Discussion in 'Immunological' started by undiagnosed, Mar 20, 2016.
Ya, I agree. I am not treating or monitoring any HHVs, just testing for exposure at the moment.
Unfortunable the data and studies that can prove that have been discredit or retracted, most of them always under mysterious circunstances, always leaving behing a conspirancy theorie and many unanswere questions.
I have perosonally talk to this researchers several means more than 4 of them, people with an incredible background in virology, retrovirology, infectious disease cancer etc, world class, people
That were playing with viruses and retroviruses in labs when lipkin was playing with toys in house, all this authorities in virology and Retrovirology strongly believe that most of this auto neuro immune illnesess including Me/cfs are the result of retrovirus infections.
Retroviruses that like Hiv after infections take time to develpe immune deficiency and many times co infections reom the herpes viruses family are fuel to accelerate the process of entring diferent type of cell Cd4lynphocites and others and replicate faster.
They also belive whatever ia causing this illness is a retrovirus that replocate slower, but with co infection, hormonal changes etc it accelerate especially with herpes viruses co infections, look at yourself how many herpes viruses you have and need to control..i do to.
They also belive there is unknow hiv strains that have recombine and doesnt not react to conventionals assays.
This theory of undiagnosed is not so far from the truth, but not exactly either.
Yes we all have diferent positions, you believe in an hiv theory that not body else seem to belive, even though i do belive there is strains of hiv, recombinations that are infecting humans and have not been diacover or ( validated to the world).they are not reactive to conventional assays.
Im one of the very few people here that seem to couple with your idea of retroviral etiology on ME/ CFS, i just think is a diferent retrovirus.
But any way im sorry if you dont like my comments and they bothered you.
Hope you have great success with evrything you are doing, if at any point i could be of any help dont hesitate to contact me.
I just want to keep the discussion grounded with evidence and data. We can talk in circles speculating but it's not going to be constructive so I want to avoid it. I'm not opposed to the idea of a retroviral etiology for a subset of ME/CFS patients. If you have gathered any data or studies that you believe supports that hypothesis we could discuss them. However, there is not much to be discussed by making vague claims without supporting evidence.
I wouldn't call it a theory, more of a historical observation. There have been a number of case reports of false negative HIV test results. The question I am seeking an answer to is whether I am one of those cases. There are a number of different reasons that a false negative test result can occur. Below is a list references for some of the different causes:
No humoral response without apparent underlying immunodeficiency
Seronegative hiv-1 infection: a review of the literature
Underlying primary immundeficiency (CVID)
Common Variable Immunodeficiency and Testing for HIV-1
Suspected slow replication rate resulting in low or no antibody production
Seronegative HIV-2 carriers in India
Test not sensitive to implicated HIV strain
Identification of HIV-1 Group O Infection —Los Angeles County, California, 1996
As for the possibility of influencing the results of the ELISA test for HIV hypoglobulinemia, it should be noted that the test of the 4th generation ELISA system, for example, such as AxSYM-HIV Ag / AB, reveals not only the presence of antibodies but also the presence of p24 antigen. If there are no antibodies, the protein p24 is detected. If the antibodies are produced and bind to the p24 antigen, the test works for the presence of antibodies.
ELISA and immunoblot are currently the "gold standard", the rest - hypotheses and artifacts.
In any case it is difficult to explain how I am still alive if I have HIV, given the fact that in 2004 the number of my helpers was 275 with a relative value of 18%.
Hi @ Knockknock.
Yes, there is certainly intuition, hard to explain facts and guesses in this area.
Here is an example.
Do not get sick black mangobes monkey HIV, unlike rhesus monkeys, which from the same virus get sick and die. And the reason is that the immune system of black mangobee for some unknown reason is not activated by the HIV virus, although the virus itself in CD4 + cells is thriving.
But, I'm afraid, this is not a topic for discussion in this thread.
Yes they do detect p24 antigen, although not with the same sensitivity as the antibodies. Also, the antigen detection doesn't work for HIV-2 as the HIV-2 capsid is composed of p26 proteins, not p24. I could point out edge cases in all of the clinically available tests where they will give false negatives, but that is not my goal. I'm not trying to convince anyone that HIV tests are unreliable. The issues I am talking about are rare, but rare doesn't mean they don't happen. I'll cut to the chase. The following pieces of evidence are what I would need to see in order to be confident HIV is not implicated in my case.
No reverse transcriptase activity
If I had a replicating virus with a detectable viral load, there would be detectable reverse transcriptase activity. This is a direct method of detection that doesn't rely on any humoral response so that variable can be eliminated. In addition, it can detect activity across the lentivirus family so it would be able to detect divergent or rare types that RNA PCR tests would miss due to their high specificity.
No proviral lentivirus sequences
Again, this is a direct method of detection that doesn't rely on any humoral response. It's possible that there would be no detectable viral load or reverse transcriptase activity especially for HIV-2 variants. To mitigate this possibility, proviral DNA sequences must be looked for. Proviral DNA PCR tests for HIV are highly specific and are only sensitive to the subtypes for which they were designed. PCR with less specific primers would be needed to ensure coverage of all HIV variants.
Just to be clear, I'm not advocating seronegative HIV as an explanation for anyone with ME/CFS symptoms. I don't even meet the CFS diagnostic criteria. This investigation applies only to myself. I realize that doesn't help you as it is apparent from the evidence you've provided so far that we likely have different pathologies.
I do not have information on how to fix the activity of reverse transcriptase. Share, if you know.
The search for universal primers for HIV DNA, especially the family of lentivirus, is just as insoluble.
I'm focused on supporting the most achievable in my position level of the T-cell link of immunity. B-cell link is rarely touched. Often, the level of activation of the T-link by the markers CD45 + CD3 + CD8 + HLA-DR + and CD45 + CD3 + CD4 + HLA-DR + goes off scale, which means that the therapy must be suspended.
For HIV reverse transcriptase, reverse transcriptase inhibitors are used. There are a number of available reverse transcriptase inhibitor medications available. I could purchase antiretrovirals including these from India but it doesn't solve the problem. Without the ability to monitor viral load it would be extremely difficult to properly manage. That's why I've been focused on getting access to the necessary research assays, but I haven't been able to get access to them. If you know any contract research organizations or other labs that could do the work, let me know. I've had some back and forth with one organization but they've been really unprofessional. They were supposed to send me a quote but never did and now aren't replying to my calls or e-mails.
I agree that you couldn't guarantee that new novel sequences would be detected, you could with high confidence detect all known HIV sequences. For example, in this paper degenerate PCR primers were designed targeting a conserved region across 5 different lentivirus sequences to look for evidence of a lentivirus in rheumatoid arthritis patients. I started looking into how well those primers would work against the HIV sequences in genbank but haven't completed that analysis. I was doing in silico PCR analysis with re-PCR to determine the detection coverage.
And by therapy do you just mean IVIG?
As far as I understand you, you want to be able to determine the presence of reverse transcriptase in the blood, as the most reliable marker of the presence of the virus.
How can inhibitors help here? Or did I misunderstand you all the same?
Unfortunately, I do not have access to laboratories that can detect the presence of reverse transcriptase in the blood.
Immunoglobulins in the schemes of treatment with my doctor I use occasionally, only if there is a significant deficit of IgG. The main treatment is using gamma interferon, sometimes in combination with alpha interferon. Dosage from 500 thousand to 1 million IU in a day intramuscularly.
I quote the results of my treatment in the second half of last year. As soon as activation of helpers and killers goes off scale, I stop treatment.
According to the graphs, one can see a tendency of a certain increase in the level of T helpers and the ratio of CD4 + / CD8 + after treatment courses with some delay.
This year, the treatment was supplemented by peptides obtained from embryonic planetary and cerebral tissue of cattle.
To date, I have no results.
Sorry, I misunderstood your previous post. When you said "fix the activity of reverse transcriptase" I thought you meant treatment, not detection. There are a wide range of possibilities for detecting reverse transcriptase activity. The most studied and validated commercial option with respect to HIV is the Cavidi Exavir Load V3 assay. It'd also be nice as it gives a viral load measurement based on the amount of reverse transcriptase activity, which is needed to monitor HIV treatment efficacy. I contacted Cavidi but they wouldn't give me a list of labs offering the test and wouldn't work directly with me. I know it's available in the developing world but so far I haven't found any specific labs offering it even though I know there are some somewhere.
There are other options as well. Some contract research organizations offer reverse transcriptase activity assays such as PERT. These services are used by pharmaceutical companies to ensure their cell lines aren't contaminated with retroviruses that would get into vaccines or other products. As I mentioned, I communicated with one of these companies who offers this assay and they were preparing a quote but then never sent it and cut off communications.
Also if you do a little googling, you can see that there are many companies offering assays to labs for detecting reverse transcriptase activity. For example:
EnzChek® Reverse Transcriptase Assay Kit
Reverse Transcriptase Assay, colorimetric
I see. I haven't researched treatment options, but I remember seeing a post on thebody.com where they mentioned IL-2 (interleukin-2) and gamma interferon for treatment of ICL. It was from 2008 so it may be out of date.
If you dont mind expain what is you diagnosted??
I mean would of swear you were a cfs suffer pursuing the idea of a retrovirus like hiv at the culprit of your illness.
What do you have what are your symptoms etc??
!! Strongly agree that finding reverse transcriptase is one of many ways of denostraring retroviral infection, even though it does not pin point to any particular retrovirus, reverse transcriptase, micr electron, isolation, are proof of retroviral infection adding the ( fact) of the patient been asymptomatic, especially in the case of IDL, CFS...
This kind of testing are in many cases more acure than an antibody test. Even the p24/26 protein since the retrovirus that we may be looking at could be diferenf, could be a mutation or diferent recombine Hiv? , could be an animal retrovirus, there is to many type of retrovirus C type, delta, gama etc...
!! Unfortunably many virologist and researchers have found hard evidence of retroviral presence in me/cfs patients using this methods, but this ( facts) have been ignored by science and the Governments.
If you have an asymptomtic patient, with evidence of defiency and disfuntional immune system, with evidence of reverse trabscripase under micr electrom
Why you dont pursuit that with the fullpower of science??
I don't have a diagnosis. You can read about most of my symptoms in my paper if you're interested.
Also, here is something I said previously in this thread regarding why I do not meet the criteria of CFS.
I had some blood drawn earlier this week and have some new data to share.
I had tests for exposure to two HHVs, EBV and CMV. You can see the results below:
The EBV results were unexpected for a few reasons. One is the high prevalence of EBV in the general adult population which has been found to be over 95%. Another reason is it is evidence that the previous visual diagnosis of oral hairy leukoplakia was a false positive. Oral hairy leukoplakia is caused by EBV so if EBV is not present, evidence suggests the lesion would have been a different type of leukoplakia. Of course this depends on the relative sensitivity and specificity of the test methods, namely visual inspection and IgG antibody detection. Presumably the EBV assay used has higher sensitivity/specificity and would be stronger evidence. Once I find some numbers, I'll recalculate the probabilities.
CD4 & CD8 Subsets
I had my CD4 & CD8 subsets measured again and have updated data. The figure below shows the data scaled to the respective reference ranges and a line fit using OLS regression for trend visualization purposes.
Showing the full scale makes it hard to discern changes in the data. The latest measurements include the following historic lows:
WBC: 4.4 x10E3/uL
CD4 Abs: 420 /uL
CD8 Abs: 335 /uL
I will be doing some hypothesis testing and forecasting analysis on this data which I will include in a future post.
The first sign of the presence of intracellular infection is relative lymphocytosis and a relative (even worse absolute) neutrophilia. You do not have this. CD4 + and CD8 + cells are almost normal. It is rare to find a patient who does not have a significant amount of antibodies to HHV4 (VCA) and HHV5. Besides, you, if I'm not mistaken, have no clinical symptoms. I think you should not worry. Congratulations.
If neurologic symptoms still exist, it's worth checking in on HHV6, HHV7.
I'm assuming you mean a transient phase during acute infection. I was infected 6 years ago so any acute reaction is not relevant. I am looking for markers of chronic infection with HIV. It would be the opposite of what you stated, I would expect lymphopenia and neutropenia in the long term.
The reference range doesn't tell all. The trends are downward and I will establish the statistical significance of them in a future post.
I am not sure what type of patient you are referring to here. Are you referring to any particular disease?
I have a number of symptoms significantly impacting my quality of life. You can read about most of them in my paper if you want.
Unfortunately I do not agree with your conclusion as it does not explain the evidence.
These are the typical causes of lymphocytosis and lymphocytopenia.
Causes of increased levels of lymphocytes (lymphocytosis) - more than 3.0 × 109 / l:
* Viral infections,
* Some bacterial infections (tuberculosis, syphilis, whooping cough, leptospirosis, brucellosis, yersiniosis),
* Autoimmune connective tissue diseases (rheumatism, systemic lupus erythematosus, rheumatoid arthritis).
The causes of a decreased level of lymphocytes (lymphocytopenia) are less than 1.2 × 109 / l:
* Aplastic anemia,
* HIV infection (primarily affects a variety T-helpers),
* Some forms of tuberculosis,
* Acute infections,
* Excess of glucocorticoids.
Intracellular infections (all viral infections, NOT only acute, but also chronically active) cause, first of all, relational lymphocytosis. I know very, very many of my friends suffering from chronic herpes infection having this symptom. At me it during last 20 years at least. You do not have it. In addition, I say that in most people, IgG levels to HHV4 are high, practically all cases of infectious mononucleosis were diagnosed in childhood. Most have also increased IgG titers and to HHV5. That's what I mean when I talk about patients.
Of course, a deficit of T helper and T killers can cause lymphocytopenia, but you have it insignificant, and the trend you are talking about is statistically insignificant.
Therefore, I want to believe that you are all right.
I do not think that with your number of helpers and negative serology of HIV there are any reasons to worry.
Among the clinical manifestations of the greatest attention, in my opinion, deserves a fungal infection, most likely associated with a relatively low number of T killers.
Can you mesage me.
I see you really know alot about immune deficiency, i would like to ask you a couple questions with out making undiagnosed thread out of topic.
I would apreciated
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