UPDATE: Critique of EM Paper by Andrew Maniotis: OMSJ Deserves a Refund

UPDATE: It looks like the paper has been taken down from the site I had linked to in this post! I am trying to figure out how to post the paper as a pdf file here. If I cannot, I will at least post the text without the pictures. This is proof that this site has them running scared.

I have found the EM paper by Dr. Andrew Maniotis that I mentioned in my previous post.  At first I was excited to read the paper. I know some people will not believe me when I say I was keeping an open mind, but I was. Unfortunately the excitement and open mind quickly changed to frustration simply because the paper is so poorly written. That is NOT intended to be a jab. It is the truth. Before you continue reading this post, do me a favor and read the paper:


(NOTE: The beginning of my critique will be to highlight some of the obvious deficiencies. The second part provides a response by an actual expert as to why EM is not proper and sufficient for diagnostic purposes.)

Other than just professional curiosity, I was also excited by the title of the paper. The “Review of the Literature” especially intrigued me. The first thing I did was look at the footnoted references. There are 122 references and just glancing through them, it seemed they were from actual peer reviewed publications! That got me really excited until I read the end of the introduction. Out of the 122 references, 120 of them were simply citations about the “more than 100 other known reasons to register positive on either nucleic acid or protein-based “HIV” tests [1-11, 13-59, 61-120].” That does not leave much literature to “review” in the other 20 pages of the body.  (I won’t mention how the dissidents love to trot out that tired old trope about cross reactivity and exaggerate it…because Maniotis did it for me in this very paper)

Maniotis supplied us a great example of how the dissidents exaggerate the fact that some antibody tests cross react:

In 2004, the Red Cross reported in The New England Journal of Medicine that even after repeated testing using different test kits, low-risk populations, such as blood donors (or military recruits) will typically yield 12 (PCR-positive) or 2 (ELISA positive) out of 37,000,000 samples, leaving potentially 10 out of 12 false positives, depending on which test kit you believe accurately detects “HIV’s” molecular signatures [101].

So, out of 37 Million tests, 12 were false positives! Actually, two of the 12 were later confirmed to have been true positives. So 10 false positives out of 37 Million does not seem like a big deal to me. But I’m not really sure what percentage that is. As Shirley Q. Liquor says: “I ain’t too good at math: I ain’t my glasses on.”

A bigger source of concern highlighting the deficiencies of this paper is the many places that demand a reference.  I know the Abstract of a paper does not necessarily contain references, but the very first sentence was a huge red flag. However, this sentence was also the first sentence of the Introduction, just slightly re-written. A reference was definitely required:

Abstract: “Viral load tests have been under increasing suspicion of detecting false-positive signals.”

Introduction:  “In only the past several years, “HIV/AIDS” diagnoses have encountered a series of increasing challenges regarding the specificity of any of the protein or nucleic acid tests.”

Here are a few more examples of statements that required referencing:

  • Alternatively, we considered that “HIV” PCR and protein readings for years have likely represented extreme oxidation states in ill persons.
  • To date, “viral-like particles” only  have been documented by AIDS researchers to occur in Petri  dishes or in test tubes after certain oxidizing chemicals are added such as PHA, IL2, interferon antibodies, and the like. 
  • And these in vitro studies demonstrate,  rather than infectious or pathogenic  “HIV” harboring surface projections or any other pathogenic viral parts, that most,  if not all of these viral load readings are spurious chemical reactions that probably represent endogenous “junk” nucleic acid sequences or HERVs that are synthesized by oxidized cells or caused by various local or systemic pathologies.
  • Roche’s viral load tests typically test 3-10 times higher than LabCorp’s tests or others.
  • It is known that the  freezing of biological material can create ice-crystals that could in principle disrupt “HIV” structural and infectious integrity, as the CDC, blood banks, Factor XIII and IX preparative industries first discovered in their quest to to protect the blood supply, and to establish the pathogenic requirements and/or disruptive conditions that would destroy the virulence of various blood borne pathogens including “HIV.”

That is just a small sampling of statements that require referencing. It also demonstrates extreme bias on the part of the researcher as it is obvious that much of this is speculation and opinion.  However, the last example (above) leads me to my next problem with the paper:


Immediately following the above quoted sentence comes this:

Therefore, ten blood samples processed for EM in this study were not dry-ice frozen and thawed, in order to avoid disruption of “HIV,” avoiding this potential pitfall regarding how these physical changes were thought to destroy structure and pathogenicity of “HIV” early in the AIDS era. The samples were fixed in gluteraldehye shortly after the blood draw, and thus were shipped to diagnostic EM labs in a protein cross-linked state, that is impervious to degradation.

OK, now we are getting to the actual specimens and getting away from the jumble of confusing info about the “dominant case history featured here”: This mysterious “professional boxer who battled ‘HIV’ diagnoses that ruined his professional boxing career for 23 years…” ALL of that information can be disregarded for several reasons most notably are that many of the specimens are as old as two years. There is no discussion as to how those specimens were stored for that period of time. As I point out above, Maniotis admits that old, frozen specimens could “disrupt ‘HIV’ structural and infectious integrity” and that is the reason he used 10 fresh specimens that were never frozen.

But wait, Maniotis only pretends to discuss the 10 specimens. He goes back to the “professional boxer” and rehashes the different VL readings: None of which he provides documentation for. Also, Maniotis claims that all of these VL readings were “in the absence of ARVs” but conveniently provides no proof for this. Actually, if you were to put these results into a table, (as I have done below) it is quite easy to see how they could very well be the result of said boxer going on and off ARVs:


Date Viral Load
June, 2010 252,000
December, 2011 4,100,906
June, 2012 204,000
August 8, 2012 1,930,000
Augusts 28, 2012 9,090,000
December, 2012 14,000

Quite frankly, including the entire saga of “the boxer” case only serves to highlight the conspiracy theory perpetuated by dissidents that HIV tests are worthless. It also detracts from the credibility that no ARVs were consumed when one reads the many contradicting news articles about “the boxer”. Furthermore, why would you want to call into question the very methodology (PCR) that you have used to “calibrate” your comparison theory?

“Here we present a case in which we calibrated an “HIV-1” viral load measurement of 204,000 / mL as determined by PCR tests…”

Oy ve, this paper is more like a study in contradictions than one of EM! But I digress…

Instead of actually discussing the 10 fresh, never frozen samples, Maniotis begins to SPECULATE and make ASSUMPTIONS for many long, poorly constructed paragraphs as to what, other than HIV, was actually being detected by PCR in the blood from “the boxer”. I cannot decide if I am upset, disappointed or just saddened by the quality of this paper. The dissidents have waited all these years to finally do some actual laboratory research to confirm their hypothesis, and this monstrous mess is what they get.  I cannot continue with this critique.  I will leave the last part for an actual expert in the field.

Analysis by an ACTUAL EXPERT

Here is the succinct question posed to a PhD Scholar with the California Institute of Technology, Division of Biology:

Q: I am just curious if you have a short answer for why HIV is typically not seen in a EM from patient plasma?

A: Historically, electron microscopy has served as an effective method to identify viral agents of infection.  However, the use of electron microscopy as a diagnostic tool is limited by its requirement for a high concentration of particles in the clinical sample.  The limit of detection for diagnosis of a virus by electron microscopy is widely accepted as 10^6 -10^8 particles/ml.1  For HIV-1 patients, a “high” viral load may range from 10^4 – 10^6 HIV RNA copies/ml. Because each HIV particle carries 2 copies of the viral genome, 1×10^6 copies/ml would translate to 5×10^5 particles/ml, placing, in many instances, the positive detection of virus outside of the detection limit of electron microscopy.  Another consideration is that although HIV can be transmitted through blood and blood products, the viral burden in an infected individual is found primarily in the lymphatic tissue, not in the blood (HIV in the blood may represent just 2% of the total viral burden).  Finally, the detection of HIV in blood by electron microscopy may be further complicated by the structural pleomorphism the virus displays. 

  1. Hazelton and Gelderblom Emerg Infect Dis. Mar 2003; 9(3): 294–303
  2. Courtney V. Fletcher, Kathryn Staskus, etal January 27, 2014, doi: 10.1073/pnas.1318249111


If we can believe this actual expert who has had real life in-lab HIV research experience (and we can) then we see what Maniotis is trying to do cannot work. There are simply not enough virions in the peripheral blood.  Again, let’s look at an example taken directly from the Abstract:

Here we present a case in which we calibrated an “HIV-1” viral load measurement of 204, 000 / mL as determined by PCR tests, against the actual number of “HIV-1” viral-like particles in the peripheral blood of the same patient.

204,000/mL is much too low for detection by EM. If this is what they used as a calibrator, then the entire experiment is set for failure from the very beginning.  What is even more questionable is the fact that Maniotis used the specimen with the 204,000 VL. Why not use the specimen from the same patient with the VL of over 9 million?

It gets even worse. This is from the portion describing Gluteraldehyde Fixation:

Twenty-two mL of peripheral blood is drawn from an arm vein. 2 mL of thiws plasma.Two mLs of plasma is then sent to Roche.  Roche’s viral load tests typically test 3-10 times higher than LabCorp’s tests or others. We tried to obtain the highest viral loads available from people naive of ARV’s to increase the probablitity of finding one virion in 10 people’s plasma samples.

Spelling issues, punctuation and sentence structure aside, this is a great example of how bad this paper is. Maniotis either needs to provide a peer reviewed reference for his ridiculous statement that “Roche’s viral load tests typically test 3-10 times higher than LabCorp’s tests or others” or he should have sent duplicate samples of each specimen for PCR VL testing: One to Roche and one to LabCorp and provide the results in this paper. However, that may have put a huge damper in Maniotis’ unfounded, non-referenced opinion.

The rest of the method describing Gluteraldehyde Fixation is terrible because it does not so much describe the method that was actually done, but speculates and makes assumptions about the method. Maniotis makes it very clear that the method was not completely performed by him or his associates. He makes it equally clear that portions of the method in his control were not necessarily standard procedure:

This speed and time is warranted because when they do (emphasis mine) genotyping of “HIV” of a sample that contains less than 1000 VL, in order to “boost” the “virion particles” in that sample of peripheral blood to amplify it to more than 1000 VL/mL, which is the limit needed for genotyping.


Most diagnostic EM labs will comply with this approach, (emphasis mine) because they only take glut-fixed blood samples from patients.

This is all I can stand for now. I have sent a request for other experts to weigh in, but it seems that once they read the paper they just do not see the point in wasting their time. One thing is for sure, I finally feel sorry for OMSJ. NOT!



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