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HHS Funds Experiments Determining How to Make H5 Influenza More Pathogenic: Journal ‘Science’

Bird flu study carried out by infamous gain-of-function virologist Ron Fouchier.

Scientists funded by the U.S. Department of Health and Human Services (HHS) say they have identified the molecular mechanism that allows low-pathogenic H5 avian influenza to acquire the defining genetic feature of highly pathogenic bird flu, according to a study published March 12 in Science.

Pathogenicity is the ability of a microorganism or agent to cause disease in a host.

Americans are paying for experiments that determine the molecular steps said to make H5 influenza more dangerous.

The study was carried out by Dr. Ron Fouchier of Erasmus Medical Center—best known for his controversial H5N1 bird flu gain-of-function experiments—along with researchers from Erasmus Medical Center, EMBL Grenoble, University Grenoble Alpes, Leiden University, and Princeton University.

The controversial experiments come as Congress asks for $3.3 billion for a future influenza pandemic, including the construction of new influenza vaccine manufacturing facilities, in a newly introduced House bill.

They also come as the FDA’s Vaccines and Related Biological Products Advisory Committee (VRBPAC) clears the way for approval of Moderna’s new mRNA influenza vaccine, despite the shot claiming to offer less than 1% absolute benefit.

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The study centered on the multibasic cleavage site (MBCS), which the authors describe as the genetic basis for the transition from low-pathogenic avian influenza viruses (LPAIVs) to highly pathogenic avian influenza viruses (HPAIVs).

To determine that mechanism, the researchers claim to have engineered influenza RNA sequences and structures and measured how frequently the virus acquired the nucleotide insertions that generate the multibasic cleavage site.

According to the paper:

“We show that transient H5 RNA structures, predicted to trap the influenza virus polymerase on purine-rich sequences, drive nucleotide insertions.”

The researchers then say they experimentally altered those RNA structures.

When they disrupted the structures, the frequency of pathogenicity-generating insertion events fell sharply.

When they strengthened them, the insertion events increased dramatically.

In one engineered construct, heteropolymer insertion frequencies increased approximately eightfold over the parental construct.

Meaning the engineered virus was said to have become about eight times more likely to acquire the genetic change that turns low-pathogenic H5 influenza into highly pathogenic bird flu.

The scientists also transferred H5 RNA features into H6 influenza, creating chimeric “Frankenstein” genetic hybrids.

According to the paper:

“Introduction of H5-like sequences and structures into an H6 hemagglutinin resulted in MBCS-yielding insertions.”

The study further reported that the insertions generated by the engineered system produced multibasic cleavage site sequences that were “similar or identical” to those observed in naturally emerging highly pathogenic H5 influenza viruses.

The authors concluded they had identified the mechanism responsible for generating the multibasic cleavage site.

They wrote:

“We show that the trapping of the influenza virus RdRp on A/U-rich sequences by transient RNA structures formed by the template is the mechanism by which nucleotide insertions occur at the H5 cleavage site.”

You can contact NIAID here, NIH here, and HHS here to voice opposition to taxpayer-funded research on pandemic pathogens—particularly after Congress, the White House, the Department of Energy, the FBI, the CIA, and Germany’s Federal Intelligence Service (BND) all acknowledged that the COVID-19 pandemic was “likely” the result of a laboratory incident involving engineered pathogens.