (which looks for genetic traces of virus) of both samples was positive for influenza A and for the H5 protein, which is indicative of avian influenza. That test also suggested that the amount of virus in the eye sample was very high. The CDC performed additional testing that confirmed that the virus was A(H5N1) and genetically the same as the virus detected to be circulating among dairy cows.

The patient was instructed to isolate at home and was started on an oral antiviral medication (oseltamivir). Over the ensuing days, the patient’s conjunctivitis resolved and no family members developed signs or symptoms of infection.

Additional testing of the virus genetic material revealed that it had not mutated in a way that would change the receptor-binding protein from the avian form (α- 2, 3-linked sialic acid [we do have this form or receptors in our eyes]) to the human form (α- 2, 6-linked sialic acid [this is the receptor type in the human respiratory tract]). On the other hand, the virus retrieved from the infected farm worker had acquired a mutation in the PB2 protein that has been associated with adaptation of the bird virus to mammals, including humans. Fortunately, the virus did not have the mutations that we associate with developing resistance to our usual influenza A virus antiviral agents.

This is good news/bad news. The bad news is that cows can transmit the virus to humans who are in close and prolonged contact with infected cows, though we still don’t know how transmission occurred – respiratory droplets from infected cows? Contact with virus in the milk of infected cows and then touching or rubbing one’s eyes? Aerosolization of virus from the milk when cleaning floors or equipment used in milking the cows?

The good news is that the patient did well and appeared to recover well, the virus did not show worrisome changes that would suggest that the virus can now efficiently transmit to and among humans, and the patient did not appear to infect anyone in his household, though we were not provided with any information as to what precautions were used in the home and how many persons were in the home. I suspect that the disease was relatively mild and mostly caused conjunctivitis is that the avian influenza virus involved had not acquired the ability to bind to α- 2, 6 sialic acid receptors and therefore, was unable to infect the person’s lungs.

There remain many questions. One question is whether the antiviral treatment prevented him from becoming more ill and/or did it shorten his course of illness? I also hope that they will carefully follow this farm worker over time. We know that in other mammals, this virus has seemed to produce significant neurological disease. The eyes can be a route for viruses to access the brain. It would be good to follow this patient to ensure he does not develop any signs of neurological disease in the future.

The continued transmission of A(H5N1) in cattle and in wild birds with spillovers to humans and domestic and peridomestic animals continues to concern me in that we are rolling the dice and giving this virus more chances to mutate and reassort. As I mentioned, this is an RNA virus and RNA viruses are more prone to acquire mutations because they often do not have the same proof-reading systems in place to catch errors when the RNA is being transcribed to produce viral proteins.

Many mutations are of no significance, some are detrimental to the virus and those viruses will generally lose in competition to more fit forms of the virus, so they disappear over time, and then some may be advantageous to the virus (increase viral fitness through increasing transmissibility, receptor binding or evading immune defenses).

The viruses that infected the cows and the humans that are generally causing conjunctivitis and mild illness are the same version of virus (B.1.1 or B.1.3). The viruses that have infected wild birds and then transmitted to humans causing much more severe disease are a different one that has infected cows (D.1.1).

We can look at the phylogenetic trees for this virus (you probably have seen these, but not known what they are called or what they mean, if you have followed the developments with SARS-CoV-2 over the past five years. These are diagrams that plot out the various versions of the virus starting (usually at the left side of the diagram) with the original form (wild-type) or at least the first discovered form of the virus and then those new versions of the virus with the fewest mutations will be closer and those with the most mutations will be further away from the original form of the virus. When the collection of mutations has been found to be significant, then the SARS-CoV-2 virus was assigned a new variant name (and appears on a new branch of the phylogenetic tree) or in the case of this A(H5N1) virus, it is assigned to a new clade.

We can look at a phylogenic tree for the changes in each of the viruses’ major proteins that we are interested in. We previously discussed the H or HA (hemagglutinin) protein and its role (especially in virus attachment to the host cell and fusion with the host cell’s membrane in order to allow the virus to enter the cell). This virus has the H5 subtype protein, and the phylogenic tree shows that there have been relatively minor mutations to this protein (that is good, because this protein is a vaccine target due to the fact that neutralizing antibodies are made to this protein as a result of infection). We can look at the tree for the N or NA (neuraminidase) protein (important in facilitating the release of newly formed viral progeny from the cell), in this case, the N1 protein, and see that it too, has relatively minor mutations, though certainly more than have occurred within the H protein (again, good news, because the H1 subtype is also a target for vaccines, but also of some of the antivirals we use).

There is a mutation required to the PB2 protein (not a vaccine target) that is necessary for transmission to mammals, though not sufficient in and of itself to allow for transmission to humans, and we see that has occurred, but only in the samples taken from infected humans, suggesting that this was an “in-host” mutation (occurred in the human after infection during translation and replication within human cells rather than in any of the cattle or prior bird samples). However, there are many more mutations to this protein and far more “divergence” (distance away from the prior forms – due to the large number of mutations), and I would not be surprised to find that it is developing in wild birds, and we are just not detecting it because we are not doing enough testing, as we did detect the mutation in a dead mammal. Perhaps one of these mutations explains the increased transmission in mammals.

Of course, this discussion just addresses mutations. As mentioned above, influenza viruses are known for reassortments with other influenza viruses, where they can exchange gene segments. This would potentially result in far more drastic change in the nature of the virus than simple mutations.

We fast forward to a year later and we now have concerning news coming from Texas dairy cattle. An article published in Nature Scientific Reports from March 14, 2025 titled “Superior replication, pathogenicity, and immune evasion of a Texas dairy cattle H5N1 virus compared to a historical avian isolate” reports on the development of a concern that I warned about last year. That is to say, if we allow certain viruses (especially RNA viruses, of which avian influenza is such a virus) to continue to spread, we risk the virus evolving and developing traits that can increase viral fitness, and potentially even develop changes that would allow it to evolve to infect humans.

The article reports that after spreading to nearly 900 dairy farms (including Idaho) and resulting in at least 39 (at the time of this study) known human infections, the avian influenza virus that has been spreading among cows has developed superior growth capability and rapid replication kinetics when studies in human lung cells in vitro (meaning in a laboratory setting as opposed to in the human body).

Worrisome for us, when the more recent isolates of the virus were tested in laboratory mice, the virus demonstrated more pathogenicity than earlier forms of the virus did, and infection in mice was accompanied by high virus titers in the brain and high mortality in the mice. Further, the virus had acquired new capabilities to thwart innate immune responses (these are our immune defenses that occur most immediately (as opposed to antibodies that take time to develop, don’t require prior exposure to the invading pathogen, and are far less specific and targeted than our antibody or cellular immune responses.)

A quick word on virologic studies. Information we gain from studies varies in its application to real-life human bodies and disease. For example, at the low end, during COVID-19 and future pandemics, we do studies referred to as in silico, which means that the study was done by computer modelling. For example, when we know the protein of a new virus that we want to target for antivirals or vaccines, the computer can generate a 3D model of the protein, as well as the medication of interest or the vaccine candidate to give us an idea as to whether the medication or vaccine might be likely to be effective. This is good for helping us prioritize our drug and vaccine candidates, but it only provides a low degree of confidence that the drug or vaccine will actually work in real life human bodies and in disease. For example, there were indications from in silico modeling that ivermectin might be a drug candidate because ivermectin appeared likely to bind an amino acid on the spike protein and an amino acid on the ACE-2 protein receptor. Further, it even seemed to be effective in the next step up of evidence, in vitro experiments, where we take a sample of the virus, a sample of human cells that the virus is known to infect and mix in the drug, in this case, ivermectin, in the laboratory to determine whether it impedes the virus from entering the cells, and it did. But, plenty of in silico and in vitro experiments that appear promising fail to pan out when taken to the next steps of clinical investigation.

When we have a promising drug or vaccine candidate, it is common to next move to studies in animals, particularly mice, because they are abundant, easy to manage, and cheap. The advantage of mice over laboratory experiments is that mice are living creatures, and unlike experiments in test tubes and cell cultures in a laboratory, they have circulatory systems, respiratory systems, immune systems, and actual functioning organs. This will often give us more indication as to whether the medication or vaccine that seemed to work in a test tube does work in a living being, however, mice still are much different than humans, and success in mice does not necessarily mean that it will work in humans leading to a common saying among scientists – “mice lie and monkeys exaggerate.”

However, different human diseases are often better suited to different animal models. For example, ferrets more closely resemble the anatomy and functioning of the human lung than mice do. On the other hand, mice develop cancers years faster than humans do, and so they can be very helpful in testing substances for carcinogenicity (the ability to induce cancer) such as has been done with food dyes. Again, mice are different than humans. When the substance does not cause cancer in the mice, that is reassuring, but not conclusive evidence that the same substance will not do so in humans, and conversely, if the substance does cause cancer in mice, that is concerning and calls for close observational studies in humans, but we often do not see cancer develop in humans.

When studies in common laboratory animals tend to further support the effectiveness of a drug or vaccine, it is common for us to then study it in larger animals that are more biologically related to us, especially mammals, and even better primates. These animals are much more expensive and it is harder to do studies in as large a group of these animals as it would be to do in mice. Studies in these animals are far more predictive of success or failure in humans and give us additional insights as to dosing and potential safety issues.

Now returning to the study referenced above, these findings related to increase in pathogenicity, severity of disease and antagonism of the innate immune response are important and concerning, but we have to keep in mind that they are results in mice, which may not be exactly the same in humans.

I’ll conclude with this. Whatever we think we know about this avian influenza outbreak in North America, particularly, the United States, it is an incomplete picture. Our government is not doing enough testing, surveillance and research into potential therapies and vaccines. The past administration did make an effort, but it was delayed and inadequate. Unfortunately, unconfirmed reports from people inside the CDC indicate that they are being told not to test dairy and poultry workers (recall the President’s comments in his first term when dealing with the COVID-19 pandemic – we wouldn’t have so many cases if we weren’t testing) and not to publicly report their symptoms. Many of the experts that were investigating and tracking this outbreak were fired in the government layoffs until someone realized this. Efforts were made to rehire them, but I don’t know how many were successfully retained. The NIH has made drastic cuts to research at a time when we need more influenza research. We are already suffering the loss of scientists from the government and universities due to personnel cuts and cuts to funding. Further, the Secretary of HHS is distracted and causing distraction by directing attention away from these real-time threats and to revisiting settled issues such as whether vaccines are associated with the development of autism, promoting elimination of fluoride from drinking water, and stoking the flames of a measles epidemic.

Again, I don’t know whether this will become a pandemic, but I can pretty much assure you that given all these changes, if it does, we will be delayed in recognizing it and we will be unprepared to deal with it. There is good reason to believe that this virus would be at least 20 times more fatal than SARS-CoV-2, and would kill many more children and possibly disproportionately so relative to older persons.