A group of scientists has used gain-of-function research to engineer a deadly mutated strain of “bird flu” that has been weaponized to spread among humans.
South Korean researchers combined three strains of the bird flu to create a new mutant version of the virus.
The researchers boast that the newly engineered mutant has increased viral stability, altered host targeting, and enhanced human cell entry.
The new virus can spread rapidly through human populations due to the potential for aerosol transmission, the scientists reveal.
The development of the new chimeric virus was revealed in a new study.
The study’s paper was published this week in the Virology Journal.
The paper reveals that scientists constructed a chimeric virus with altered heat resistance, receptor binding, and cell entry capabilities.
They were able to engineer this new virus by combining gene segments from three distinct influenza viruses.
They then applied directed mutations to increase replication and stability.
Highly pathogenic bird flu viruses require BSL-3 containment due to their potential for aerosol transmission and serious health risks.
The experiments come as President Donald Trump’s administration has announced a fresh crackdown on “dangerous gain-of-function research.”
The timing raises alarm over the use of high-risk virological techniques to create brand new, pandemic-level viruses under the guise of vaccine development.
Just last week, the White House confirmed that the Covid pandemic was caused by a virus engineered during gain-of-function experiments.
Researchers introduced specific mutations to enhance the thermal resilience of the virus.
These modifications mean the mutant virus can survive longer under higher temperatures.
“We identified a key mutation (R90K) that increases heat stability while preserving antigenicity,” the researchers wrote in the study’s paper.
“Combining the R90K and H110Y mutations (22W_KY) resulted in a synergistic increase in thermal stability and maintained HA activity without measurable reduction even after 4 h at 52 °C.”
These alterations directly transform the physical durability of the virus.
It allows the virus to persist in conditions that would otherwise degrade its infectivity.
Thermal stabilization is a functional enhancement, meeting the definition of gain-of-function.
The authors further engineered viral replication traits by modifying the PB2 gene to boost replication in chicken eggs.
This method also impacted replication in other mammals aside from humans.
“The PB2 gene of PR8 was replaced with a prototypical avian PB2 gene to increase replication efficiency in embryonated chicken eggs and reduce replication efficiency in mammalian cells,” the scientists wrote.
“The PB2 gene of 01310, modified with I66M, I109V, and I133V mutations (referred to as 310-MVV), increased the replication efficiency of Y280-lineage H9N2 viruses compared with the wild-type PB2 gene of 01310.”
This deliberate alteration of replication in non-natural hosts like eggs is a textbook example of gain-of-function manipulation.
The scientists rebuilt influenza viruses from scratch, using the pHW2000 plasmid-based system.
“Recombinant viruses were generated using a pHW2000 plasmid-based reverse genetics system,” they note.
Reverse genetics systems are commonly used in gain-of-function research to design viruses with novel traits not found in nature.
The study confirms altered receptor interactions in the modified virus.
This is a critical determinant of which species or tissues the virus can infect.
“The N193D mutation led to a reduction of the affinity of the 22W_MVV virus for 2,3-SA,” the researchers explain.
Although the change reduced binding in this case, modifying receptor preference alters the host-virus interface, meaning it is still classed as gain-of-function by definition.
The deadly new virus is a lab-built chimera formed by fusing gene segments from three separate flu strains.
“22 W HA and 22 W NA genes, along with six internal genomic segments (PB2, PB1, PA, NP, M, NS) from PR8 and a PB2 gene from 01310 containing the I66M, I109V, and I133V (MVV) mutations,” they note.
This means the final virus included:
- Hemagglutinin (HA) and neuraminidase (NA) from clade 2.3.4.4b H5N1
- Internal genes from A/Puerto Rico/8/1934 (PR8)
- PB2 gene from A/Chicken/01310/Korea/2001 with MVV mutations
Such multi-strain reassortment is inherently risky.
This type of mutation falls under the highest classifications of gain-of-function due to the unpredictability of the resulting virus.
The virus was also engineered to spread more effectively and rapidly through human populations.
It manipulates the immune response and quickly enters human cells after being inhaled.
“BEI-inactivated 22W_KY also elicited significantly stronger systemic IgG, mucosal IgA, and T-cell responses, especially in the lungs,” they explain.
“The highest level of intracellular entry was observed for BEI_22W_KY, confirming its superior effectiveness in penetrating cells.”
These enhancements suggest the modified virus is more effective at invading host cells.
This is a major safety red flag when discussing lab-created pathogens.
This study was published without mentioning gain-of-function oversight or biosecurity risk assessment.
Should this engineered virus escape containment accidentally or intentionally, it could ignite a global pandemic.
Ironically, it would create the disaster that the experiments were allegedly set up to prevent.
