H5N1 'Bird Flu' is the Result of Gain-of-Function 'Research'

Ah, 'the Science™' is baaaaack, and speaking of the past, here's a 2013 piece advocating for Chloroquine vs. 'man-made' H5N1

As this new year picks up steam, we’re left with the same, shale aftertaste of having experienced this before.

I’m, of course, talking about a respiratory virus—Avian or Bird Flu—that is poised to wreck havoc in everybody’s daily lives due to its ‘pandemic potential’.

While we’re on the subject, let’s not forget that science once was a more helpful endeavour, but that was when a) researchers weren’t totally mesmerised by both big gov’t/pharma grants, b) peer-review still worked (to certain extents), and c) highly relevant outlets still published ‘contrarian’ (sic) content.

And thus we turn to Cell Research, specifically a short letter to the editors by Yiwu Yan and colleagues entitled ‘Anti-malaria drug chloroquine is highly effective in treating avian influenza A H5N1 virus infection in an animal model’. Published 4 Dec. 2012, in appeared in Cell Research, 23 (2013): 300–2, and it contains a few very interesting snippets of information to which we now turn.

References omitted, emphases and [snark] mine.

Dear Editors…(H5N1 is ‘man-made’)

The recent controversial studies of man-made avian flu viruses [I bet you didn’t know that] caused a media storm, and brought new concerns to the potential of an avian influenza H5N1 virus pandemic, which has been pending since 1997. Although the estimated mortality rate of avian influenza A H5N1 virus infection in humans could be as high as 60%, the World Health Organization (WHO) phase of pandemic alert is currently set at 3, due to that there has not been human-to-human or community-level transmission [remember: this was penned in late 2012]. However, the newly created H5N1 virus strains, which are genetically altered, are transmissible among ferrets, and thus may trigger a real pandemic that could potentially result in millions of deaths according to Science Insider [I’ll discuss this one below]. While it is arguably a bit too late to debate whether regulations or mandatory reviews should be applied to these dual-use studies, in the matter of fact, these viruses that are probably among the most dangerous infectious agents known already exist [so, why do ‘we’ create them in the first place?]. Therefore, a top priority at present is to find effective prophylactic or therapeutic agents that would help to control a pandemic of avian influenza A H5N1 viruses.

Two brief things to note here: contrary to whatever BS is peddled in legacy media about, say, ferrets, monkeys, pangolins, and/or bats, these foursomes or whatever are not what’s behind the ‘mysterious bird flus cases’ (Salon) or, my personal ‘favourite’ in the category of ‘gaslighting galore’, comes to us via Newsweek’s Peter Aitken (dated 27 Dec. 2024) who is the magazine’s ‘Politics Weekend Editor’:

Where Did Bird Flu Come From, and How Does it Spread?

Most cases have come from exposure to birds—just by mere coincidence—with five cases coming from probably exposure to infected commercial poultry. The CDC has tentatively tied those cases to three instances from Washington and two from Arizona.

Some cases have come from dairy herds, which is where the CDC believes the bulk of cases occurred in California—all but one case, which the CDC put down as ‘unknown’ source.

Los Angeles health officials warned residents to ‘avoid unprotected contact with sick or dead animals including cows, poultry and wild birds; avoid consuming raw or undercooked animal products, such as raw milk; and protect pets and backyard poultry from exposure to wild animals.’

‘It is also important for everyone to get the seasonal flu vaccine’…a statement from the Los Angeles Department of Public Health (LA DOH) said.

Oh, here we TF go again.

This also means, by the way, that ‘public health™’ officialdom is all-in on spreading misinformation by their tried and tested methods (lying by omission and/or commission), as this wondrous—of course ‘archived’—scheme entitled ‘Emergence and Evolution of H5N1 Bird Flu’ does: it simply leaves out the entire gain-of-function, or bioweapon, ‘research’.

See how easy that is? Trust ‘the Science™’.

Bird Flu’s Infectious Potential Likely Due to GoF

Back in 2012, though, Martin Enserink and Jon Cohen penned the following essay for Science: ‘One of Two Hotly Debated H5N1 Papers Finally Published: With four mutations, a hybrid H5N1 virus jumps between ferrets via respiratory droplets’, which I’ll excerpt here but recommend you read it in its entirety:

One of two influenza papers at the center of an intense, 6-month international debate has finally seen the light of day. Today, Nature published a controversial study in ferrets that shows how scientists can engineer an avian influenza strain to transmit between mammals through respiratory droplets such as those created by coughing or sneezing [repeat after me: ‘no-one knows where bird flu came from’].

The 11-page study, led by Yoshihiro Kawaoka of the University of Wisconsin, Madison, and the University of Tokyo, describes how the research group stitched a mutated version of a key viral protein called hemagglutinin from the bird flu virus known as H5N1 onto the human H1N1 virus that caused a relatively mild pandemic in 2009. A mere four mutations in the avian hemagglutinin—the H5—allowed this hybrid virus to bind more strongly to mammalian cells and copy itself at high enough levels to readily transmit via respiratory droplets [oh, would you have thought that…]. If the same holds true in humans, that means the virus might be able to trigger a pandemic.

The paper is one of two studies that the U.S. National Science Advisory Board for Biosecurity (NSABB) in December said should not be published in full. After an expert panel convened by the World Health Organization (WHO) disagreed with the decision, NSABB reviewed revised versions of the manuscripts and changed its position. That cleared the way for Nature on 2 May to publish the first of the two experiments. (The other of the two papers, by Ron Fouchier of Erasmus MC in Rotterdam, the Netherlands, has been held up because the Dutch government insisted that Fouchier obtain an export license to submit it, which he has done. It is now under review by Science.)

So, I recommend revisiting that CDC’s ‘archived’ version of events, which—however (in)conveniently leaves out that gain-of-function (bioweapon) ‘research’ described in Science in 2012.

Kawaoka's study is an ‘important additional step along the way’, says Malik Peiris, a flu researcher at the University of Hong Kong, who co-wrote an article in Nature about the Kawaoka paper.

Influenza infection begins when hemagglutinin binds to receptors on the host cell…on 5 November 2011, while NSABB was debating the wisdom [sic] of publishing the Kawaoka and Fouchier papers in full, a report appeared online in Virology that identified two such mutations. But the mutations alone still didn’t make the virus transmissible between ferrets through respiratory droplets.

Kawaoka's group carried out a series of experiments that coaxed out additional mutations with that effect. The effort included screening 2 million randomly created mutants and infecting ferrets to let strains further adapt to them. Eventually, they found a virus that transmitted from infected animals to four of six healthy ferrets in neighboring cages [I’m unsure if these 4-6 ferrets are the basis for the WHO’s claim of human lethality of up to 60%, but at this time, I wouldn’t be surprised if they are]. It did not kill any of them [note that infection ≠ death].

If you wish to read a summary report about the licensing for that other study required by the Dutch gov’t, click here.

And with the man-made origins of this charade masquerading as ‘research’ now established, let’s return to the chloroquine paper.

On the Pathology of Bird Flu

Previous reports have demonstrated that the high mortality in humans infected with avian influenza A H5N1 is partly due to acute lung injury or the resulting severe condition, acute respiratory distress syndrome (ARDS)^4,5. There are few treatment choices for ARDS, aside from mechanical supporting equipment and empirical treatments. The use of cortisones is controversial.

We have recently discovered that avian influenza A H5N1 virus infection causes acute lung injury by inducing autophagic alveolar epithelial cell death⁶. Importantly, we found that autophagy inhibitors are effective in ameliorating murine acute lung injury induced by live avian influenza A H5N1 virus infections⁶. We thus hypothesize that if a drug that is currently in clinical use can act to inhibit autophagy, then such a drug might be a good candidate for treating H5N1 infections [isn’t science beautiful, almost like an art (if done right)?].

To test this, we have focused our efforts on chloroquine (CQ), as CQ is the only oral clinical drug that is known to be an autophagy inhibitor⁷. CQ, or N′-(7-chloroquinolin-4-yl)-N,N-diethyl-pentane-1,4-diamine, was discovered in 1934 by Hans Andersag and his co-workers at Bayer Laboratories and was introduced into clinical practice in 1947 as a prophylactic treatment for malaria⁸. Currently, CQ and its hydroxyl form, HCQ, are used as anti-inflammatory agents for the treatment of rheumatoid arthritis, lupus erythematosus and amoebic hepatitis. More recently, CQ has been studied for its potential use as an enhancing agent in cancer therapies as well as novel antagonists to chemokine receptor CXCR4 in pancreatic cancer^8,9.

And thus we learn that which ‘the Science™’ had tried to suppress in 2020 was perfectly common knowledge less than a decade prior.

On the Efficacy of Chloroquine vs. H5N1

We first tested whether CQ could inhibit cell death in the human lung carcinoma A549 cells infected with live avian influenza A H5N1 virus. The cell viability was improved both prophylactically and therapeutically in a dose-dependent manner with CQ treatments, and the efficacy of CQ was much higher than that of the potent autophagy inhibitor 3-methyladenine (3-MA) (Figure 1A). [line break added]

Next, we tested the potential therapeutic effect of CQ in a mouse model of live H5N1 infections. We found that when CQ was administered therapeutically at a dose equivalent to that for human clinical use, the survival rate of H5N1 virus-infected mice was improved dramatically (from 0% to 70% at day 8 post infection), and the body weight changes also showed a trend of improvement, but prophylactic application of CQ showed no protective effect (Figure 1B and 1C) [so, if push comes to shove with Bird Flu, have a few treatment kits of CQ available (note I’m not an MD, but it might be useful to consider talking to a trustworthy one)]. We analyzed the lung histopathology in these mice and found fewer infiltrating leukocytes in the CQ therapeutic group, but not in the CQ prophylactic group (Figure 1D). Lung edema, as determined by the increased wet/dry weight ratio of lung tissue, was also significantly reduced by therapeutic CQ treatment, but not by prophylactic CQ treatment (Figure 1E). [line break added]

Taken together, our results demonstrate that CQ, a known autophagy inhibitor that is in clinical use, could efficiently ameliorate acute lung injury and dramatically improve the survival rate in mice infected with live avian influenza A H5N1 virus…

CQ was therefore proposed to be a candidate prophylactic agent for influenza virus. However, government-sponsored clinical trials have shown insufficient prophylactic effects against influenza infection¹², which is consistent with our mouse results. CQ could also inhibit the innate immune responses through TLR signaling pathways and act as novel antagonists to chemokine receptor CXCR4 in pancreatic cancer^9,13. We have shown that CQ treatment clearly inhibited the autophagy in mouse lung induced by avian influenza A H5N1 virus while the virus loads and proinflammatory cytokines were not significantly affected (Figure 1F, 1G, Supplementary information, Figure S1)…

Our study strongly suggests that CQ (and potentially its derivatives) should be evaluated as a candidate drug for clinical treatment of H5N1-infected patients. Moreover, a systematic screening of common clinical drugs for potential autophagy inhibitors may lead to the identification of other novel treatments against avian flu.

And thus the continued importance of evidence-based approaches.

Bottom Lines

As far as worn-out adages go, ‘doing the same thing over and over again expecting different results’ being ‘the definition of insanity’, I suppose it fits.

Once upon a time—actually, not that long ago—Western Civ knew what to do, how to do things, and more or less carefully juxtapose risks vs. benefits of its own actions.

This time, I fear, things won’t be different from the WHO-declared, so-called ‘Pandemic™’.

Note, though, that these researchers have Chinese names and were working on CQ in China—which is hardly surprising as the Japanese-US teams doing this kind of gain-of-function = dual-use bioweapon ‘research™’ could (sic) be considered as enemy activities.

Now, with the experiences of the past 5 years behind us, though, I suppose we, the people need to consider the notion that these lunatics are merely doing the bidding of whoever oligarch/deep state funding agency is tasking them to do so.

There’s literally nothing new under the sun.

Yet, as I type these lines in early January 2025, we, the people look like we’re poised to repeat history, all the evidence and experiences notwithstanding.