Virus turned against itself – HIV/AIDS research uses Tat

Associate Professor David Harrich

Associate Professor David Harrich, who works in the QIMR’s Molecular Virology Laboratory on HIV. PIC: Liam Kidston. (c) The Courier-Mail

Associate Professor David Harrich has been researching HIV for thirty years, since starting as a research assistant at the University of California, Los Angeles (UCLA) in the early 1980s when the first cases of HIV/AIDS emerged.

“I’ve come close to giving up in the past. But today I’m so encouraged. I feel very fortunate because not a lot of scientists are able to stay in the same game long enough to see these sorts of developments. It involves perseverance, dedication and, of course, sustained research funding.

After years of research, he has had a breakthrough. Associate Professor Harrich has determined how to modify a protein in HIV,  so that it instead provides strong, lasting protection from infection.

“This is like fighting fire with fire,” Associate Professor Harrich said.

“If this research continues down its strong path, and bear in mind there are a many hurdles to clear, we’re looking at a cure for AIDS.”

Associate Professor Harrich runs the only research laboratory and containment facilities in Queensland working with the HIV virus, QIMR’s Molecular Virology Laboratory at the Queensland Institute of Medical Research in Brisbane.

He invented the Nullbasic protein by mutating an existing HIV protein. Nullbasic has shown remarkable abilities to stop the virus replicating in a lab environment. Animal trials are due to start this year.

“I have never seen anything like it. The modified protein works every time,” Assoc Prof Harrich said.

“You would still be infected with HIV, it’s not a cure for the virus. But the virus would stay latent, it wouldn’t wake up, so it wouldn’t develop into AIDS. With a treatment like this, you would maintain a healthy immune system.”

The successful development of this type of one-off treatment would also have economic implications. HIV patients currently take a regime of drugs for the rest of their lives, which can be a significant financial burden.

This research is published in the current issue of Human Gene Therapy and can be found online at http://www.ncbi.nlm.nih.gov/pubmed/23298160


5 comments on “Virus turned against itself – HIV/AIDS research uses Tat

  1. Dear Professor Harris, I would like to address an issue with the findings, which may have your interest. It is great that you have managed to modify a protein to counter the HIV replication, thus also protecting the immune system etc. However, virus are living beings/active crystalline substances (at least HIV as a microscopic Retro Virus is characterized like that) and anything you modify which makes your strand of the virus less replicative, will hamper its own survival among other viruses of its same kind. Thus, you may be in the same scenario as the many treatments against malaria out there – ie. DDT – where resistance develops pretty fast.

    Thus, I am of the professional opinion, that in order for your strand to have success, you must apply something to the strand which makes it replicate well – in that chaotic way it does it (multiple viral strands in a cacophony being assembled more or less by random) – and then have that part of it, which attacks the white blood cells modified, such that the your modified HIV virus (HIVm) has a better survival than the original one (HIVo), and such that HIVm has less probability of replicating with the strands of the HIVo, for instance due to modification of proteins, modification of the reverse transcriptase for the HIVm strands.

    Now, the HIVo replicates via triggers which makes the mother cell ‘explode’, thus the process could be assumed working better if the HIVm works WITH the mother cell, rather than against it.

    You would need, that your new HIVm strand actually replicates better, while it does not fight the human body’s immune system.

    Thus, to have real success, you would need to create your HIVm strand such that this protein modification in all creates a better survival for the HIVm than for the HIVo, thus, by injecting (once!) the HIVm, the HIVm would take over, due to its statistical better survival.

    The world of genetic treatment is full of real good research, real good lab results, but exposed to the usual gravity test, they fail as the litmus test is, whether or not the genetic treatment itself has better survival than the existing genes.

    Thus, one of the serious attempts for genetic treatment are those treatments meant to enter, then do their job, then self-destruct. However, as for instance the HIVo hides inside of cells, in that they have replicated themselves into the genome of the host cell, it is not possible to “cure” the host (the human being), as there will always be something “left over” in that human being.

    The trick is therefore, to ensure that what ever your HIVm strand will be doing, it will always take over the HIVo’s position due to better survival in the human body…

    What is your take on this?
    Warmly David Svarrer, Nairobi, Kenya
    +254 734 936 145 – david.t.svarrer@gmail.com

    Computer Software specialist and HIV / hepatitis / influenza researcher since 1984.

    In short, I am researching creation of softwares which runs like retrovirus’es, but in controlled forms, thus, utilizing the phenomenal survival of the retroviral principle in software for so called agent technology. I expect to have a system out working with that principle some time in 2016-2018… I have worked with this (thereby naturally also with certain Hepatitis viruses and the Influenza’s), as a way to improve software security in general, and to create ways for software to work, which works in new ways.

    Your work is very inspiring, by the way…

    • Dear David,

      Thank you for your compliment.

      The technique that you are describing is different to what this research is doing. The Nullbasic protein is inserted into the immune cells rather than altering HIV itself.

      For more information, you can read the full article here:

      Or view an interview with David Harrich here:

      He talks about the technique used at 1:59.

      Kind regards,

      Sarah-Jane Matthews
      QIMR Science Communication (Online)

  2. Thanks a lot for your comments, Sarah-Jane, I think that I’ll invite one of my good friends and also a researcher nature, Mr. Saidimu Apale, Twitter @saidimu , he might have interest in this, too… I’ll sign up for postings on this thread here – it could grow hot. Very interesting thing about the therapy being inserted into the immune cells. I’ll read your link above with pleasure…

  3. Now, Dr. Harrich, it was a mind boggling article to read, I have read most of the 42 pages preliminary report from you and must admit it is mind boggling. However, now what is your take on the dynamic immune response? What are the possibilities of creating a dynamic response from the modified Nullbasic, such that this attenuating gene you have created becomes active given presence of HIV-1? The next question which I think is very important to address, and which I did not see being addressed very strongly in your report was the mutating capabilities of HIV, which – just like in Hepatitis and Influenza viruses – poses the maybe most significant threat to a passively “injected” genetic cure in the CD4+. We all know that in the assembly hall, the many bits and pieces of HIV-virus are assembled more or less helter-skelter – more or less like if you took the maybe 16 parts of a childrens puzzle and put them together with glue, rather than finding the markers on each piece and matching them perfectly. That in itself is part of the hectic mutation taking place by both Influenza, Hepatitis and HIV. It means that the signature towards the human body host changes radically from time to time, thus – in Influenza and HIV – a vaccine cannot be prepared properly due to that next time the same Influenza or HIV “passes by” the immune system, it is recognized as something the body has never seen before, thus, the protein defence and other immuno-reactions restart from scratch, finding out how to attack the “New” intruder. This is therefore part of the HIV’s survival mechanism. Thus, what are your thoughts in regards to a relatively passive gene, spliced into the CD4+ cell, and then the very hectic mutation process of the HIV virus, which – even if attenuated strongly as you put it – over time will provide a strong survivor over a passive barrier? I mean: It is likely that a HIV-strand by sheer coincidence, in the chaos in the assembly hall, will produce a strand of HIV which will not be inhibited by the Nullbasic genetic modification?? As you know it, the existing anti viral therapy is partially successful solely due to that the patient is not allowed to stop the treatment even for a day, or some hours, due to the (big) risk of mutated HIV taking over the control due to having developed immunity against the current, relatively passive, therapy. I hope my question makes sense to you. I have worked – naturally not as intensively as you have – in the field of retroviruses – since 1984 – due to the enormous impact on computer viruses and on the so called agent technology. Now, after Sarah-Jane Matthews answer, I think it may be prudent to mention that agent technology resembles what you could describe as “friendly virus”, in that we build friendly hosts which provides friendly handles for the visiting agents (intruding viruses), but maintaining the viral environment otherwise the way it is.
    Warm regards
    David Svarrer

  4. Now, what happened to the about 130 HIV like virus like structures in the humane genome, which entered throughout our evolution? Apparently, the current world epidemic of AIDS is not a new phenomenon.. Thus – what incapsulated the former HIV-strands and made these passive in the human genome? This is particularly of interest, due to that the HIV in its current form, stores itself in the CD4+ cells’s DNA, thus could at a first glance appear as “irremovable”, while studying the more than 130 existing HIV-similar structures in our human genome and studying how come the ribosomes don’t produce outcome, would maybe give an answer as to how we shall block the HIV already “ingested” by the CD4+ cells.. Synthesis on the DNA of proteins, enzymes etc. – and naturally herewith, also synthesis of HIV from HIV-implants in the human CD4+ cell’s DNA – is normally highly based on presence of the necessary building blocks for the protein in the cytoplasma. Thus, what could be a starvation process for the HIV-virus? I mean – just as well as you can see a human, having what appears as diabetes – suddenly appear “cured” when given simple vitamins, thus indicating that maybe the insulin-synthesis was missing due to lack of the necessary building blocks in the Langerhall cells in the Pancreas, thus it should be possible to apply various starvation / gene blocking therapies which would identify the HIV in the CD4+ cells, and then apply appropriate attenuation or elimination? Would it for instance be far fetched to use some of the research done within analgesics, where certain sugar-like OH-groups has been introduced linked to the medication thus making it possible to target the ingestion groups on the various cells in the human body pretty accurately. For instance it may be known to you, that the difference between Clavulin and Augmentin (two Amoxicillin + Clavulinic Acid formulations from same vendor) are only different in that the Augmentin has certain sugar-like formations on the medication, thus targeting the destination bacterias much more efficiently. As an example, the current diabetes treatment research also is focused on transporters, such that it hopefully one day becomes possible either to synthesize the insulin AFTER the stomach (acid) has been passed, or possible to encapsulate the insulin into various transporters which will release the insulin after the stomach. I hope you can use my contributions positively in this research.
    Warm regards
    Digital Age Institute Ltd.
    David Svarrer

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