A NEW study finds that H5N1 influenza viral lineages are beginning to evade human immunological defenses. This indicates current and future H5N1 viral lineages pose a greater risk to human health—including the possibility of increased transmission in humans. 1/
This new computational modeling of avian influenza variants' immunoprotein interactions reveals the H5N1 influenza virus is evolving to escape immunological defenses raised by previous infection or vaccination in mammals. 2/
This rapid adaptation means that if one makes an H5N1 vaccine with a previous vaccine candidate virus, the vaccine will have less efficacy, based on the measurements of how much the virus has evolved in recent years. 3/
The continuous transmission of H5N1 from birds to mammals and the increase in strains with immuno-evasive HA in mammals sampled over time suggest that antigenic drift is a source of zoonotic risk. 4/
Using high-performance computational modeling, the researchers documented a trend of weakening binding affinity of a wide variety of existing antibodies, collected from vaccinated and or infected hosts, against H5 viral isolates over time. 5/
In assessing the possible pandemic risk spurred by H5 bird flu spread and mutation, global researchers agree that the avian virus remains high on lists of potential pandemic agents. 6/
As of today, no human-to-human transmission has been reported. However, cattle in at least 17 states have tested positive for H5N1 in addition to millions of cases among wild birds, small mammals, commercial chickens, and other flocks. 7/
Between January 2022 and March 2025, the CDC reported:
-12,510 outbreaks among wild birds in U.S.
-51 jurisdictions w/ bird flu among wild birds.
-166,417,923 poultry affected
-70 human cases of H5N1, one fatal, in the U.S. 8/
Fibrinoloid (amyloid-containing) microclots are resistant to degradation and are found in a variety of diseases including #LongCOVID, ME/CFS, and sepsis. A NEW review looks at the use of laser speckle imaging (LSI) and laser Doppler imaging (LDI) to assess how fibrinaloid microclots can disrupt the microcirculation. 1/
The microcirculation typically refers to those capillaries less than 100 mm in diameter. Having shown that blood can clot into an anomalous amyloid form that is rather resistant to fibrinolysis, researchers have previously developed the idea that endothelial dysfunction can both lead to and be caused by the fibrinaloid microclots so formed, such that this can slow or block entirely parts of the microcirculation. 2/
The microclots might be thought of as a ‘structural’ manifestation. This impairment of the microcirculation is referred to as ‘blood stasis’. It is thus desirable to have ‘functional’ methods that can measure these effects on the microcirculation directly. 3/
A NEW study finds that infection with SARS-CoV-2 during the first year of the pandemic was associated with three to five times higher odds of cognitive impairment 2 years after infection. 1/
Survivors of the disease may require special attention from clinical doctors to diagnose and treat cognitive impairment, namely, those who were hospitalized for more than 15 days, in intermediate or intensive care units, and presented disorientation, changes in vision, gait or balance, during infection. 2/
Conversely, although cognitive impairment was less frequent and severe in COVID-19 cases who had been followed in the community during infection, this population is younger. Causality between SARS-CoV-2 infection and cognitive impairment could not be inferred from the present study. 3/
A NEW study finds that anti-SARS-CoV-2 antibodies play a protective role against vital organ-related #LongCovid (LC) symptoms, especially cardiovascular symptoms, but are insufficient in preventing or limiting other highly prevalent LC symptoms, such as neurological, psychiatric and pulmonary. 1/
These data underscore the complexity of the potential involvement of anti-SARS-CoV-2 immune responses in either protecting against or contributing to the development of different #LongCovid phenotypes. 2/
The disturbed immunological profile supports the idea of some sort of silent longCOVID, that may eventually manifest as critical clinical events, such as acute myocardial infarction or cerebral vascular accidents. 3/
A meta-analysis from Egypt of 125 studies involving over 4 million COVID survivors shows that months to years after infection, fatigue was the most common symptom at 43%. Around 27% of people experience cognitive impairment after COVID infection. 1/
Further, 28% experienced memory issues, 24% sleep disorders, 20% headaches, 16% dizziness, 14% depression, and 13% anxiety, with significant variability depending on follow‑up time, disease severity, sex, and BMI. 2/
Neurological symptoms are common & persistent in COVID survivors. This study highlights significant burden these symptoms place on individuals, emphasizing the need for well-resourced multidisciplinary healthcare services to support post-COVID recovery. 3/3
A new review on neuroimmune pathophysiology of #LongCOVID explores how SARS-CoV-2 can cause lasting neurological symptoms through a combination of direct infection, immune dysregulation, and persistent inflammation. 1/
Key mechanisms include viral antigen persistence, autoimmunity, blood–brain barrier disruption, neurotransmitter imbalances, and glial cell dysfunction. The authors link these processes to cognitive impairment, fatigue, dysautonomia, and other Long COVID symptoms. 2/
Despite the perception that COVID-19 is now a mild disease, there is overwhelming evidence indicating that SARS-CoV-2 infection is capable of producing widespread post-acute sequelae in a significant percentage of infections. 3/
As people get older, a growing population of cells starts to consume more energy — perhaps because the cells accumulate damage that leads them to rev up processes such as inflammation. 1/
An emerging hypothesis suggests that the brain accommodates these energy-hogging ‘senescent cells’ by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass. 2/
It’s one example of a growing understanding of how our brains control ageing and how psychological stress can accelerate the process at a molecular level. 3/