Thursday, April 16, 2026

Nature Med.: Rapid expansion of genotype D1.1 A(H5N1) influenza viruses in wild birds across North America during the 2024 migratory season

 
Abrupt Shift in H5N1 Genotypes in Wild Birds in US/Canada

#19,120

After its arrival in eastern Canada in late 2021, HPAI H5N1 spread quickly to the U.S. - reassorting with local LPAI avian flu viruses as it traveled - producing more than 100 new genotypes.  

While most of these reassortants were unremarkable, in early 2024 a B3.13 genotype emerged that was particularly well-suited for infecting dairy cattle. Six months later, another new genotype appeared in North American birds; D1.1. 

In short order (see chart above), this upstart D1.1 genotype went from zero detections to dominating in wild birds, spilling over into poultry farms, infecting poultry workers, and sometimes displaying signs of antiviral resistance (see Emerg. Microbes & Inf: Oseltamivir Resistant H5N1 (Genotype D1.1) found On 8 Canadian Poultry Farms).

Unlike the `bovine' strain - which typically produced mild (primarily conjunctival) symptoms in humans, D1.1 produced more serious illness in a number of cases.

In addition to this increased virulence in humans, D1.1 further demonstrated its versatility by spilling over into cattle in at least 3 states (Nevada, Arizona & Wisconsin).  

All of which brings us to a Brief Communications - published in Nature Medicine - which details the origins, and rapid spread, of D1.1 in North American birds.  I've only posted some brief excerpts, so follow the link to read it in its entirety. 

I'll return with more after the break.

Published: 15 April 2026

Rapid expansion of genotype D1.1 A(H5N1) influenza viruses in wild birds across North America during the 2024 migratory season

Walter N. Harrington, Anthony Signore, Lisa Kercher, Jolene A. Giacinti, Ahmed Kandeil, Christina A. Ahlstrom, Sarah Bevins, Beate Crossley, Karlie Eure, Thomas P. Fabrizio, Trushar Jeevan, Julianna Lenoch, Jacqueline M. Nolting, Daniel Rejmanek, David Stallknecht, Trent Bollinger, Evan J. Buck, Deborah Carter, Bradley S. Cohen, Krista E. Dilione, Jamie C. Feddersen, John Franks, Dayna Goldsmith, Cory J. Highway, …Richard J. Webby 

Nature Medicine (2026)Cite this article 

Abstract

In late 2021, high pathogenicity avian influenza A(H5N1) clade 2.3.4.4b viruses entered North America and reassorted rapidly with local avian influenza viruses. In September 2024, we detected a new reassortant later classified as genotype D1.1. Using active and passive avian influenza surveillance across Canada and the USA, we tracked the emergence and rapid spread of D1.1 viruses in wild birds during the 2024 fall migration.

Phylodynamic analysis showed that D1.1 viruses formed a monophyletic group and displaced earlier A(H5) genotypes across several flyways. Their expansion coincided with detections in other hosts, including 17 human cases, 4 of which were severe or fatal. None of the mammalian-adaptive markers detected in human cases were found in wild bird viruses, and candidate vaccine viruses retained antigenic cross-reactivity with D1.1 strains.

(SNIP)



Conclusion 

The emergence and rapid spread of HPAI A(H5N1) genotype D1.1 viruses across North American migratory flyways during the 2024 migration season represents a notable shift in clade 2.3.4.4b epidemiology. Several factors may explain the unusually efficient transmission of D1.1. Genomic analyses show that this genotype includes a distinct North American–derived neuraminidase (NA) segment, which may provide antigenic advantages because population immunity to this NA is probably lower than to NA segments circulating widely before 2024.

Although principal mammalian adaptation markers were absent in the wild bird samples, some D1.1 viruses carried several mutations with reported phenotypic effects (Supplementary Table 2), which may have contributed to their dominance. Increased densities of immunologically naive juvenile birds during southbound migration may have facilitated rapid viral amplification at staging areas14.

Environmental conditions also probably played some role in the dissemination of genotype D1.1 viruses. Persistent drought and altered habitat use at important breeding and staging areas may have led to increased mixing and density of wild birds, facilitating interspecies viral transmission15. These ecological factors, combined with the novelty of the genotype in wild populations, may have enabled the rapid geographic spread observed. 

Although D1.1 viruses circulating in wild birds currently lack principal mammalian adaptation markers, their sustained replication in mammalian hosts, such as US dairy cattle16, increases the evolutionary potential for zoonotic transmission. D1.1 viruses detected in poultry in British Columbia were found to carry the NA-H275Y mutation—a known marker for resistance to oseltamivir17, demonstrating that resistance and adaptation markers can emerge stochastically, even without selection pressure. 

(SNIP)

In conclusion, the emergence of the D1.1 viruses coincided temporally with the southward autumn migration of North American waterfowl, favoring their dissemination. Their spread highlights the need for an integrated One Health response18 that aligns wildlife surveillance, agricultural biosecurity and public health preparedness.

        (Continue . . . )

 

D1.1 likely remains a key player in North American birds, but the lack of genomic specificity in recent reporting makes it difficult to quantify how prevalent it remains in 2026.  The USDA's dashboard of wildbird detections does not specify genotype, and instead classifies viruses as:

  • EA = Eurasian; AM = North American; the EA H5 (2.3.4.4) viruses are highly pathogenic to poultry.
  • EA/AM: reassortant of H5 goose/Guangdong and North American wild bird lineage
A little over a year ago, in Nature: Lengthy Delays in H5N1 Genome Submissions to GISAID, we looked at some of the many obstacles in analysing surveillance data which are often missing crucial metadata (i.e. collection date, exact location, host-specific information, genotype, etc.).

While D1.1 has demonstrated remarkable ecological success - and a concerning ability to spillover into mammals - it doesn't appear to be ready for prime time. 

It does, however, remind us how abruptly the novel fluscape can change.  

Whatever critical zoonotic traits D1.1 (and other genotypes) currently lack could easily be rectified by some future untoward reassortment event.

But without substantially improved wildlife and agricultural surveillance under a One Health framework - and the rapid and open sharing of data - we'll likely never see it coming. 

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Wednesday, April 15, 2026

Obstetrics & Gyn: Recovery of Pregnancy-Related Death Ratios After the Coronavirus Disease 2019 (COVID-19) Pandemic


CDC MMWR Sept 2020


#19,119

While we've known that pregnant women and their unborn offspring are often among the hardest hit during influenza pandemics (see 2009's Pregnancy & Flu: A Bad Combination), COVID's impact on pregnancy remains less well understood. 

Early in the pandemic we looked at a number of studies that found increased risks for pregnant women, including:
  • ~3–4× higher risk of ICU admission
  • ~5× higher need for critical care
  • ~7–8× higher risk of maternal death (relative risk)
  • Much higher risk of mechanical ventilation and pneumonia

But today we've a analysis, published in Obstetrics & Gynecology, that quantifies the impact of pregnancy-related deaths during the COVID pandemic (up 60% in 2021), and the fact that those deaths - while lower now - still remain elevated for some sociodemographic subgroups

The full report is very much worth reading.  I'll have more after the break.
Original Research
Disparities by Age, Race and Ethnicity, and Geography
MacCallum-Bridges, Colleen L. PhD; Daw, Jamie R. PhD; Admon, Lindsay K. MD, MSc
Obstetrics & Gynecology ():10.1097/AOG.0000000000006255, April 2, 2026. | DOI: 10.1097/AOG.0000000000006255
 Abstract
 
OBJECTIVE: 

To describe trends in pregnancy-related death ratios from 2018 to 2024, assess the contribution of coronavirus disease 2019 (COVID-19) to these trends, and evaluate whether pregnancy-related death ratios have recovered to prepandemic levels.

METHODS: 

We conducted an observational study that used vital statistics data to calculate the annual pregnancy-related death ratio (the number of pregnancy-related deaths per 100,000 live births) for female individuals aged 15–49 years between 2018 and 2024. We compared the pregnancy-related death ratios across prepandemic (2018–2019) pandemic (2020–2022), and postpandemic (2023–2024) periods; to assess the contribution of COVID-19, we calculated the pregnancy-related death ratio including and excluding COVID-associated deaths (ie, those with ICD-10 U07.1 listed as a cause). Pregnancy-related deaths were identified using International Statistical Classification of Diseases, Tenth Revision codes (A34, O00–O99), and the total pregnancy-related death ratio was decomposed into the early pregnancy-related death ratio (deaths during pregnancy or within 42 days after pregnancy) and the late pregnancy-related death ratio (deaths 43–365 days postpartum). We conducted subgroup analyses by maternal age, race and ethnicity, or geographic region.

RESULTS: 

From 2018 to 2024, there were 8,298 pregnancy-related deaths (32.3/100,000 live births). From the prepandemic period to the pandemic period, the early pregnancy-related death ratio increased by 7.5 deaths per 100,000 live births (95% CI, 6.1–8.8) and the late pregnancy-related death ratio increased by 3.7 deaths per 100,000 live births (95% CI, 2.7–4.6). Most of this increase (76% for the early pregnancy-related death ratio, 50% for the late pregnancy-related death ratio) was COVID-associated deaths. 
By 2023–2024, the early pregnancy-related death ratio had returned to prepandemic levels, but the late pregnancy-related death ratio remained elevated (1.4 additional deaths/100,000 live births; 95% CI, 0.4–2.4). Most subgroups experienced an increase in early and late pregnancy-related death ratios during the pandemic, but recovery varied.
Notably, both early and late pregnancy-related death ratios remained substantially elevated among non-Hispanic Black mothers in 2023–2024 compared with the prepandemic period (early pregnancy-related deaths increased by 7.0/100,000 live births [95% CI, 1.3–12.8]; late pregnancy-related deaths increased by 5.4 /100,000 live births [95% CI, 1.3–9.5]).

CONCLUSION: 

Pregnancy-related death ratios increased dramatically during the COVID-19 pandemic, and by 2023–2024, recovery differed by the timing of death relative to pregnancy and across sociodemographic subgroups. Additional efforts are needed to identify drivers of differential recovery from the COVID-19 pandemic and inform clinical and policy initiatives to reduce pregnancy-related deaths, improve maternal health, and promote health equity.

       (SNIP)

Pregnancy-related deaths increased dramatically during the COVID-19 pandemic, peaking in 2021 with 32.7 early pregnancy-related deaths per 100,000 live births and 13.1 late pregnancy-related deaths per 100,000 live births. Pandemic era increases in pregnancy-related deaths were largely explained by COVID-associated deaths, but by 2023–2024, recovery from the COVID-19 pandemic differed across sociodemographic subgroups.
Although some groups had returned to prepandemic levels, pregnancy-related death ratios remained elevated for other groups, including non-Hispanic Black mothers, a demographic that already faced substantially higher rates of pregnancy-related deaths before the COVID-19 pandemic. Additional research is needed to identify drivers of differential recovery from the COVID-19 pandemic and inform clinical, public health, and public policy initiatives to reduce pregnancy-related deaths and promote maternal health and health equity.

       (Continue  . . . ) 

As the following CDC chart illustrates, pregnancy related mortality rose sharply in 2020, peaked in 2021, and began dropping significantly in 2022.

It is worth noting that while available, uptake of the COVID vaccine was quite limited among expectant mothers in 2021, with the CDC reporting:
Data from the COVID-19-Associated Hospitalization Surveillance Network (COVID-NET) in 2021 indicate that approximately 97% of pregnant people hospitalized (either for illness or for labor and delivery) with confirmed SARS-CoV-2 infection were unvaccinated.
In late September 2021 the CDC Issued a HAN For Pregnant Women Urging COVID Vaccination, which helped to increase its uptake.  

It seems likely that the COVID vaccine, along with acquired immunity, better medical care options, and the arrival of less virulent Omicron variant in 2022, all contributed to this sharp decline. 

Today, according to the latest (March 2026) ACOG COVID-19 Vaccination Considerations for Obstetric–Gynecologic Care Practice Advisory update, only about 11% of pregnant women in 2026 have received a COVID-19 vaccine. 

However, vaccine uptake has waned, with a 25.7% year-to-date decrease in the 2025–2026 season compared with 2024–2025 (CDC 2025d). As of February 21, 2026, 11.1% of pregnant women overall have received a COVID-19 vaccine (CDC 2026). Clear, strong clinician recommendation remains one of the most influential factors in maternal vaccination acceptance and is essential to reducing preventable morbidity.
While many choose to view COVID as a non-threat today, it continues to cause significant morbidity and mortality (see WHO Statement: COVID-19 Still Causes Severe Disease & Renewed Vaccination Recommendations).

A few recent studies include:
Nature Comms: The Risk of Kidney Disease Increases Following SARS-CoV-2 Infection Compared to influenza
Unfortunately, our growing societal laissez-faire attitude towards this virus means that some people are only going to learn this the hard way. 
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Tuesday, April 14, 2026

The Lancet Microbe: Characterisation of Immune Responses Targeting HPAI A(H5) Viruses in Health-care Workers in the Netherlands

 

Credit CDC Antigenic Characterization

#19,118


Until relatively recently it was assumed that most of the world's population had little to no immunity against HPAI H5 viruses. In June of 2024 (see CDC A(H5N1) Bird Flu Response Update: Population Immunity to A(H5N1) clade 2.3.3.4b Viruses) the CDC reported: 

Data from this study suggest that there is extremely low to no population immunity to clade 2.3.4.4b A(H5N1) viruses in the United States.  Antibody levels remained low regardless of whether or not the participants had gotten a seasonal flu vaccination, meaning that seasonal flu vaccination did not produce antibodies to A(H5N1) viruses.
This means that there is little to no pre-existing immunity to this virus and most of the population would be susceptible to infection from this virus if it were to start infecting people easily and spreading from person-to-person. This finding is not unexpected because A(H5N1) viruses have not spread widely in people and are very different from current and recently circulating human seasonal influenza A viruses.

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. 

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

How much `real-world' protection any of this might offer is anyone's guess. But with a pandemic specific vaccine unlikely in the opening months of an outbreak, and growing concerns over our antiviral armamentarium, any immunological edge - no matter how small - would be welcome. 

While most of the studies we've seen to date have focused on the American Bovine B3.13 strain, today we've a study from the Netherlands which uses two European clade 2.3.4.4b H5N1 viruses along with an older Chinese (2005) clade 2.3.4 virus. 

The research summary reads:


Evidence before this study

We searched PubMed from Jan 1, 1997, to July 1, 2025 in English using combinations of “influenza”, “heterosubtypic”, “immunity”, “cross-immunity”, “baseline”, “population”, “humans”, “H5N1”, “avian influenza”, “clade 2.3.4.4b”, “humoral”, “antibodies”, “hemagglutinin”, “neuraminidase”, “cellular”, and “T-cells”. Previous reports on immunity to A(H5) influenza viruses on a population level are fragmented, because most examined binding or functional antibodies exclusively, and few examined T-cell responses.

Added value of this study

We profiled immune responses targeting A(H5) influenza viruses in a presumed unexposed cross-sectional cohort of health-care workers (n=107) by combining the measurement of antibody binding, haemagglutinin inhibition, antibody-dependent cellular cytotoxicity (ADCC), neuraminidase (NA) inhibition, and T-cell responses. A(H5) antibodies binding the haemagglutinin stalk, and NA inhibition-mediating and ADCC-mediating antibodies were common. Cross-reactive T cells targeting the haemagglutinin and NA of A(H5) influenza viruses were detected. Our rational selection of antigens from both seasonal and avian influenza viruses enabled a direct comparison of multiple effector mechanisms, establishing the first integrated baseline map of humoral and cellular responses against A(H5) influenza viruses.
 
Implications of all the available evidence

Our findings, in combination with existing research, show that partial immunity to A(H5) influenza viruses is widespread. Repeated exposure to seasonal influenza viruses likely led to the development of a cross-reactive antibody and T-cell repertoire recognising A(H5) influenza viruses. Although the protective value of cross-reactive immune responses remains speculative, evidence from animal model systems suggests that these responses might confer partial protection.

The full study, while fairly technical, is well worth reading. I've posted the abstract below.  I'll have a bit more after the break.


Mark A Power, MSca,∗ ∙ Willemijn F Rijnink, MSca,∗ ∙ Widia Soochit, PhDa ∙ Lennert Gommers, BSca ∙ Anne van der Linden, BSca ∙ Felicity Chandler, BSca ∙ Femke Volker, BSca ∙ Theo M Bestebroer, BSca ∙ Babs E Verstrepen, PhDa ∙ Alba Grifoni, PhDb ∙ Ngoc H Tan, MPharma ∙ Susanne Bogers, MSca ∙ Gijsbert P van Nierop, PhDa ∙ Prof Alessandro Sette, PhDb,c ∙ Prof Marion P G Koopmans, PhDa ∙ Corine H Geurts van Kessel, PhDa,† ∙ Reina S Sikkema, PhDa,† ∙ Mathilde Richard, PhDa,‡ ∙ Rory D de Vries, PhDa,‡ r.d.devries@erasmusmc.nl Show less
 
Published April 13, 2026
DOI: 10.1016/j.lanmic.2026.101367 External Link
 
Download PDF
 
Summary

Background

Highly pathogenic avian influenza A(H5) viruses pose a pandemic threat, with a history of mammalian adaptation and zoonotic spillovers into humans. We aimed to determine whether pre-existing cross-reactive immune responses to A(H5) clade 2.3.4.4b influenza viruses detected between 2020 and 2024 are present in the general population.

Methods

We conducted an observational, cross-sectional study within the prospective Surveillance of Respiratory Viruses in Healthcare and Animal Workers in the Netherlands (SENTINEL) cohort, in which we analysed a subset of health-care workers aged 18 years or older who provided blood samples at a periodic study visit in August or September, 2024. Blood samples were analysed for influenza A(H5)-specific antibody binding, haemagglutination inhibition, Fc-effector functions, neuraminidase (NA) inhibition, and T-cell responses.

Findings

We included 107 health-care workers. Participants’ median age was 50·0 years (IQR 40·0–58·0); 77 (72%) health-care workers were female, 29 (27%) were male, and one (1%) did not report their biological sex. Virus-specific antibodies were measured in 106 serum samples.
Low-level binding antibodies directed against the A(H5) haemagglutinin (HA) head were detected in up to 28 individuals (depending on the antigen), but without haemagglutination inhibition activity.
Nevertheless, we detected A(H5)-reactive antibodies with Fc-effector functions in all participants. Additionally, we observed high levels of antibodies with NA inhibition activity (geometric mean titre 208 [95% CI 153–284]) in up to 97% of the health-care workers against avian N1, and T-cell responses against HA and NA from A(H5) influenza viruses in 43–69% (46–74 of 107) health-care workers. A(H5)-specific responses correlated with immune responses targeting A(H1N1).

Interpretation

Together, our findings suggest that partial cross-reactive immunity to A(H5) influenza viruses exists in humans, likely induced by previous exposures to seasonal influenza viruses. This partial cross-reactive immunity might play an important role during future outbreaks, potentially by blunting disease severity. Characterising pre-existing baseline immunity is crucial for accurate pandemic risk assessment and preparedness planning.
While some of the headlines overnight in the European press (see Likely no deadly bird flu pandemic: Immunity against regular flu also works on H5N1) overstate these findings, any degree of immunity to H5N1 beats no immunity at all. 

Since this study utilized a convenience sample of healthcare workers, it did not include children or adolescents (< 20), or the elderly (> 70). 

But they did report:  In an age-stratified analysis, antibody levels against A(H5) influenza virus HA0 antigens appeared higher in health-care workers older than 60 years.

This increased immunity is likely the consequence of a lifetime of exposure to influenza viruses, but the majority (61%) of the test cohort also reported receipt of the seasonal flu vaccine over the past 4 years

Since we've seen other studies showing some limited protection against H5N1 (in ferrets) from the seasonal flu vaccine, it is possible that prior flu vaccination contributed to - or amplified - some of the preexisting immunity reported in this study.

While I find plenty of good reasons to get the flu shot each year, perhaps for some, that will provide an added incentive to get one this fall.  

At least, one can hope.

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Monday, April 13, 2026

Front. Immunology: Thymidine phosphorylase promotes SARS-CoV-2 spike protein-driven lung tumor development

 

#19,117

While the world continues to treat COVID as if it is now a mild illness, over the past 6 years we've seen compelling evidence that repeated COVID infections can seriously affect one's health (see Nature: Acute and Postacute Sequelae Associated with SARS-CoV-2 Reinfection), along with a long litany of post-COVID sequelae. 

A few (of many) recent studies include:


EID Journal: Thrombotic Events and Stroke in the Year After COVID-19 or Other Acute Respiratory Infection

European Society of Cardiology: Major Consensus Statement Released on Long-Term Cardiovascular Impact of COVID Infection 

Referral: JAMA - COVID-19 in Pregnancy Linked With Risk of Neurodevelopmental Disorders in Early Childhood



It may take years to fully parse out the long-term health impacts of COVID on society, but some researchers have expressed concerns over increased lung cancer risks due to SARS-CoV-2 infection (see 2022's SARS-CoV-2 and probable lung cancer risk). 

While it wasn't limited to COVID, last year in Nature: Respiratory Viral Infections Awaken Metastatic Breast Cancer Cells in Lungs, we saw a study in mice that demonstrate that common respiratory viruses may awaken dormant cancer cells.  The authors wrote:

Studies have shown that cancer metastasis can be triggered by inflammation. Infection by respiratory viruses, such as influenza and SARS-CoV-2, often causes inflammation. 

Last last year, Molecular Aspects of Medicine published The double-edged sword: How SARS-CoV-2 might fuel lung cancer, which suggested that Post-COVID-19 pulmonary fibrosis could be a precursor to lung cancer.

While we aren't at the point where we can say with any certainty that COVID infection causes cancer, researchers continue to find plausible reasons why it may create conditions that exacerbate the risks. 

Which brings us to a new study, which also suggests a potential link between COVID infection and an increased risk of lung cancer. First the Abstract, followed by some excerpts from a press release. 

Thymidine phosphorylase promotes SARS-CoV-2 spike protein-driven lung tumor development
Abstract

Background:

COVID-19 survivors exhibit increased interstitial lung fibrosis, a known risk factor for lung cancer. We investigated whether SARS-CoV-2 spike protein (SP)-induced lung injury and elevated thymidine phosphorylase (TYMP) promote lung tumorigenesis.

Methods:

A TriNetX retrospective cohort analysis was combined with mechanistic studies in K18-hACE2TG and K18-hACE2TG/Tymp–/– mice. Mice received intratracheal SP or control lysate followed by a urethane-induced lung cancer protocol. Lung injury, inflammation, thrombosis, fibrosis, STAT3 activation, cytokine profiles, and tumor burden were assessed. In vitro assays evaluated SP- and RBD-induced ACE2 processing.

Results:

Propensity score-matched TriNetX cohorts demonstrated an increased lung cancer risk after COVID-19, particularly among current smokers (n = 166,807; RR 1.22; HR 1.50; P<.001). In mice, SP induced acute lung injury, neutrophil infiltration, and microthrombi, which were reduced in TYMP-deficient mice. SP markedly increased lung tumor incidence and aggressiveness, whereas TYMP deficiency reduced tumor formation from 50% to 18% of lung lobes. SP-induced STAT3 upregulation and collagen deposition were significantly attenuated in K18-hACE2TG/Tymp–/– mice. Cytokine profiling revealed a tumor-promoting, myeloid-dominant inflammatory milieu in K18-hACE2TG mice, in contrast to a T cell-inflamed, anti-tumor profile in K18-hACE2TG/Tymp–/– mice. SP and RBD altered ACE2 processing, generating lower-molecular-weight fragments consistent with enhanced turnover.

Conclusions:

SARS-CoV-2 SP drives lung injury, fibrosis, and tumorigenesis through a TYMP-dependent mechanism involving STAT3 signaling and inflammatory microenvironment remodeling. COVID-19 significantly increases lung cancer risk, especially in current smokers. TYMP represents a potential therapeutic target to mitigate long-term pulmonary consequences of COVID-19.

       (Continue . . . )

 

Researchers explore potential link between COVID-19 and lung cancer risk 

Marshall University Joan C. Edwards School of Medicine

New findings from researchers at the Marshall University Joan C. Edwards School of Medicine and The Hebrew University of Jerusalem have identified a potential association between COVID-19 and increased lung cancer risk, driven by underlying biological mechanisms in the lung.

The study, published in Frontiers in Immunology, integrates human clinical data with mechanistic research in animal and cellular models to better understand how SARS-CoV-2, the virus that causes COVID-19, may contribute to long-term lung disease.

“Our findings suggest that COVID-19 may do more than cause acute illness—it may also create biological conditions in the lung that could contribute to increased cancer risk over time,” said Wei Li, Ph.D., professor of biomedical sciences at the Joan C. Edwards School of Medicine and co-corresponding author on the study. “Understanding these pathways is critical as we continue to study the long-term health impacts of the virus.”

The study identified a key role for thymidine phosphorylase (TYMP), a protein that may interact with the SARS-CoV-2 spike protein to promote inflammation, fibrosis and tumor-related pathways in the lung. Researchers found that this interaction may activate processes associated with cancer growth and alter the lung’s immune environment in ways that could support tumor formation.


While there is growing circumstantial evidence that COVID may promote tumor-promoting environments, we still lack causal proof. That may come in time, but even without it, we've pretty good evidence that repeated COVID infections are best avoided if at all possible. 
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WHO Burundi: Investigation into a `Mystery' Disease in Mpanda

 

#19,116

Caveat : Reports of `mystery' diseases are fairly common around the globe, and while these reports usually turn out to be something already known, on rare occasions they can alert us to a new, or re-emerging threat.

Yesterday on FluTrackers, Pathfinder posted two reports on a `mystery' illness affecting several households in Burundi, in east Africa.  Since late March, at least 5 deaths, and roughly 3 dozen illnesses have been reported, `. . . primarily among members of the same household and close contacts.'

According to the WHO: `Symptoms include fever, vomiting, diarrhoea, blood in urine, fatigue and abdominal pain. Some severe cases have also presented with jaundice and anaemia.'

So far, tests have ruled out many of the `usual suspects'; Ebola virus disease, Marburg virus, yellow fever, Rift Valley fever, and Crimean-Congo hemorrhagic fever.  Further testing is underway. 

While this could be something new, there are still a number of diagnoses that must be ruled out including infectious diseases like Severe Malaria, Leptospirosis, Enteric Fever, etc., environmental contaminants (heavy metals or pesticides), or food or alcohol poisoning. 

The CIA Factbook describes Burundi as:

Burundi is a landlocked, resource-poor country with an underdeveloped manufacturing sector. The economy is predominantly agricultural with roughly 90% of the population dependent on subsistence agriculture.

According to the WHO:

In Burundi, life expectancy at birth (years) has improved by ▲ 19.6 years from 44.4 [43.5 - 45.4] years in 2000 to 64 [63.3 - 65] years in 2021.

But this still puts it in the bottom 20% among african nations. The WHO AFRO statement follows:

Burundi investigates illness that has caused five deaths
11 April 2026

Bujumbura—The health authorities in Burundi, with support from the World Health Organization (WHO) and partners, are deepening investigations to determine the cause of an illness that has led to five deaths and sickened 35 people in Mpanda district in the north of the country.

Laboratory analysis has turned negative for Ebola and Marburg virus diseases, Rift Valley fever, yellow fever and Crimean-Congo haemorrhagic fever. An alert about the undiagnosed illness was received on 31 March 2026, primarily among members of the same household and close contacts. Symptoms include fever, vomiting, diarrhoea, blood in urine, fatigue and abdominal pain. Some severe cases have also presented with jaundice and anaemia.

“While it’s reassuring that preliminary analysis is negative for these serious infections, further investigations are ongoing to determine the cause of the disease,” said Dr Lydwine Badarahana, Burundi’s Minister of Health. “All the necessary measures are being taken to safeguard public health and prevent potential spread of infection.”

A joint team of experts from the country’s public health emergency operations centre and the national reference laboratory has been deployed to the field to support ongoing investigations.

WHO is supporting the Ministry of Health to strengthen disease surveillance, field investigation, clinical care, laboratory diagnosis and infection prevention and control, while also providing logistical support to sustain key operations. The Organization has also facilitated the shipment of samples to the National Institute of Biomedical Research in neighbouring Democratic Republic of the Congo for further analysis.

The Ministry of Health is leading the response, working with partner organizations to coordinate joint efforts. 
The old medical adage that; if you're in Central Park and hear hoofbeats, think `horses' not `zebras' still applies. But of course, Burundi is a long way from Central Park, so this is an outbreak worth keeping our eye on. 
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Sunday, April 12, 2026

CHEST Review: Examining the Threat of H5N1 Highly Pathogenic Avian Influenza to Human Health

#19,115

This morning we've an open access review published in CHEST® - the monthly clinical research journal of the American College of Chest Physicians - which looks at the continued evolution of HPAI H5N1's threat to human health.
 
At a time when many government agencies appear to have reduced their coverage of HPAI (the CDC's last Avian Flu News & Spotlights update was Sept 8th, 2025), this review for clinicians is particularly timely. 

This article covers a lot of ground, starting with a a literature search and evidence review which documents HPAI's shift from being primarily a disease of birds to increased mammalian adaptation. 


While focusing primarily on H5N1 clade 2.3.4.4b, this review also briefly discusses the Cambodian 2.3.2.1e clade.  While H5N5 is mentioned, this article went to press prior to last year's announced human infection in Washington state.

Much of this review is focused on practical concerns for clinicians, including testing, treatment, and isolation of cases.  A few `pearls' from the narrative include:
  • Exposure to cattle or commercial poultry operations thus may be indicative of potential clade 2.3.4.4b A(H5N1) infection; however, lack of exposure cannot rule out potential infection, as observed in 5 patients with unknown exposure or exposure to other animals.39,41
  • Timely identification and isolation of infected patients is essential and is enabled by a low threshold of suspicion for patients with consistent clinical presentations and epidemiologic factors, including exposure to sick birds or cattle within 10 days of symptom onset.
  • Patients with positive findings may go undetected if they do not seek diagnosis or treatment in the absence of access to health care or because they experience only mild symptoms.
 While this review acknowledges the `low' risk today, it warns that could change:
Future Directions

At this time, the risk posed to the general public from AIV is considered low.29 However, that reality could change at any time given the rapidly evolving situation involving infection in mammals and substantial knowledge gaps surrounding clade 2.3.4.4b A(H5N1) and human infections.

This is an excellent review for clinicians, and makes for a good Sunday morning read for anyone interested in the topic. 

Highly recommended. 

Open access

Examining the Threat of H5N1 Highly Pathogenic Avian Influenza to Human Health

Juliette Blais-Savoie, Emily Halajian, Kuganya Nirmalarajah, Andra Banete, Juan C. Corredor, Jonathon D. Kotwa,Yaejin Lee, Sugandha Raj, Shayan Sharif ,Nicole Mideo, Samira Mubareka

Publication: CHEST
Publisher: Elsevier
Date: April 2026

Abstract

Topic Importance
The clade 2.3.4.4b highly pathogenic avian influenza (HPAI) virus H5N1 is the etiologic agent for an ongoing panzootic with a rapidly increasing number of human infections. Although morbidity and mortality in humans with this clade seems to be limited to date, previous HPAI H5N1 viruses have been associated with mortality rates of approximately 50% in humans. Not all cases of clade 2.3.4.4b influenza A(H5N1) HPAI in humans have been associated with known exposure to infected animals. Therefore, clinicians must be aware of the changing viral ecology, human risk factors, and clinical presentations associated with H5N1 viruses to facilitate early case recognition and management of clade 2.3.4.4b A(H5N1) HPAI infection in humans.
Review Findings
Historic H5N1 presentations have involved multiorgan systemic disease, notably including severe neurological disease. Common symptoms associated with clade 2.3.4.4b A(H5N1) HPAI include conjunctivitis, fever, and upper respiratory tract infection. Exposure to infected dairy cattle is a novel risk factor.
Summary
The rapid global spread of clade 2.3.4.4b A(H5N1) viruses has been associated with severe disease and high mortality in many farmed animal species and wildlife. The composite picture of emerging risk to human health comprises an unprecedented number of mammalian infections, viral adaptations to mammalian hosts, severe neuroinvasive disease in naturally infected mammals, and spillover into novel species such as dairy cows with forward transmission to humans. Preparedness measures are crucial to mitigating significant human health impacts from this virus and must include a Canadian One Health Training Program in Emerging Zoonoses approach that promotes both animal and human health

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While HPAI H5Nx remains our biggest concern, recents human infections with other subtypes (see Taiwan CDC Update: Novel H7 Infection Identified as H7N7 and WHO DON: Avian Influenza A(H9N2) - Italy (Ex Senegal)) remind us that Nature's laboratory is open 24/7, and we could easily be blindsided by something unexpected coming out of left field.

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