For When The Bough Breaks

CDC Infographic

#19,416

Over the past 20 years the secondary focus of this blog has been on personal preparedness, and the growing fragility our our increasingly high-tech dependent infrastructure. 

Much of this comes from my 15 years of living aboard boats, and constantly thinking about what could fail (usually at the worst possible moment), and how to limit its impact. 

The events of the past few days (Microsoft outage, FAA 4-hour emergency groundstop, and several very large cyber-heists) remind us how fragile or vulnerable our systems are.  

Last January, in NERC: Long-Term Reliability Assessment (Jan 2026), we looked (again) at growing concerns over the stability of the nation's electrical grid, followed last May by NERC Issues Level 3 Alert As Grid Faces `Unprecedented Challenges' Due to Surge In Large Power Consumers.

Every four years the ASCE (American Society of Civil Engineers) releases a report card on America’s infrastructure, and their most recent report (2025) warns that our cumulative GPA for infrastructure sits at only a C, and one of our most vulnerable infrastructures is the electrical grid (D+). 

This D+ rating is shared by Aviation, Dams, Roads, Levees, Wastewater, and Schools, while Stormwater and Transit are rated even lower.  And every day that passes without addressing these problems only increases the risks. 

Regardless of what conspires to bring these systems down (age, neglect, deliberate sabotage, etc.), the impact will often first fall upon the American public.  

I was in New Orleans 5 weeks after Hurricane Katrina in 2005, and there was still no electricity, or running water, across most of the city.  The streets were lined with debris and dead refrigerators filled with rotting food, pharmacies were still boarded up, and any semblance of normalcy was still months away.

In 2014's Water, Water, Everywhere But Not A Drop To Drink we saw hundreds of thousands of Ohio residents without  potable water for days due to harmful toxins produced by a microcystis algae bloom.  This was neither the first or last such event. 

A similar emergency was declared in Oregon in 2018 (see Tapping Into Your Preps).  

(2018 advisory)

Eight years ago, in NIAC: Surviving A Catastrophic Power Outage, we looked at a presidential commission's report on the risks of a major, prolonged, grid collapse.

https://www.hsdl.org/?view&did=819354

This 92-page report was released a little more than a year after hurricane ravaged Puerto Rico suffered the longest (11-month) grid failure in American History  and a year following another report - DHS: NIAC Cyber Threat Report - August 2017 - that warned of growing cyber threats to our critical infrastructure and called for `bold, decisive actions'.

Over the past 10 years I've gone through 2 hurricane-induced extended (4-7 day) power outages, and one prolonged community well failure, that had me relying on my personal preps for food, water, and power for days. 

Yet I've been lucky.  Many others have had to deal with far worse. 

In recent months we've seen increased calls by governments around the world for increased personal preparedness (see UK National Risk Register 2026 - Urges Citizen Preparedness). While the reasons given are often vague, concerns over natural or man-made disasters appear to be rising. 

California and the Pacific Northwest are bracing for what could be an unprecedented winter El Nino (see California Declares State of Emergency to Bolster Statewide El Niño Preparedness), while Florida has just completed its first El Nino Awareness week.

This year, I've beefed up my solar preps, adding a second solar panel, and additional battery capacity (see #NPM26: It's a 12 Volt Life).  I've added a battery operated camp shower, a better shortwave radio, and have recently gone through and thrown out long out-of-date canned food from my pantry. 

None of which guarantees I'll come away unscathed from an emergency, but I firmly believe it greatly increases my chances. 

While I'm far from a luddite (I love my gadgets), I know that things break. And as a (former) computer programer I know the more complicated a system becomes, the more likely it is to fail and the harder it will be to fix.

Given the complexities of our aging infrastructure, it follows that more failures can be expected.  Whether due to natural disasters, failed upgrades, `bad actors', or simply bad luck . . . the odds increase a little each day that you will be adversely affected.

The question isn't whether another emergency will arise, it is whether you and your family will be ready to deal with it.  How you should prepare will depend upon where you live, the likely threats you will face, and logistical, physical, or financial limitations. 

I'm unlikely to freeze to death here in Florida, but heat-related deaths are relatively common.  And while Southern California doesn't worry about hurricanes, they do have a significant seismic threat. 

How you go about preparing may be different, but your goals are pretty similar. So if the power goes out today - and stays out for a week - do you have?

• A battery operated NWS Emergency Radio to find out what was going on, and to get vital instructions from emergency officials
• A decent first-aid kit, so that you can treat injuries
• Enough non-perishable food and water on hand to feed and hydrate your family (including pets) for the duration
• A way to provide light when the grid is down.
• A way to cook safely without electricity
• A way to purify or filter water
• A way to handle basic sanitation and waste disposal.
• A way to stay cool (fans) or warm when the power is out.
• A small supply of cash to use in case credit/debit machines are not working
• An emergency plan, including meeting places, emergency out-of-state contact numbers, a disaster buddy, and in case you must evacuate, a bug-out bag
• Spare supply of essential prescription medicines that you or your family may need
• A way to entertain yourself, or your kids, during a prolonged blackout

A good place to get started is by visiting Ready.gov, or by hitting this link which will serve up a series of my preparedness blogs.

While you may go years without needing it, with emergency preparedness it is better to be ready 5 years too soon than 5 minutes too late.

WHO DON: Middle East respiratory syndrome coronavirus - Qatar

 

#19,415

Although reports of human infection with MERS-CoV have dwindled in recent years, this family of coronaviruses still circulates (and evolves) in dromedary camels both in the Middle East and Africa, and still poses a zoonotic threat.

A month ago - in WHO DON: Middle East respiratory syndrome coronavirus - Kingdom of Saudi Arabia - we looked at the WHO's first Saudi MERS update of 2026, which chronicled  8 cases reported by KSA since last December.

Last August, in WHO: Risk assessment of the introduction, spread, and zoonotic spillover of MERS-CoV Clade B in camel populations of the Nile Basin and Across Africa, we looked at concerns over the cryptic spread of MERS in Africa. 

But whether in Africa or the Arabian peninsula, MERS-CoV spillover to humans is viewed as likely underreported (see (Referral) Nature: Human MERS-CoV cases are falling but pose an ongoing pandemic threat).

While some of this decline is likely due to difficulties in identifying cases, at the same time some Middle Eastern countries have shown past reluctance to report cases.

Yesterday the WHO published a DON (Disease Outbreak News) on two (apparently unrelated) MERS cases from Qatar which occurred in August, but were only recently (Oct 29th) reported to the WHO. 

Of particularly note, the first case fell ill on July 22nd - was hospitalized on July 25th, but not diagnosed with MERS-CoV until the 5th of August - a delay which may help explain the large number of contacts (73), including 62 healthcare workers. 

The second case was identified relatively quickly, but 22 HCWs were identified as close contacts.   In both instances, no secondary infections were reported. 

Due to its length, I've only posted excerpts from the WHO DON report. Follow the link to read it in its entirety.  I'll have a brief postscript after the break.

Middle East respiratory syndrome (MERS) – Qatar
13 November 2026

Situation at a glance

On 29 October 2026, the National International Health Regulations (IHR) Focal Point of the State of Qatar notified the World Health Organization (WHO) of two laboratory-confirmed cases of Middle East respiratory syndrome (MERS). The cases were confirmed on 5 and 25 August 2026 and are the first MERS cases reported from Qatar since 2022. MERS is a viral zoonotic infection, principally transmitted to humans through direct or indirect contact with infected dromedary camels. Both patients were men aged over 50 years with underlying medical conditions and occupational exposure to dromedary camels. Both were hospitalized and subsequently discharged in a stable condition. A total of 99 contacts from both cases were identified, tested, and monitored for 14 days following their last exposure. All contacts tested negative for MERS-CoV, and no secondary cases were identified. The two cases reported exposure to dromedary camels at geographically separate farms, with no epidemiological link identified between them. The cases appear to represent sporadic infections associated with zoonotic transmission from dromedary camels rather than human-to-human transmission.

Description of the situation

On 29 October 2026, the National IHR Focal Point of Qatar notified WHO of two laboratory-confirmed cases of Middle East respiratory syndrome (MERS). The cases were confirmed on 5 and 25 August 2026. These are the first MERS-CoV cases reported by the State of Qatar since 2022.

The first case was a man aged over 50 years who worked with dromedary camels and had chronic medical conditions. He developed symptoms on 22 July 2026 and was admitted to hospital on 25 July. Real-time reverse transcription-polymerase chain reaction (RT-PCR) on an upper-respiratory tract specimen initially tested negative for MERS-CoV. A subsequent lower-respiratory tract specimen tested positive by RT-PCR, and infection was laboratory-confirmed on 5 August. He reported longstanding occupational exposure to dromedary camels, including during the 14 days before symptom onset. He did not report consuming raw camel milk or any recent travel. He recovered and was discharged in a stable condition after two consecutive negative PCR test results.

A total of 73 contacts were identified for this case, comprising 11 close contacts and 62 health and care workers. All contacts were tested and monitored for 14 days following their last exposure. All tested negative for MERS-CoV, and no secondary cases were identified.

The second case was a man aged over 50 years who was involved in camel breeding and rearing and had underlying chronic medical conditions. He developed symptoms on 23 August 2026. Two nasopharyngeal specimens tested positive for MERS-CoV by RT-PCR on 25 August. He reported sustained occupational exposure to dromedary camels, including directly caring for recently ill young camels during the 14 days preceding symptom onset. He also reported consuming raw camel milk during this period but had no recent travel history.

He developed severe MERS-CoV pneumonia complicated by acute hypoxemic respiratory failure and required high-flow nasal oxygen and non-invasive ventilatory support. He subsequently recovered and was discharged in a stable condition after two consecutive negative PCR test results.

A total of 26 contacts were identified for this case, comprising four close contacts and 22 health and care workers. All contacts were tested and monitored for 14 days following their last exposure and tested negative for MERS-CoV. One high-risk contact who was a health and care worker developed respiratory symptoms but tested negative for MERS-CoV on two specimens. No secondary cases were identified.

The two cases reported occupational exposure at geographically separate camel farms, with no epidemiological link identified between the farms or the cases. The precise sources of infection remain undetermined. However, their sustained occupational exposure to dromedary camels, including direct contact with recently ill camels in one case and the consumption of raw camel milk by the same case, suggest probable zoonotic acquisition.

       (SNIP)

These are the first MERS cases reported from Qatar since 2022. Both cases had occupational exposure to dromedary camels, and one reported tending to sick camels and consuming raw camel milk during the 14 days before symptom onset. The cases were exposed at geographically separate farms, with no epidemiological link identified between them. All 99 identified contacts tested negative for MERS-CoV, and no secondary cases were identified. The available information therefore suggests that these were sporadic infections associated with zoonotic transmission rather than human-to-human transmission.

The occurrence of two apparently unlinked cases highlights the continued risk of zoonotic spillover among people with frequent or occupational exposure to dromedary camels, particularly those with underlying medical conditions.

As per WHO’s rapid risk assessment of 29 January 2026, the overall risk associated with MERS-CoV remains moderate at both the regional and global levels. This assessment reflects continued sporadic zoonotic spillover into the human population and the potential for subsequent health care-associated transmission and international importation into countries where the disease is not endemic.

Based on the information reported by the State of Qatar, there is no evidence of sustained human-to-human transmission associated with these cases. Continued surveillance and animal health investigations remain important to detect and assess any potential further transmission.

        (Continue . . . )


Prior to COVID's emergence in late 2019, MERS-CoV was the top contender for sparking a coronavirus pandemic, sporting a high mortality rate (>30%), and spreading easily through hospitals in the Middle East (and South Korea) (see Ziad Memish: Two MERS-CoV Hospital Super Spreading Studies).

In the summer of 2025 we looked at an editorial in Journal of Epidemiology & Global Health on the importance of continued healthcare preparedness and surveillance (see Al-Tawfiq & Memish On Recurrent MERS-CoV Transmission in Saudi Arabia), with an emphasis on identifying asymptomatic carriers.

Whether MERS-CoV will re-emerge as a global health threat remains unknown, but it continues to circulate and evolve - largely out of our view - on both the Arabian Peninsula and in Africa.

Which makes it very much worth our attention.

UK: Defra Upgrades AIPZ to Include Housing Order Due to Avian Flu

 

#19,414

On Wednesday, in UK Scotland: H5N5 Reported In Eurasian Otters - AIPZs Declared for England and Scotland, we looked at the robust start to the UK's fall avian flu season, including 3 detections of H5N5 in local otters.  

Today - after 2 more outbreaks -  the AIPZ (Avian Influenza Protection Zone) order has been upgraded to include mandatory housing of flocks > 50 birds (or small flocks where meat or eggs are sold).

The updates from Defra include:

12 November 2026: avian influenza prevention zone (AIPZ) with housing measures

The avian influenza prevention zone (AIPZ) with mandatory biosecurity measures covering all of England has been updated to include housing measures. The housing measures apply from 00:01 on 13 November 2026.

All bird keepers should continue to take steps to prevent bird flu and stop it spreading and be vigilant for signs of disease.

Read guidance on housing your birds safely.

Declaration

Declaration of Avian Influenza Prevention Zone (England) – mandatory biosecurity and housing measures (PDF)

From 00:01 on 13 November, this declaration revokes and replaces the declaration made at 23:30 on 10 November 2026, which came into force at 9:00 on 11 November 2026:

Avian Influenza Prevention Zone (England) declaration (PDF)

Defra defines the mandatory housing order as:

In the AIPZ in England there are mandatory housing measures which mean you may have to house your birds.

• If you have 50 or more birds you must house them. This applies to all types of birds.

• If you keep less than 50 birds and they are for your own use only (for example you do not sell or give away their eggs or meat), you do not have to house them.

• If you keep less than 50 birds but you do sell or give away their eggs, poultry products or live birds, you must house them. These birds are known as ‘poultry.

• If you’re in a protection zone or a captive bird (monitoring) controlled zone, you must house your birds. Check what zone you’re in using the bird flu disease zone map and follow the rules for that zone.

Housing your birds reduces the risk of contact with wild birds, which can spread bird flu.

Meanwhile, here in the United States the number of backyard outbreaks continues to outpace commercial farms (see below). 

Canada's CFIA also reports a surge in detections, with 11 new outbreaks since November 1st.

While most commercial poultry producers have long experience dealing with outbreaks, surveys indicate that backyard producers are generally less well aware of the signs of avian flu, and may be less inclined to wear PPE.

Which means, if you raise backyard birds, now would be a good time to familiarize yourselves with the risks of avian flu, and the things you can do to reduce those risks to you and your families.

A couple of good places to start include:

UF/IFAS Extension: What Backyard Flock Owners Need to Know about Bird Flu (Influenza H5N1)

CDC Guidance Backyard Flock Owners and Bird Flu 

Referral (NEJM): Autoantibodies against Type I Interferons and Death from H7N7 Avian Influenza

 
AutoAb development in population
credit Human autoantibodies against type I
interferons in severe viral disease

#19,413

We've a fascinating correspondence  - published yesterday (Nov 11th) in the NEJM - which links a relatively rare autoimmune dysfunction (autoantibodies against Type I Interferons) to increased severity of novel flu infection.  

The authors hypothesize that those with this condition could potentially act as “patients zero” in emerging viral pandemics. 

Since this correspondence is not open access, I'm only able to give some background and a brief synopsis. Those already familiar with the events of the 2003 H7N7 outbreak, and the recent discoveries surrounding this autoimmune condition, may prefer to proceed directly to the link below.   

Autoantibodies against Type I Interferons and Death from H7N7 Avian Influenza
Published November 11, 2026
N Engl J Med 2026;395:1963-1965
DOI: 10.1056/NEJMc2608446
VOL. 395 NO. 19 Copyright © 2026

For those preferring a review:

In 2003, the Netherlands saw an outbreak of H7N7 that resulted in the loss of 30 million birds across 1,000 farms, and saw scores of mild human infections and the death of a veterinarian (see Eurosurveillance Human-to-human transmission of avian influenza A/H7N7, The Netherlands, 2003).

Another analysis, performed by the RIVM (Ministry of Health) found the spread of the virus to be much greater than originally reported, citing as many as 1,000 human infections (see Executive summary Avian Flu Epidemic 2003: Public health consequences).

Both reports cited likely human-to-human transmission, with the RIVM study finding ` . .  58.9% of the family contacts of persons having direct exposure to poultry had a measurable response in the HI test.' 

Most of these cases reported mild symptoms; primarily conjunctivitis.  A minority reported mild-or-moderate flu-like symptoms (often in conjunction with conjunctivitis), and one patient died. 

While nowhere as deadly to humans as H5N1 or H7N9, this H7N7 outbreak serves as a cautionary tale on the susceptibility of humans to novel influenza.  It also raises questions about the wide spectrum of outcomes from novel flu infection.

Relatively recently a rare immune dysfunction - autoantibodies against type I interferons - has been tagged as a likely determinant of severity in viral infections.  

Six months ago, a review article in Current Opinion in Virology (Human autoantibodies against type I interferons in severe viral disease by Groen & Hale) reported:

Highlights

• AutoAb development is influenced by age, genetics, immune tolerance, and infections.

• IFN-I autoAbs heighten risk for severe infections and live-vaccine adverse events.

• Targeted diagnostic screening for IFN-I autoAbs could benefit certain individuals.

• Understanding autoAb mechanisms will help devise potential therapeutic strategies.

While first discovered in the early 1980s, it wasn't until COVID that AutoAbs impact on viral infections was really appreciated (see Nature Human genetic and immunological determinants of critical COVID-19 pneumonia).

All of which brings us to the NEJM correspondence, where the authors went back and tested stored serum from 35 patients from the 2003 H7N7 outbreak, including the 58 y.o. veterinarian who died. 

They found the fatal case had autoantibodies neutralizing interferon-α, -ω, and -β, while 2 of the remaining 34 mild cases had autoantibodies neutralizing interferon-β only.

Since antibodies against all three subtypes are rare in people under 60, the authors say this is unlikely to be by chance.  Strengthening their case, the fatal H5N1 case in Louisiana in early 2025 carried IFN-I autoAbs. 

Autoantibodies neutralizing type I IFNs in a fatal case of H5N1 avian influenza

Qian Zhang Corresponding Author , Taylor S. Conrad , Marcela Moncada-Velez , Kaijun Jiang ,Anastasija Cupic , Jonathan Eaton , Kimberley Hutchinson ,Adrian Gervais ,Ruyue Chen , Anne Puel , Paul Bastard  , Aurelie Cobat ,Thersa Sokol , RyanA. Langlois  ,Lisa Miorin  , Adolfo García-Sastre  ,John A. Vanchiere , Jean-Laurent Casanova Corresponding Author

Author and Article Information
J Exp Med (2026) 223 (3): e20251962.
https://doi.org/10.1084/jem.20251962

While it is well established that avian flu viruses have a hard time establishing themselves in humans, and that human-to-human transmission is uncommon, this rare autoimmune condition could provide a foothold for novel viruses like H5N1, H7N7, and H9N2 to adapt to humans. 

At least that's the theory. Admittedly, one based on limited evidence.

But if it turns out to be correct, it becomes even more imperative that we take steps to prevent spillovers (PPEs, seasonal flu vaccines to prevent coinfection and reassortment, etc.), and to treat even mild cases as potential public health threats. 

Policies which, based on recent anecdotal reports (see Newsweek Farm Workers Sound Alarm on Underreported Bird Flu Numbers), still appear to be lacking.

UK Scotland: H5N5 Reported In Eurasian Otters - AIPZs Declared for England and Scotland

 

#19,412

We've been watching the co-circulation and spread of an H5N5 subtype of avian flu - primarily in the high latitude regions of the Northern Hemisphere - for the past 3 years (see Preprint: H5N5 virus transmission is driven by repeated cross-Atlantic introductions and transmission among high latitude seabirds).

We've seen numerous reports of H5N5 from Norway, Svalbard island, Iceland, and eastern Canada, often infecting mammals, including cats, polar bears, raccoons, foxes, and walruses.

In the spring of 2025, the UK reported 15 grey seals infected with H5N5. The following November, in UK: HPAI H5N5 Rising, we saw a sudden shift in H5N5 activity in wild birds in the UK, with the APHA reporting:

Since our previous outbreak assessment on 7 October 2024, there have been no new reports of high pathogenicity avian influenza (HPAI) H5 clade 2.3.3.4b in domestic poultry in Great Britain (England, Scotland and Wales). There have, however, been 15 more HPAI H5 clade 2.3.3.4b events involving 26 “found-dead” wild birds in Great Britain. Of these, 25 were HPAI H5N5 with 1 case of HPAI H5N1.

Also in November of 2025 the United States reported the first (and fatal) human infection with H5N5.  While still a minor player in the global scheme of things, H5N5 continues to show surprising resilience and spread. 

While most of these reports have involved wild birds and/or small mammals, in early October Scotland reported an outbreak of H5N5 in commercial poultry in Ness, Isle of Lewis.

3 October 2026

Highly pathogenic avian influenza (HPAI) H5N5 was confirmed in commercial backyard poultry in Ness, Isle of Lewis, Scotland (AIV 2026/20). A 3km protection zone and 10km surveillance zone has been declared around the premises. This is the first outbreak of the 2026 to 2027 season and following confirmation of this case, GB has lost its freedom from highly pathogenic avian influenza (bird flu) status.

In an update, posted today by defra, the UK government has announced AIPZs (avian influenza protection zones) have been declared for both England and Scotland.

11 November 2026
AIPZ declared in England and Scotland from 11 November 2026

Following a number of findings of highly pathogenic avian influenza in wild birds and detections in poultry and increased risk levels, an avian influenza prevention zone (AIPZ) has been declared covering England and Scotland to mitigate the risk of further outbreaks of disease occurring.

This means that it is a legal requirement for all bird keepers in England and Scotland to follow strict biosecurity to prevent bird flu and stop it spreading.

You can read more information on the requirements for certain types of bird:

in the declaration for the AIPZ in England
In the declaration for the AIPZ in Scotland

Additionally, today defra has updated their avian flu in on-avian wildlife list for the first time since early March, adding three recent H5N5 detections over 5 weeks. 

The most recent High pathogenicity avian influenza (HPAI) in Great Britain and Europe Update Assessment (#11) - dated Nov. 6th,  but released yesterday- carries the following map showing 81 detections of HPAI H5 since Oct 1st. 

I've circled the H5N5 detections.  For now, all are on the western and northern coastlines, which fits the narrative that it is primarily carried by sea and shore birds. 

Whether it can establish itself further inland remains to be seen. But for now, it seems to be holding its own against H5N1.

EID Journal: Cross-Protection against Influenza A(H5) Clade 2.3.4.4b Viruses after A(H1N1)pdm09 Infection

#19,411

Over the past 32 months we've seen at least six dozen human infections from HPAI H5 (H5N1 & H5N5) in the United States, and while most have been described as mild or moderate, 3 people have died. 

It seems likely, based on limited seroprevalence testing (see JAMA Open: Asymptomatic Human Infections With Avian Influenza A(H5N1) Virus Confirmed by Molecular and Serologic Testing), that the actual number of infections is higher.

Which suggests that H5N1 may not be quite as deadly as originally feared.  Of course, even a 2%-3% fatality rate would put it in the same league as the 1918 pandemic. 

An early assessment by the CDC (July 14th, 2024 H5N1 Update) reported that `. . . that there is extremely low to no population immunity to clade 2.3.4.4b A(H5N1) viruses in the United States'.

Since then, however, we've seen a number of studies which have reported serological evidence of limited immunity - particularly in older cohorts - against some strains of H5N1.

Probably not enough to prevent infection, but perhaps enough to reduce the severity of infection.

Initially, the focus was on HA immune imprinting (see Nature: Declan Butler On How Your First Bout Of Flu Leaves A Lasting Impression), where the HA group (1 or 2) you are first exposed to is thought to provide some degree of protection against other HAs in that group.

How much real-world protection early or past H1/H2 exposure might offer against H5Nx - or how long it might last - are unknown, but it has been suggested it might provide an `edge' against severe disease.

More recently, we've seen attempts to quantify the impact of the first NA (Neuraminidase) one is exposed to (see last December's Nature Comms: Pre-existing Cross-reactive Immunity to HPAI 2.3.4.4b A(H5N1) Virus in the United States).

This study found`very low levels of pre-existing binding antibodies to the HA head of the HPAI A(H5N1) 2.3.4.4b virus', but slightly more encouragingly, `. . . substantial cross-reactive binding antibodies to N1 neuraminidase (NA) of 2.3.4.4b A(H5N1).

Regarding the the value of cross-reactive antibodies to the N1 Neuraminidase, the authors wrote:

Neuraminidase antibodies have been considered as an independent correlate to protect against influenza 20. Although they cannot prevent infection, neuraminidase antibodies can prevent virus egress, reduce viral shedding, and thus could attenuate disease and lessen disease severity 21,22,23.

All of which brings us to a new research letter, published yesterday in the EID Journal, which reports that ferrets pre-exposed to H1N1 saw less severe illness when challenged with H5N1 or H5N5 than influenza-naive ferrets.

A few caveats:

• While an encouraging finding, this was a relatively small study, and ferrets aren't a perfect analog for humans.

• Also, pre-exposed ferrets only had one prior exposure - to H1N1pdm09 - whereas the human population typically has a much messier exposure history to a variety of flu viruses (many first imprinted with H3N2, or pre-2009 H1N1). 

• The challenge experiments appear to have been conducted roughly 3 months after H1N1 infection, and it is unknown if - or how quickly - protection might wane.  

Not unexpectedly, pre-exposed ferrets exposed to H5N5 did not fare quite as well as those challenged with H5N1, and there are no guarantees that any future H5 pandemic would carry a closely matching N1 Neuraminidase. 

Still, this is a fascinating report, and it may partially explain why recent H5N1 infections have been less deadly than originally feared.

Follow the link to read the report in its entirety.

Volume 32, Number 12—December 2026
Research Letter

Cross-Protection against Influenza A(H5) Clade 2.3.4.4b Viruses after A(H1N1)pdm09 Infection

Xiangjie Sun, Jessica A. Belser, Zhu-Nan Li, Nicole Brock, Joanna A. Pulit-Penaloza, Troy J. Kieran, Claudia Pappas, Hui Zeng, Jessie C. Chang, Paul J. Carney, Brandon L. Bradley-Ferrell, James Stevens, Min Z. Levine, and Taronna R. Maines  

Abstract

We challenged ferrets previously infected with influenza A(H1N1)pdm09 virus with H5N1 or H5N5 clade 2.3.4.4b viruses to assess cross-protection. Results show that previous A(H1N1)pdm09 virus immunity conferred partial protection against both viruses, with slightly reduced protection against H5N5 compared with H5N1, potentially reflecting the absence of cross-reactive N5 neuraminidase antibodies.

(SNIP)

Preimmune ferrets challenged with either H5N1 or H5N5 virus shed similar levels of virus in nasal wash samples during days 1–4 postinfection (range of mean peak titers 103.8–105.2 PFU/mL) as naive controls but exhibited reduced titers in throat swab samples on day 4 for H5N5 virus and days 2 and 3 for H5N1 virus (Figure 2, panels A, B).

Viral clearance from nasal washes occurred 2–4 days earlier in preimmune ferrets. We detected H5N1 virus less frequently in rectal swab samples from preimmune animals than from naive controls, whereas we did not observe that reduction for ferrets infected with H5N5 virus (Figure 2, panels A, B).

Influenza A(H1N1)pdm09 virus preimmunity did not substantially reduce viral titers in the upper respiratory tract (nasal turbinates) or soft palate after H5N1 or H5N5 virus challenge (Figure 2, panels C, D). However, A(H1N1)pdm09 preimmunity largely prevented viral dissemination to the lower respiratory tract (trachea and lungs) and extrapulmonary tissues for both viruses, with only sporadic low-level viral detection. However, intestinal viral titers were comparable between preimmune and naive ferrets challenged with H5N5 virus (Figure 2, panels C, D).

Detection of group 1 HA stalk antibodies after A(H1N1)pdm09 infection (Appendix Figure), together with previous evidence of HA stalk-mediated cross-protection against disease caused by the influenza A viruses within the same phylogenetic group (3,9), suggests that cross-reactive HA stalk antibodies might contribute to protection against A(H5) viruses. In addition, N1 cross-reactivity might further enhance protection against H5N1 virus. Consistent with our findings, limited N5 cross-reactivity has been reported in humans despite detectable N1 responses (10).


Further studies using H5-specific HA stalk antigens and functional assays are needed to determine the contribution of cross-reactive antibodies and cellular immunity to protection against zoonotic influenza A viruses. Our findings showed that previous A(H1N1)pdm09 viral infection conferred partial cross-protection against H5N1 and H5N5 viruses in ferrets, reducing disease severity, lethality, and viral dissemination.

Dr. Sun is a microbiologist in the Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Her research primarily focuses on using the ferret model to understand influenza virus pathogenicity and transmissibility.