New retrovirus: HIAP-II

My blood has been to CDC-Atlanta twice now. Facilitated by the United Nations, I have been out of the USA twice now to meet with Nobel-awarded scientist(s). My blood has been to Path labs in Washington, DC and a 100 other scientific places. In a conversation I had, with the Head of CDC's Retroviral Division, he mentioned Tulane's work to me. I do not have any retroviral activity in my body, so I know that this does not pertain tome. But, perhaps it might explain other CFS cases. Be well.

New retrovirus, HIAP-II (Source:

Idiopathic CD4+ T-lymphocytopenia, or Non-HIV AIDS, is associated with a patented retroviral particle called Human Intracisternal A-Type Particle-Type II, or HIAP-II.

Autoimmune Technologies is developing viral protein antibody tests based on HIAP-II that the Company believes will be useful in diagnosing Non-HIV AIDS. These tests may have other important uses as well, including use in the screening of blood products.

These tests are still in the laboratory stage and are not yet generally available for investigational, clinical, or other use.
Non-HIV AIDS patients may comprise perhaps one percent of all AIDS patients. While the majority of Non-HIV AIDS patients do not belong to any of the risk groups such as blood transfusion recipients, male homosexuals, and intravenous drug abusers in which AIDS was first identified, some Non-HIV AIDS patients do belong to these groups. This suggests that Non-HIV AIDS may also be transmissible.

Research conducted at Tulane University Medical Center suggests that Non-HIV AIDS is associated with a retroviral particle called Human Intracisternal A-Type Particle-Type II, or HIAP-II. Antibodies to this particle have been found in a high percentage of patients with Non-HIV AIDS. Tulane has patented HIAP-II, and Autoimmune Technologies is licensing HIAP-II technology in order to develop screening and diagnostic tests and therapies for Non-HIV AIDS and to study the possibility of generating vaccines against Non-HIV AIDS, autoimmune disease, and AIDS.
Likes: Misfit Toy


I forgot to mention that... I've always understood that retroviruses are not cytotoxic; they do not kill cells. I don't see how any retrovirus (like xmrv) can be the cause of any Immune Deficiency Syndrome (like CFIDS).

HIV (another retrovirus) causing AIDS is unproven theory.

Actually being that I am a HIV-Negative AIDS patient, my case shatters HIV-->AIDS theory...and is the reason why so many scientists want my blood. I have been blogging about it for years. This is the first letter I ever wrote (to about 5,000 people that year) about the subject:

This is a good award-winning documentary on the HIV/AIDS story being rewritten. 2.5 minute trailer: I got a copy at my public library. If your library doesn't have it, you can just ask the circulation desk to obtain a copy for their circulation collection.
The term I think you are after is cytolytic. Many viruses use cytolysis to release their virions, killing the infected cell. This would defeat the purpose of inserting viral genes. Retroviruses may not contain genes that deliberately kill cells, but this doesn't stop them from triggering apoptosis, cell suicide. This process could even be a last-ditch defense against retroviruses and cancers.

Intracisternal A-type particles are well known in species with retroviral infections. These particles are not fully functional viruses. They get their name because they fail to carry out some stages of their life cycle and accumulate inside cells without even reaching the cell membrane. The DNA sequences which produce these non-functional particles may become retrotransposons, inserting themselves multiple times in chromosomes. Murine IAP sequences are all over the mouse genome in about 2,000 copies per cell. This is used as a test for contamination by mouse cells. I urge caution about this interpretation because human IAP sequences have been observed in people with known retroviral infections. The distinction comes from the number of copies. Should a very similar virus infect humans, as is possible in vitro, the resulting IAP sequences would be very similar to mouse IAP sequences.

The important point here is that the presence of the particles strongly suggests an active retroviral infection somewhere. It may be in some tissue reservoir not sampled. It may have been present in the recent past. If you find HIAPs you should be looking carefully for a corresponding active retrovirus.

Non-HIV AIDS is not new. There was even a chapter on it in the first edition of "Osler's Web" in 1996. My argument has always been that there is more than one cause. This would shatter the implication AIDS => HIV, without addressing the implication HIV => AIDS, a subtle logical distinction.
With a typical latency from infection to onset of symptoms of immune deficiency of something like 5 years it seems obvious there must be considerably more to the story than the life cycle of a single virus. This does not let the virus off the hook for causing the ultimate train wreck. My knowledge of the effect of contaminated blood on hemophiliacs who had no other risk factor prejudices me in the direction of believing the virus alone can start the process. I knew one hemophiliac fairly well.

Looking over the literature for a variety of long-term diseases with varying rates of progress convinces me there are pathological processes which have a great deal of similarity to retroviral infections without meeting the criteria set up by virologists to make study easier. Those criteria are likely to fail in human hosts where unusually long latency is necessary to pass the virus to another generation.

Just as an example, I'll mention the known human ERV Fc1. This has complete open reading frames for every gene except one, which has a misplaced stop codon and a frameshift event between it and complete functioning. Inserting a complete viral genome via an exogenous virion would be required for standard criteria of infection. However, the insertion of one mRNA sequence for the defective gene would be enough to "resurrect" the virus. In fact that is not the minimal change possible. A stop codon is only 3 base pairs long; a frameshift can be caused by an RNA fragment that is not a multiple of 3 base pairs long. It is entirely possible for an RNA fragment as small as those called micro RNA to cause such a change.

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