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/
A new Israeli study demonstrates why some people develop #LongCOVID.
➡️ By analysing immune responses, gene expression and plasma proteins in blood samples, scientists found that people with longCOVID show persistent chronic inflammation and disrupted immune signalling months after infection — patterns not seen in those who fully recovered. 1/
These immune differences help explain lingering symptoms — such as fatigue, brain fog and breathlessness — and point to specific inflammatory pathways that could be targeted for treatment. This work opens new avenues for better therapies for millions living with longCOVID. 2/
Researchers performed immunological, virological, transcriptomic and proteomic analyses from a cohort of 142 individuals between 2020 and 2021, including uninfected controls (n = 35), acutely infected individuals (n = 54), convalescent controls (n = 24) and patients with LC (n = 28).
➡️ The LC group was characterized by persistent immune activation and proinflammatory responses for more than 180 days after initial infection compared with convalescent controls, including upregulation of JAK-STAT, interleukin-6, complement, metabolism and T cell exhaustion pathways.
➡️ Similar findings were observed in a second cohort enrolled between 2023 and 2024, including convalescent controls (n = 20) and patients with LC (n = 18). 3/
Can past COVID-19 weaken the body’s ability to fight tuberculosis?
➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).
➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/
Key finding:
➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.
➡️ Suggests prolonged immune downregulation after COVID-19. 3/
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.
➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.
➡️ Flu does not drive the same long-term immune activation. 3/
A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.
➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/
Key Findings
➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.
➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).
➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.
➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/
Implications
➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology
➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.
➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/
New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.
The key? Differences in the immune system, gut, and hormones. 1/
Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.
➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/
The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.
➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/