PAHO Epidemiological Alert: Simultaneous Circulation of Seasonal Influenza and Respiratory Syncytial Virus - 9 January 2026

 

#19,015

While it is not exactly `news' that the Northern Hemisphere is being battered by a particularly intense H3N2 flu season (see When Seasonal Flu Exceeds Expectations), on Friday PAHO released an updated Epidemiological Alert that also warns of a slow rise in RSV (Respiratory Syncytial Virus) activity. 

This double-viral whammy has the potential to put even more pressure on already stressed healthcare delivery systems.  As we saw yesterday, we've already seen Sporadic Tamiflu (Oseltamivir) Shortages Reported In U.S. & Canada. 

Yesterday PAHO published a press release (excerpts below) summarizing the Alert.

PAHO issues alert on simultaneous circulation of seasonal influenza and respiratory syncytial virus in the Americas

Washington, D.C., January 10, 2026 (PAHO) – The Pan American Health Organization (PAHO) has urged countries across the Americas to remain vigilant and strengthen health system preparedness in response to the simultaneous circulation of seasonal influenza and respiratory syncytial virus (RSV). This situation could place additional pressure on hospitals and clinics for the remainder of the winter season in the Northern Hemisphere.

The epidemiological alert updates an advisory released on December 4, 2025, which warned of the possibility of an earlier or more intense respiratory season than usual.

       (SNIP)

"The simultaneous circulation of influenza and RSV is a significant challenge that requires us to prioritize vaccination—which protects against severe cases that may require hospitalization—and maintain close surveillance, enabling timely action to prevent larger outbreaks and avoid hospital overcrowding," said Dr. Marc Rondy, PAHO Regional Adviser in Epidemiology of Epidemic- and Pandemic-Prone Diseases.

PAHO emphasizes that interim studies show current influenza vaccines are effective at preventing hospitalizations (30–40% effectiveness in adults and 75% in children), and calls on countries to achieve high vaccination coverage, especially among priority groups such as children, pregnant people, older adults, and those with chronic conditions.

In light of this situation, PAHO recommends that countries in the region:

• Strengthen integrated surveillance of influenza, RSV, SARS-CoV-2, and other respiratory viruses, reporting weekly data to FluNET and FluID to support regional and global monitoring.
• Prepare and adjust health service response plans to address possible simultaneous increases in influenza and RSV cases and hospitalizations.
• Prioritize influenza and COVID-19 vaccination for at-risk groups, including older adults, young children, pregnant people, individuals with chronic conditions, and healthcare workers.
• Implement RSV prevention strategies, including maternal vaccination and long-acting monoclonal antibodies for newborns and infants, in line with PAHO/WHO recommendations.
• Strengthen risk communication, promoting key preventive practices.

PAHO reminds the public that vaccination against influenza, frequent handwashing, covering the mouth when coughing or sneezing, wearing masks indoors if symptomatic, staying home when experiencing fever or respiratory symptoms, and seeking prompt medical care for severe symptoms are simple and effective ways to protect themselves and their families, especially young children and older adults

 
The full 22-page Epidemiological Alert provides nation-specific data for the Americas, and recommended guidance for public health authorities, with sections on Surveillance, Clinical management and prophylaxis, Vaccination, and Risk Communications. 

While PAHO reports that Respiratory Syncytial virus levels remain below last year's, the combined impact of a `drifted' H3N2 virus - which has impacted young children and the elderly the hardest - and an expected further rise in RSV (which affects the same cohorts), is a concern. 

PAHO's advice is pretty straightforward; those at high risk should get vaccinated, everyone should practice good `flu hygiene' (wash hands, wear masks, stay home if sick, etc.), and those who are ill should immediately seek medical treatment in case of respiratory distress. 

But getting people to follow it remains a challenge.

Sporadic Tamiflu (Oseltamivir) Shortages Reported In U.S. & Canada

 

FluView Week #53

#19,014

With seasonal influenza raging in North America, Europe, and Asia it isn't terribly surprising that we are - once again - seeing reports of sporadic shortages of the antiviral oseltamivir by both the media, and industry watchdogs. 

Two days ago, Becker's Hospital Review published Tamiflu shortages emerge during severe flu season, which reports in some regions pharmacists - and even hospitals - are scrambling to find doses. 

Similarly, on the 7th, Bloomberg reported Flu Patients Struggle To Find Tamiflu As Virus Surges Across US.  But the problem isn't limited to the United States; Drug Shortages Canada lists both actual and anticipated shortages of several strengths of oseltamivir.

While not every community is affected, shortages are concerning since delays in starting tamiflu can reduce its effectiveness. The CDC urges: 

There are prescription flu antiviral drugs that can treat flu illness; those should be started as early as possible and are especially important for patients at higher risk for flu-related complications.1

We've looked at the importance of starting oseltamivir early (1st 48 hrs. of illness) many times before, including in 2024's Clinical Inf. Dis.: Benefit of Early Oseltamivir Therapy for Adults Hospitalized with Influenza A: An Observational Study.

While the FDA hasn't weighed in on these most recent reports, the American Society of Health-System Pharmacists’ (ASHP) drug shortage database lists (as of Jan 7th) 10 oseltamivir products (various manufacturers and strengths) are in short supply. 

Sporadic shortages and delays in getting Tamiflu are not uncommon, as we saw in 2022 in the CDC HAN #0482: Prioritizing Antiviral Treatment of Influenza in the Setting of Reduced Availability of Oseltamivir. 

That shortage led to the HHS Releasing Some Tamiflu Supplies From the Strategic National Stockpile.

Since the demand for oseltamivir is elevated globally, it isn't clear how long it will take for supply chains to adjust, alleviating these delays.  While there are other options such as Baloxavir, they aren't well stocked by many pharmacies in the United States. 

All of which makes it more important than ever to take steps to avoid, or at least reduce the impact, of getting the flu. 

As we discussed yesterday in Preprint: Antibodies elicited by the 2025-2026 influenza vaccine in humans, serological evidence suggests this year's flu shot isn't a complete miss - and while it might not prevent infection - for many it may  help reduce its severity. 

Masking, avoiding crowds, increasing indoor ventilation, and using hand sanitizers can add additional valuable layers of protection. And if you do get sick, stay home.

While exact numbers have never been disclosed, our National Strategic Stockpile supposedly has somewhere around 50-60 million courses of oseltamivir on hand; sufficient to treat 15-20% of the nation during a severe flu pandemic (assuming a single, standard dose).

Stockpiles of Baloxavir are similarly unknown, but according to a media report in 2024 (see The U.S. strategic drug stockpile is inadequate for a bird flu outbreak) likely numbers only in the hundreds of thousands of doses.

How to get those vital medications from the government warehouses, to thousands of hospitals and pharmacies, and then the `last mile' to the patient (who will need to start them within 24-48 hours of falling ill) - is a legitimate logistical challenge. 

While I'm hopeful our antiviral armamentarium will help `take the edge off' the opening months of the next pandemic, it is by no means guaranteed. Meanwhile, vaccines may be a year or more away (see SCI AM - A Bird Flu Vaccine Might Come Too Late to Save Us from H5N1).

Once again, our first line of defense will likely rely heavily on NPIs (non-pharmaceutical interventions), like face masks, hand washing, ventilation, staying home while sick, and avoiding crowds.

Which is why I'm recommending that people consider now (see #Natlprep 2025: Personal Pandemic Preparedness).what they will do if another pandemic flu should embark on a new world tour.

Preprint: Antibodies elicited by the 2025-2026 influenza vaccine in humans

CDC FluView Week 52

 #19,013

While reporting of flu activity is probably still lagging due to the holidays, later today we should get the latest CDC FluView report on what - by all accounts - is shaping up to be a brutal seasonal flu season (see map above).

The subclade K H3N2 virus we began tracking more than 2 months ago (see Increasing Concerns Over A `Drifted' H3N2 Virus This Flu Season) continues to plague Australia long after their flu season should have ended, and has now become dominant in the Northern Hemisphere. 

Despite significant antigenic changes in this `drifted' subclade K, we've seen early indications that this year's vaccine may not be a total `miss', and is still worth getting (see UKHSA Preprint: Early Influenza Virus Characterisation and Vaccine Effectiveness in England in Autumn 2025, A Period Dominated by Influenza A(H3N2) Subclade K).

When I got my flu shot in October I already had a strong inkling that the H3N2 component was going to be `suboptimal', as the WHO had already changed the formulations for next year's Southern Hemisphere flu shot.

Still, some protection is better than no protection, and so I gladly rolled up my sleeve.  

Yesterday a new preprint appeared from Scott Hensley and others at the University of Pennsylvania, which further characterizes this year's vaccine match, conducting  serological testing (hemagglutination inhibition (HAI) assays) on blood samples from 76 adults taken before - and about a month after - vaccination

While they report reduced antibody titers compared to the vaccine strain, they found the vaccine was likely `somewhat effective' against subclade K, and still worth getting. 

After vaccination, about 70% had antibody levels usually associated with protection against the vaccine strain (J.2), while nearly 40% reached that level for the subclade K virus.

As with all studies, there are some limitations worth noting, including.

• Only 1 vaccine formulation (standard dose egg-based 2025-2026 Flulaval Trivalent influenza vaccine) was tested
• Challenge was limited to 1 strain of the subclade K virus (A/New York/GKISBBBG87773/2025)
• Follow-up sera collection was 27-30 days post-vaccination, telling us relatively little about the duration of protection.  

How all this plays out in terms of real-world protection (against both infection, and severe disease) won't be fully known until after the flu season has ended, but these are fairly encouraging results.

First the link, and a few excerpts from, the preprint.  I'll return with more after the break. 

Antibodies elicited by the 2025-2026 influenza vaccine in humans
Jiaojiao Liu, Shuk Hang Li, Naiqing Ye, Tachianna Griffiths, Elizabeth M Drapeau, Reilly K. Atkinson, Ronald G. Collman, Scott E. Hensley

doi: https://doi.org/10.64898/2026.01.05.26343449
This article is a preprint and has not been certified by peer review

Abstract

A new H3N2 variant (named subclade K) possesses several key hemagglutinin substitutions and is circulating widely during the 2025-2026 influenza season. In this report, we completed experiments to determine if the 2025-2026 seasonal influenza vaccine elicits antibodies in humans that recognize this variant.

We find that H3N2 subclade K viruses are antigenically advanced; however, the 2025-2026 seasonal influenza vaccine elicited antibodies in many individuals that efficiently recognized these viruses.

Thus, the current seasonal influenza vaccine will likely be somewhat effective at preventing H3N2 subclade K virus infections.

       (SNIP)

Conclusions 

Collectively, our data suggest that H3N2 subclade K viruses are antigenically advanced compared to the 2025-2026 H3N2 vaccine strain; however, the antigenic differences that we observed in sera from some humans are not as large as previously reported in ferrets2 .

While we find that human antibodies elicited by vaccination react more efficiently to the H3N2 vaccine strain relative to subclade K H3N2 viruses, we found that many individuals produced antibodies that efficiently recognized subclade K H3N2 viruses after vaccination. 

Our study highlights the benefits of receiving influenza vaccinations, even in seasons that include circulation of variant viruses.

        (Continue . . . )

There are other good reasons to get this year's flu shot, if you haven't done so already

• It is always possible we could see an extended flu season, much like Australia has reported;  one that lingers on into April or May. 

• Even if  H3N2 begins to wane in the weeks ahead, we could see a late season surge in H1N1 or Influenza B.

• And with increasing levels of  HPAI H5 in the environment, there is (a likely small) potential for a co-infection with H5 and seasonal flu to produce a pandemic strain (see Preprint: Intelligent Prediction & Biological Validation of the High Reassortment Potential of Avian H5N1 and Human H3N2 Influenza Viruses).

Antigenic `Shift' or Reassortment

While rare, this isn't just a theoretical concern; twice in my lifetime (1957 & 1968) avian flu viruses did precisely that; reassorted with a seasonal flu virus and launched a human pandemic.

• The first (1957) was H2N2, which according to the CDC `. . . was comprised of three different genes from an H2N2 virus that originated from an avian influenza A virus, including the H2 hemagglutinin and the N2 neuraminidase genes.'

• In 1968 an avian H3N2 virus emerged (a reassortment of 2 genes from a low path avian influenza H3 virus, and 6 genes from H2N2) which supplanted H2N2 - killed more than a million people during its first year - and continues to spark yearly epidemics more than 50 years later.

While increased uptake of the flu vaccine isn't guaranteed to prevent another reassortment event, it should reduce the chances. 

As would taking other steps to prevent infection; such as wearing masks in crowded indoor areas, using hand sanitizer, and staying home when you are sick. 

Or we can do nothing, and take our chances. 

Nature Comms: Adjuvanted Influenza Vaccination Increases Pre-existing H5N1 Cross-reactive Antibodies

 

#19,012

Despite the initial CDC assessment (see July 14th, 2024 H5N1 Update) that `. . . that there is extremely low to no population immunity to clade 2.3.4.4b A(H5N1) viruses in the United States', we seen studies suggesting there may be some limited immunity; particularly in those born before 1968. 

A few recent examples include:

mBio: Low levels of influenza H5N1 HA and NA antibodies in the human population are boosted by seasonal H1N1 infection but not by H3N2 infection or influenza vaccination

Preprint: Cross-Reactive Human Antibody Responses to H5N1 Influenza Virus Neuraminidase are Shaped by Immune History

Preprint: Neuraminidase Imprinting and the Age-related Risk of Zoonotic Influenza 

Simply put, the first influenza virus you are exposed to (HA Group 1 or 2) is believed to affect your immune response for the rest of your life (see Nature: Declan Butler On How Your First Bout Of Flu Leaves A Lasting Impression). 

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.

 

Given the challenges of quickly bringing a safe, and effective, H5N1 vaccine to the masses (see SCI AM - A Bird Flu Vaccine Might Come Too Late to Save Us from H5N1), there is understandably a lot of interest in potential stop-gap measures that might help blunt the opening months of a pandemic.

So far, boosting with existing H1N1 vaccines has shown very limited value (see EID Journal: Investigation of Influenza A(H5N1) Virus Neutralization by Quadrivalent Seasonal Vaccines, United Kingdom, 2021–2024).

But today we have a study which suggests using an interesting - but potentially controversial - option; deploying a standalone booster ASO3 adjuvanted H1N1 vaccine, similar to the one used in Europe during the 2009 pandemic. 

Given its highly publicized link to an increased incidence of narcolepsy - particularly in children and adolescents (see Finland: Task Force Report On Pandemrix-Narcolepsy Link) - an ASO3 adjuvanted vaccine would likely face stiff headwinds from an already vaccine-hesitant society. 

First, a link, and the abstract to the study - which contains some surprises - after which we'll take a deeper look into their findings. 

Adjuvanted influenza vaccination increases pre-existing H5N1 cross-reactive antibodies 

Mariana Alcocer Bonifaz, Disha Bhavsar, Claire-Anne Siegrist, Arnaud Didierlaurent & Benjamin Meyer
Published: 07 January 2026article number , (2026)

Download PDF

 Abstract

Highly pathogenic H5N1 avian influenza viruses of clade 2.3.4.4b cause sporadic human infections and currently raise concerns about a new influenza pandemic. Heterogeneities in disease severity have been observed in the past and are reported among infected farm workers in the United States. These may be attributed to differences in pre-existing H5N1 cross-reactive antibodies. 

In this study, we characterize H5N1 cross-reactive antibody landscapes in the current population (#NCT05794412 and #NCT01022905) and assess the effect of AS03-adjuvanted pandemic H1N1 and non-adjuvanted seasonal influenza vaccination on H5N1 cross-neutralizing and IgG antibody titers targeting a range of influenza virus-derived antigens. We detect H5N1 cross-neutralizing antibodies using a vesicular stomatitis virus-based pseudovirus system that correlate well with antibodies inhibiting the spread of authentic H5N1 viruses, anti-group 1 hemagglutinin stalk and anti-trimeric hemagglutinin antibodies.

Additionally, we find that AS03-adjuvanted pandemic H1N1 vaccination increases H5N1 cross-reactive antibodies significantly in a pandemic H1N1 immunologically partially naïve population. Furthermore, we show that immune imprinting causes distinct H5N1 cross-reactive antibody patterns pre-vaccination.

(SNIP)

In conclusion, we could show that low levels of H5N1 cross-neutralizing antibodies exist in the population in 2009 and more recently in 2023. Low dose AS03-adjuvanted pandemic H1N1 vaccination was able to substantially induce H5N1 cross-reactive antibodies and could overcome the effect of immune imprinting on H5N1 cross-reactive antibody patterns in a pH1N1 immunologically partially naïve population.  

       (Continue . . . )

In a nutshell, the authors report:

• Most adults carry weak antibodies against today's H5N1 bird flu from past human flu infections or vaccines, which may reduce the severity of infection.

• A low-dose AS03 adjuvanted H1N1 vaccine increases these antibodies nearly 4-fold -  compared to just 30% from the standard seasonal flu shot.

• This effect would likely be of greatest benefit to those exposed to HA Group 2 viruses (H3N2) early in life, as HA Group 1 subjects saw less impact.

• In a bit of a twist, receipt of the regular seasonal flu shot within a few weeks of the booster actually dampened its effect. 

While there is no mention of the past safety concerns over ASO3 in this paper, it would clearly be a factor in any adoption of this strategy. Absolute risk was deemed low 15 years ago, and varied by geographic regions, but the EMA Recommended Restrictions On Use of Pandemrix Vaccine in those under the age of 20 in 2011.

It would be of interest to know if other adjuvants - like MF59 (widely used in Europe) - would produce similar gains.  But in a severe enough pandemic, even an AS03 vaccine might be an attractive option. 

As we've discussed previously (see Manufacturing Pandemic Flu Vaccines: Easier Said Than Done), producing and delivering billions of doses of a safe and effective H5 vaccine is a tall order, and success is not guaranteed. 

We've also seen warnings that our current influenza antivirals may be lacking (see St. Jude Researchers: Current Antivirals Likely Less Effective Against Severe Infection Caused by Bird Flu in Cows’ Milk) along with signs of growing antiviral resistance in avian flu (see Emerg. Microbes & Inf: Oseltamivir Resistant H5N1 (Genotype D1.1) found On 8 Canadian Poultry Farms).

Add in the growing anti-science bias of the public, often fueled by AI generated clickbait videos and political rhetoric, even a low CFR H5 pandemic could be disastrous.  

While I could certainly do without another pandemic in my lifetime, nature's laboratory may have other plans. 

Which why we need to explore a wide range of options now, before we desperately need them. 

PNAS: Reconstructing the Early Spatial Spread of Pandemic Respiratory Viruses in the United States

 
#19,011

Long-time readers are aware of my limited grasp of statistics, and probably suspect I'll drown someday trying to ford a stream that is - on average - 2 feet deep. Which is why I won't even try to dissect the advanced methods used in today's study from Columbia University's Mailman School of Public Health. 

But their findings; that early cryptic spread of pandemic viruses are hard to predict - even when viewed in retrospect - is worthy of deeper discussion.

First, in broad strokes, a brief summary from the press release.

News Release 5-Jan-2026
Study examines how the last two respiratory pandemics rapidly spread through cities
Peer-Reviewed Publication

Columbia University's Mailman School of Public Health
The researchers set out understand the geographic spread of the two pandemics to inform strategies to prevent future pandemics. They applied detailed data on the dynamics of the two infectious diseases to a computer model to simulate their spread using known patterns of air travel and commuting, as well as potential superspreading events. They focused on over three hundred metropolitan areas in the U.S.

In the simulations, both pandemics were widely circulating in most of the metro areas within weeks, before government interventions or early case detection. While the specific transmission pathways across locations were different for the last two pandemics, the spatial expansion was driven by several shared transmission hubs such as the New York and Atlanta metropolitan areas. Their spread was largely driven by air travel rather than commuting, though random dynamics introduced substantial uncertainty in transmission routes, which makes it hard to predict where the outbreaks will happen in real time.

        (SNIP)

Beyond reconstructing the historical spread of the last two pandemics, the study also provides a generalizable framework to infer early epidemic dynamics that may be applied to other pathogens. While mobility, particularly air travel, is a key driver of pandemic spread, the researchers caution that other factors also play a role, including community demographics, school schedules, winter holidays, and weather conditions.

        (Continue . . . )

A link, and some excerpts from the full study, after which we'll look at some of the real-life implications.  

Reconstructing the early spatial spread of pandemic respiratory viruses in the United States
Renquan Zhang, Rui Deng, Sitong Liu , +4 , and Sen Pei  
January 6, 2026
https://doi.org/10.1073/pnas.2518051123
Vol. 123 | No. 2

Abstract

Understanding the geographic spread of emerging respiratory viruses is critical for pandemic preparedness, yet the early spatiotemporal dynamics of the 2009 H1N1 pandemic influenza and severe acute respiratory syndrome coronavirus 2 in the United States remain unclear. 

While mobility and genomic data have revealed important aspects of pandemic spatial spread, several key questions remain: Did the two pandemics follow similar spatial transmission routes? How rapidly did they spread across the United States? What role did stochastic processes play in early spatial transmission?

To address these questions, we integrated high-resolution disease data with a robust, data-efficient inference framework combining air travel, commuting flows, and pathogen superspreading potentials to reconstruct their spatial spread across US metropolitan areas.

The two pandemics exhibited distinct transmission pathways across locations; however, both pandemics established local circulation in most metropolitan areas within weeks, driven by several shared transmission hubs. Early spatial spread was more strongly associated with air travel than with commuting, though stochastic dynamics introduced substantial uncertainty in transmission routes, creating challenges for timely detection and control.

Simulations indicate that broad wastewater surveillance coverage beyond top transmission hubs coupled with effective infection control may slow initial spatial expansion. Our findings highlight the rapid, stochastic spread of pandemic respiratory pathogens and the difficulties of early outbreak containment.

        (Continue . . . )
 

For those who are as statistically challenged as am I; `stochastic' is just a fancy word for "random" or "probabilistic".  We often talk about the R0 (r-naught) of a virus - how many people one person is likely to infect - but that's just an average. 

Some people may get sick, wisely stay home, and infect no one else. Others may mask their symptoms with OTC cold/flu meds and fly to a convention; becoming a superspreader that infects dozens. 

Individual choices - both good and bad - can affect how quickly a pandemic spreads. As can many external factors, like the weather, holidays, community demographics, and school closures. 

And of course, not all viral threats are created equal. 

The SARS-COV virus of 2022-2023 famously did not spread asymptomatically, which made quarantine of symptomatic individuals effective (see SARS and Remembrance), making containment possible. 

H1N1 and COVID, however, could be spread asymptomatically and via aerosols, and that made them virtually unstoppable.   

The reality is, it doesn't take a super virus to spread uncontrollably. Even a (relatively) mild H1N1 virus swept the world in 2009, and supplanted the old H1N1 virus, all in a matter of weeks.

While many countries implemented border closings, passenger screenings, and airport thermal scanners to try stop H1N1 and COVID; at best they only delayed entry by a matter of days or weeks.   

Most viruses take days - up to a week or longer - to incubate. And with 7 million airline passengers each day, any attempts to identify and isolate infected passengers are probably doomed from the start.

Today's study is a reminder that once a respiratory pandemic virus is transmitting efficiently in the community, our ability to stop it is laughably small. 

The authors of today's study do suggest airport wastewater surveillance at key transmission hubs (testing sewage from aircraft, airport terminals, and related infrastructure) would be a cost effective early warning system. 

This would not only pick up asymptomatic carriers, or tell us where to deploy medical assets, it might even alert us to emerging threats before they become fully transmissible.

As much merit as that idea has - given our current level of pandemic denial, and unwillingness to test and share data -  I'm not particularly hopeful.

Arch. Pub. Health: Excess Primary Healthcare Consultations in Norway in 2024 Compared to Pre-COVID-19-pandemic Baseline Trends

#19,010

From very early on in the SARS-CoV-2 pandemic, we saw concerns raised over the potential long-term impact of COVID infection; often centered around cardiac or neurological involvement.

In early April 2020, the New York Fire Department reported a 400% increase in sudden cardiac arrest death calls beginning in late March (see NBC affiliate Massive Spike in NYC ‘Cardiac Arrest’ Deaths Seen as Sign of COVID-19 Under counting).

In June, JAMA published an original investigation which found a huge increase in out-of-hospital cardiac arrests in New York City during the peak of their COVID-19 epidemic, writing:

From March 1 to April 25, 2020, New York City, New York (NYC), reported 17 118 COVID-19–related deaths. On April 6, 2020, out-of-hospital cardiac arrests peaked at 305 cases, nearly a 10-fold increase from the prior year.

Admittedly, most of these cases were never tested for COVID-19, making any link circumstantial. The following month, however, in JAMA: Two Studies Linking SARS-CoV-2 Infection To Cardiac Injury, we saw physical evidence of cardiac injury due to COVID infection, even among a relatively young cohort of previously healthy adults.

By mid-summer, it was becoming apparent that COVID was far more than just an acute respiratory infection (see Nature Med. Review: Extrapulmonary manifestations of COVID-19), and could produce blot clots, along with neurological, renal, and cardiovascular damage.

 In late July we saw this cautionary editorial published in JAMA.

Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter?
Clyde W. Yancy, MD, MSc1,2; Gregg C. Fonarow, MD3,4
JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3575

Since then, studies showing post-acute impacts of COVID infection have exploded, with many citing repeated COVID infections as increasing the risk of long-term health damage. A few (of many) include:

Nature: Long-term Cardiovascular Outcomes of COVID-19

AHA: COVID-19 May Trigger New-Onset High Blood Pressure

NIH: Study Shows SARS-CoV-2 Infects Coronary Arteries, Increases Plaque Inflammation

EHJ: Accelerated Vascular Ageing After COVID-19 Infection: The CARTESIAN Study

Terms like `Long COVID' and PASC (Postacute Sequelae of COVID) are now officially recognized, but their impact remains poorly quantified (and often disputed).

Much of the evidence is anecdotal, or inferential, because 90% of the world stopped testing, and reporting on ICU admissions and deaths, more than 3 years ago (No News Is . . . Now Commonplace).

The world desperately wanted to move on from COVID, and it decided the best way to do so was by touching up the X-rays.  But of course, the health burden of COVID - recognized or not - remains. 

Today we've a study from the Norwegian Institute of Public Health and others, that looks at the trajectory of primary care consultations in Norway both before - during - and after the COVID pandemic.

What they found was the number of consultations in 2024 were about 7% above pre‑pandemic expectations (see graphic at top of this blog). Most of these were coded as being for respiratory, fatigue, psychological, cognitive, and some infectious/gastrointestinal complaints.

Patterns that have often been associated with PASC or `Long COVID', but remain exceedingly difficult to establish a causal link.  

The authors - who cite (and are critical of) Norway’s national COVID strategy which `. . . emphasizes the assumed benefits of sustaining population immunity through repeated SARS-CoV-2 infections' - hypothesize that repeated COVID infections have led to population‑level health impacts, with PASC and post‑COVID immune dysfunction driving much of the cited excess primary care consultations.

The authors note, in particular, the impact this has had on women, children, adolescents, and young adults.

I've reproduced the abstract below, but you'll want to follow the link and read the full article.  I'll have a brief postscript when you return.

Excess primary healthcare consultations in Norway in 2024 compared to pre-COVID-19-pandemic baseline trends

Research
Open access
Published: 02 January 2026
article number , (2026)

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Abstract

Background

The risk of post-acute sequelae of COVID-19 (PASC) is estimated at 3–6% per infection in 2024. We hypothesized that widespread SARS-CoV-2 infections could lead to population-level consequences. Our previous study identified substantial increases in Norwegian primary healthcare consultations in 2023—compared to pre-pandemic levels—for conditions associated with acute COVID-19 and PASC. This study extended that analysis to 2024. We then assessed whether observed patterns were compatible with our hypothesis.

Methods

We used data from the Norwegian Syndromic Surveillance System, which captures nationwide primary healthcare consultations for 102 ICPC-2 codes (out of a possible 710) that are relevant for infectious disease surveillance and some post-acute infection syndromes. Bayesian linear regression models were fitted to 2010–2019 trends, adjusting for population changes, to estimate expected values for 2024. Excess consultations were calculated by age and sex. A COVID-19 community spread was proxied by vaccination-adjusted weekly hospitalization rates.

Results

In 2024, there were 17,800,365 consultations, corresponding to an absolute excess of 1,185,231 consultations, or a 7.1% relative excess, compared to the modelled baseline. The 10 code combinations with largest absolute excess in 2024 were respiratory infections (325,726 excess consultations; 20% relative excess), fatigue (205,381; 70%), psychological symptom/complaint other (188,978; 87%), acute stress reaction (182,079; 76%), feeling depressed (126,783; 133%), hyperkinetic disorder (112,763; 116%), abdominal pain/cramps general (84,544; 29%), memory disturbance (39,177; 63%), conjunctivitis (34,643; 59%), and infectious disease other/NOS (33,556; 81%). COVID-19 community spread showed the strongest correlations with conjunctivitis, strep throat, respiratory infections as a group (R**), fatigue, infectious disease other, memory disturbances, and pneumonia. Deviations from pre-pandemic trends varied: respiratory and psychological disorders worsened from 2020 onward and several conditions showed dramatic excess from 2022–2024. Females 15–29, children, adolescents, and young adults had disproportionately large relative excesses for consultations for memory disturbances.

Conclusions

Primary healthcare consultations in 2024 significantly exceeded pre-pandemic expectations, especially for conditions linked to acute COVID-19 and PASC, though the two cannot be differentiated in these data. While other factors undoubtedly also play a role, findings are compatible with ongoing population-level health impacts associated with repeated SARS-CoV-2 infections, particularly among women, children, adolescents, and young adults. These results emerged under a national COVID-19 strategy that does not account for post-acute consequences of SARS-CoV-2 infection.

(Continue . . . )

The author's hypothesis, and findings, certainly resonate with what I've seen, and written extensively about, for the past 6 years. But proving causality is always difficult, even when the patterns neatly `fit' the hypothesis. 

A task that is made even more onerous by the deliberate dismantling of COVID surveillance, testing, and reporting around the world.  

Society has used this lack of data to trivialize COVID infection (and reinfection) to the point that vaccine uptake has plummeted, and mask-wearing - and other protective measures - have become anathema. 

Meanwhile, COVID continues to exact a heavy toll, while the public remains oblivious to - or highly skeptical of - other threats that may be in the pipeline. 

While ignorance may yield temporary bliss, we risk a very rude awakening down the road.