Debunking a widespread myth: SARS-COV-2 does not have genetically engineered HIV fragments inserted

There are quite a few reasons, to believe that SARS-COV-2 may have come from a lab. There are the sort of things you don’t need a background in biology for to recognize: The fact that it first emerged next to a lab where scientists were performing experiments on various coronaviruses is a little suspicious to say the least.

There’s also the overall manner in which the Chinese government treats the whole affair. The Wuhan lab is now overseen by a Chinese general, scientists are not allowed into the cave were previous coronaviruses were found that were experimented on and information was purged from the lab’s website. Again, you don’t need to have a background in biology, to understand that these sort of things are suspicious.

Then there are also the suspicious things you’ll notice if you have some basic understanding of biology. It’s suspicious how little SARS-COV-2 changed during its first year. We saw just one major mutation that showed up everywhere called D614G, but other than that there was no significant change to its genome for about a year, until we all began to develop some degree of immunity. That’s strange, it suggests that this virus was already well adapted to humans when we first found out about it.

Finally, there’s the strange observation that the peptide sequences of six or seven amino acids in SARS-COV-2 closely resemble those seen in humans, but also closely resemble those seen in mice, without any significant similarity to gorillas or chimpanzees. The virus will try to resemble human proteins to avoid alerting the immune system, but for it to also resemble mice proteins suggests that during some recent step in its evolution, it would have needed to avoid alerting the immune system of mice. I’ve explained it here. One way you could expect a result like this, is if this virus was passed through naive mice with humanized ACE2 receptors.

And so as you can see, there are quite a few mysteries about SARS-COV-2’s origins that remain unanswered. We don’t know exactly what happened, the fact that the Chinese government acts so secretive and insists on blaming frozen food imported from outside the country and Evergrande handed out 120 million dollars to Harvard University all suggest that quite a few people are being threatened or bribed into keeping their mouths shut.

Always try to falsify your findings

However, if you genuinely want to understand what happened, instead of getting trapped in obscure rabbit holes or wandering into dead alleys, then you also need to look critically at the evidence you’re offered. Not all evidence is equally relevant and sometimes claims are made that are so spectacular that they spread rapidly around the world, long before anyone has a chance to point out why this is not the smoking gun you’re looking for.

That’s the case for an argument you may have encountered in the vaccine skeptic substack circles: The idea that the spike protein of SARS-COV-2 has a bunch of insertions, where genetic material from HIV was inserted to enable this virus to infect and kill your T-cells.

It’s somewhat ironic to me, that these substacks that generally came into existence because people did not want to receive an experimental vaccine for a virus that poses no significant threat to healthy young people, are now still afraid of a virus that most people, vaccinated or unvaccinated, no longer care for.

To me this seems to be a product of Leonardi’s law: The phenomenon I named after a notorious T-cell immunologist, where staring too long at a virus makes it appear uniquely scary, because you start to recognize all the ways in which it happens to be uniquely different from other viruses. This man has gained a large following of about 50,000 people who have their own anxiety amplified by him, but his fear-mongering doesn’t perform a real service to society.

We’re all susceptible to Leonardi’s law. Just as the qualities of your new lover will start to seem unmatched as you interact with them to the exclusion of other people, the threat posed by a new virus will seem unique if you obsessively look at it without asking yourself “how unusual is this”? Millions of people around the world, from Phds in virology to government bureaucrats to average dudes in the street, have spent two years gazing at one virus to the exclusion of all others, amplifying each other’s fears.

But it gets worse, when we don’t critically reflect on the evidence we’re offered. You always need to try to falsify your own findings, before sharing them with the world. That’s what nobody who shares this myth that SARS-COV-2 has HIV inserts seems to be doing unfortunately. Nobody bothers to look at the stuff they’re sharing and asking “how unusual is this finding I’m looking at”? The reason is because if they bothered to try to falsify it, they wouldn’t be sharing it. They’d realize it’s nonsense.

Convergent evolution

To start with, if you want to understand why these findings are nonsense, you need to understand that in nature, similar roles will often be performed by similar looking organisms, even when those organisms have no relationship to each other. This is called convergent evolution. There is just a limited range of viable solutions to a particular problem and from within that range of solutions, just a limited range can be arrived at through the process of natural selection. And that’s how you end up with mysteries like this:

At the top you see the Australian Tasmanian wolf, an extinct predator. At the bottom, you see the gray wolf. These two animals have no significant shared ancestry to each other. The wolf is more closely related to a hedgehog, than to a Tasmanian wolf. The Tasmanian wolf is more closely related to a Koala bear, than to a grey wolf. And yet, the two animals have a skull that looks surprisingly similar.

They’re no exception. Vultures in the New World and vultures in the Old World look highly similar to each other, yet they have no common ancestor, they’re two separate groups that evolved independently. We see it in other animals too: Carcinisation is the process of nature trying to evolve a crab. All sorts of animals that we humans call “crabs” have very little relationship to each other, despite looking similar to us. Often there’s just a limited range of solutions to problems that natural selection can arrive at, so different organisms converge on similar appearances, without having a relationship to each other.

Viruses are forced to look similar to each other

“But what does all of this have to do with viruses?” You may wonder. Well, if you understand the principle I outlined here, then you understand why biologists are not immediately alarmed when they encounter similarities between two viruses. They understand that different viruses all have to work within similar constraints, they’re all dealing with certain biological limitations.

The human genetic code is capable of producing 22 different amino acids. Imagine we’re looking at a chain of amino acids (called a peptide) of six amino acids. Theoretically you would be looking at 22^6 = 113.379.904 different possible combinations. What would be the odds that we encounter a combination seen in one virus in another virus? Well, at first hand, that would now seem like a very strange coincidence of course.

But if you think more carefully about it, you’ll start to understand why it’s not so strange. Sure, there are a hundred million different theoretically possible combinations, but certain combinations of amino acids will just not be structurally stable. You can see this in human genetic disorders: Sometimes just one single change of an amino acid because of a single mutation in a gene, where one nucleotide was replaced by another nucleotide, can be enough to render an entire protein utterly useless.

Beyond the constraints of structural stability, viruses have to deal with other constraints: The human immune system evolved to attack biological material that looks different from human biological material and shows up in places where the body doesn’t want to tolerate alien biological material. Your body tolerates a wide variety of bacteria within your intestinal tract, that help you digest your food. In your blood on the other hand? Your blood is supposed to be sterile, free from any bacteria.

For viruses to escape detection by our immune system, they have to evolve to produce proteins that look similar to our own proteins. This is why it is so strange, when we find that SARS-COV-2 resembles both the proteins of humans and mice. Viruses don’t just have to resemble our proteins to fool your white blood cells: They also need to fool the cells that they infect into going along with producing their proteins, without alerting your immune system that something is wrong.

This is important to understand: It means that viruses are limited in the combinations of amino acids that they are going to be using. They need to use combinations that are structurally stable and from within that range of structurally stable amino acids, they have to focus on combinations that look similar to those seen in proteins produced by the human body. If they don’t do this, it’s easy for them to be recognized.

Another strategy that viruses will use in certain proteins, is to develop sites that allow sugar molecules to attach. When you have sugar molecules attached at the right spot of a protein, it’s not possible for human antibodies to bind to those sites. To enable sugar molecules to attach to a protein, you need specific combinations of amino acids.

One example of such a process is called N-linked glycosylation. To enable the attachment of a sugar molecule, a virus will have a combination of: N-X-S/T. N here is the amino acid Asparagine, X can be any amino acid except proline and S/T is Serine or Threonine. In other words, you can see that the need to protect themselves from the immune system with sugar molecules, helps force viruses to use similar combinations of amino acids to each other.

We can understand that viruses will preferentially have such spots on specific locations: Places where antibodies are eager to attach and (importantly!) disrupt the function of the virus by attaching. An antibody that attached to the protein a virus uses to enter a cell, at the location where the protein touches the receptor of the cell, will be more likely to interfere with the virus, than an antibody that just attached to a random part of the membrane that covers the virus.

There are inevitably many other biological limitations that viruses have to work with, but that is outside the scope of this article.

Similarities in short sequences are not surprising

This is the picture you may have seen. Here we see three spots where SARS-COV-2’s spike protein has some extra amino acids. You can look them up in BLAST, a tool used to screen sequences of all sorts of organisms, and then you’ll find that these sequences can also be found in HIV. What does that mean?

Well, not much, if anything. Ask yourself this question: What sort of virus do you think we continually sequence? If you have one of the hundreds of different viruses known to mankind that cause a mild cold, you won’t get the virus sequenced. On the other hand, HIV is a potentially lethal virus that has no real cure and rapidly develops resistance against the various treatments we have available for it.

In other words, the database that BLAST looks at, will have a lot of HIV genomes in it, but not a lot of metapneumovirus A2 sequences in it, because metapneumovirus A2 is only known for causing mild colds in children. And so anything you look at will be compared to a lot of different kinds of HIV genomes that were uploaded, but not to the various other viruses known to man.

The other thing to remember, is that HIV is known for being an extremely rapidly mutating virus. The reason we can’t really cure HIV, is because it constantly throws new variants at us. The database that we look at (BLAST) thus has an enormous variation of HIV sequences. What’s important to note about these three supposed “HIV inserts”, is that they’re not found in all HIV sequences. Rather, they’re just seen in a small minority of HIV sequences.

For example, take a look at TNGTKR, the six amino acid peptide from SARS-COV-2 that is supposed to be the first HIV insert. When you throw it into BLAST, you get this:


You get a couple of 100% matches, but as you scroll down, you start seeing 83% matches and in fact, the whole page has more 83% matches than 100% matches. It’s not conserved among HIV variants, in fact, it’s found in a small minority of HIV genomes uploaded to BLAST.

But now let’s take a look at the supposed inserts at the level of the amino acids:

Whenever SARS-COV-2 has a spot where it has some extra amino acids, it’s treated as an “insert”. Except at 250, before “insert 3”. “Insert 3” is a spot of three extra amino acids, but before insert 3 there’s also a spot of three extra amino acids, that they didn’t bother to look at. Why would that be?

But also take a good look at those “inserts” themselves. They don’t just take the gap, they add a few letters before and afterwards. That’s as arbitrary as the similar spot before Insert 3 that goes unmentioned. In the original paper, they speak of four supposed inserts, three from GP120 and the fourth from an entirely different HIV protein, but in most modern variants of the theory circulating, they stop bothering to mention the fourth one and focus on the first three.

But here’s the important thing: If you think there’s some unusual similarity between HIV and SARS-COV-2 suggestive of genetic inserts, then you need to try to falsify your theory. One way to do that would be to look at other regions of the SARS-COV-2 genome, or the genome of other corona viruses and to throw those in BLAST. If you again see HIV showing up, you could imagine that all the corona viruses in circulation have had HIV segments added into them, or you could arrive at the correct conclusion, which is that you’re staring at random noise and starting to see patterns, the virological equivalent of seeing faces in the clouds.

So here’s an example of my point. For the SARS-COV-2 spike protein, they’re finding similarities to HIV’s GP120 protein, which forms part of HIV’s viral membrane spike that allows it to bind to the receptors of cells. But this is not shocking, if you remember that:

  1. These sequences are not conserved in HIV, they’re just found in a minority of HIV sequences.
  2. There’s a lot of HIV material to compare to, not a lot of material from other viruses.
  3. Viral proteins with similar functions from radically different viruses can still be expected to have certain similarities due to convergent evolution.

So let’s try to falsify our theory. We’re going to look at the SARS-COV-2 membrane protein, we take a peptide chain of similar length to that of these “inserts” and see if we also encounter it in HIV.

Here we have the SARS-COV-2 membrane protein:

        10         20         30         40         50
MADSNGTITV EELKKLLEQW NLVIGFLFLT WICLLQFAYA NRNRFLYIIK 
        60         70         80         90        100
LIFLWLLWPV TLACFVLAAV YRINWITGGI AIAMACLVGL MWLSYFIASF 
       110        120        130        140        150
RLFARTRSMW SFNPETNILL NVPLHGTILT RPLLESELVI GAVILRGHLR 
       160        170        180        190        200
IAGHHLGRCD IKDLPKEITV ATSRTLSYYK LGASQRVAGD SGFAAYSRYR 
       210        220 
IGNYKLNTDH SSSSDNIALL VQ       

We take the following peptide from this:

HHLGR

We look it up in BLAST. What do we find?

This membrane sequence is found in the HIV envelope! Why would that be? Is it because the membrane was edited with HIV sequences too, or is it because these are two proteins that have similar functions for these viruses?

Now let’s do the Spike protein itself. We can find the whole thing here.

We take this sequence, of six amino acids:

ISQIQQ

We throw it into BLAST. What do we find?
ANOTHER 100% MATCH TO AN HIV envelope SEQUENCE! OMFG!

If it wasn’t obvious yet, this is not because some scientist cut HIV into bits and put those bits into a coronavirus to create SARS-COV-2. Rather, it’s because different viruses are forced to work within similar natural constraints to replicate themselves.

And to illustrate that, we’re now going to look at another human coronavirus and see if we can also find scary sequences that are found in HIV.

You can find the amino acid sequence of the Spike protein of Human coronavirus NL63 (HCoV-NL63) here.

We’re going to grab a sequence of five amino acids and see if we can also find it in HIV. You can’t find every single random chain of five or six amino acids in HIV, it generally requires me two or three tries to find a match. Note again how the authors of the now infamous paper seem to have had the same problem, which is why one of these spots where SARS-COV-2 has an insertion of a few amino acids went entirely unmentioned by them.

I’m taking this peptide from halfway through NL63’s Spike protein:

>LGTVD  

I throw it into BLAST. What do we get?

Note that for competent virologists, what I’m doing here would be considered excessive, perhaps even pointless. If someone would take a peptide of five or six amino acids from any virus, throw it into BLAST, see that it’s also found in some HIV sequences and say: “THIS VIRUS HAD HIV SEQUENCES INSERTED INTO IT!” They would be laughed out of the room, because similarities between viruses of peptides of that length just don’t really mean anything, beyond the fact that viruses are forced to operate within similar biological constraints.

The Summary

To understand why this myth of SARS-COV-2 having HIV sequences inserted into its genome is false, you need to remember the following points:

  1. Not all viruses are constantly being sequenced. HIV and SARS-COV-2 are two exceptions, most viruses known to man are very rarely if ever sequenced.
  2. HIV is unique among viruses that infect us, when it comes to its extremely high mutation rate. Because of that, it has a lot more variation against which you can find matches. This means that if you find a match with a minority of uploaded HIV sequences, it’s just not going to be very meaningful.
  3. Matches of peptides 5 or 6 amino acids in length, as the authors of this study made, are just not meaningful. You’re inevitably going to find some matches at that level, because viruses inevitably use similar building blocks, especially when they infect the same host species.
  4. The authors of the study are pretty selective in which peptides they bother comparing to HIV. Another sequence shows up in the genome that would also count as an “insertion” in accordance to their idea, but they don’t bother comparing it to HIV, because obviously they didn’t find a creepy HIV match.
  5. The reason this stuff only shows up in obscure substacks and is not a topic of debate among serious virologists and molecular biologists, is because it’s easy for them to see that this is ridiculous and the original paper is an embarrassment for the authors who put their names on it. They should have immediately understood why this doesn’t work, but they could have done some pretty basic tests to try to determine if their findings have any real significance or not.

This paper should have never been published, because the consequence is that two years later, average people who spend too much time reading about SARS-COV-2 on the Internet are still convinced that they’re going to be infected with some sort of HIV-corona hybrid that will decimate their immune system.

Similarly, for every Substack that gets a thousand hits when it proclaims that SARS-COV-2 has HIV fragments inserted, articles like this where people take a critical look at these claims will get perhaps one. If you want to be scared, there’s nothing me or anyone else can say that will prevent you from being scared:

5 Comments

  1. I can barely understand the science here but I’ll take your word for it as I’ve had COVID and don’t fancy developing stage 3 AIDS

  2. Let me summarise, and please tell me where I’m mistaken:
    -Covid genome is 32KB long
    -at 4 points in that genome, there are short snippets of code matching snippets from 4 separate HIV strains
    -The snippets in question are not found in any other coronavirii
    -The snippets in question code for changes to the tips of the spike protein, ie, the most biologically active points of the covid spike protein, a one in 32000 chance, or near enough, for each, lets make it 1 in 1000 to say there are more bioactive places that would also classify, leaving us with with the total of a 1 in a trillion chance of the 4 edits ending up there, given the 1 in a much bigger number chance of suitable snippets being in the situation to cross genetic transfer in the first place..
    – Covid/covid spike has Tcell damaging ability, similar to HIV (but not able to reproduce in Tcells, only damage), possibly gained due to said changes
    – No other HIV matching snippets were found in the covid genome, or other coronavirii (I think?)

    What are the odds of 4 such snippets from 4 separate strains of HIV being found at what seem to be effectively the 4 most biologically active points in the spike/genome, and only at those points? via cross species genetic transfer, basically nill, but you are arguing they just evolved there at random due to similar selection pressure on covid to HIV, and it didn’t seem very clear to me that you tried to quantify that, are you saying that if you pick another pre covid coronavirus (purportedly) newly jumped to humans, preferably not SARS or MERS since they are also candidates for lab editing escapees, that you would find similar length HIV matching snippets at biologically active points, and, similarly, only at bioactive points? obviously selection pressure for convergent evolution will apply most strongly at bioactive points, yet my understanding was no other coronavirii had similar HIV snippets?

    I’d appreciate a bit more depth on this than what seemed (possibly because I’m not a genetic engineer and missed the subtlety) like handwaving dismissal, if you don’t mind, Especially given that some of the work in those wuhan BSL4 labs down the street from the release location was quite literally modifying the spikes of bat sars virii, related to covid, to infect human ACE2 receptors, using human mice models, and incorporating HIV in the process somehow (can’t remember the details of that bit), ie, linking every bit of this in one paper…

    • >What are the odds of 4 such snippets from 4 separate strains of HIV being found at what seem to be effectively the 4 most biologically active points in the spike/genome, and only at those points?

      Should I really even bother to respond if you haven’t read what I wrote?

      If you randomly select other sequences of SARS-COV-2 of similar length and throw them into BLAST you also get “HIV sequences”.

      In other words, it’s not “only at those points”. Rather, the authors of the original paper only looked at those points.

  3. Further to the comments from b above, we also have 2006 publications celebrating creating a chimeric SARs spike having components of HIV, HCV and other nasties. Why would we disregard those publications? Several independent experts across the world have attested to the HIV inserts. If we have the Wuhan/EcoHealth types celebrating HIV-SARS chimeras and lo and behold we now detect inserts of HIV in the current spikes (completely unlike any previous Coronaviruses), it seems odd that we would claim it is just chance. That’s like pleading innocent while holding the smoking gun and standing over the dead body.

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