AIDS and Idiopathic CD4-T-cell Lymphopenia
Posted by Henry Bauer on 2014/05/11
When “HIV-positive” gay men who have long been healthy then become sick with an “AIDS-like” illness, perhaps they are experiencing idiopathic CD4-T-cell lymphopenia and not “HIV/AIDS”.
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The “AIDS” era had begun as GRID: gay-related immunedeficiency. As John Lauritsen pointed out as early as 1985, that naming stemmed from a bizarre, unique, misleading classification scheme which masked the fact that the prime risk factor for illness was not being gay, the prime risk factor was abusing drugs as part of a blatantly unhealthy lifestyle .
When Africans, Haitians, and drug injectors were seen to have the same illnesses, GRID was re-named AIDS: acquired immune deficiency syndrome of unknown cause, characterized by low CD4 counts. In 1984, the cause of this immune deficiency was prematurely and mistakenly attributed to a retrovirus claimed to have been discovered by Robert Gallo who subsequently reported detecting “HTLV-III” in “18 of 21 patients with pre-AIDS … [and] 26 of 72 adult and juvenile patients with AIDS” , a rate of detection that is anything but convincing proof of cause. The evidence has continued to accumulate that this “HTLV-III”, subsequently re-named “HIV”, was and is not the cause of “AIDS”, which therefore remains an immune deficiency of unknown or unspecified cause.
By 1993 so many cases of “HIV-negative AIDS” had come to official attention that these were attributed to yet another newly minted condition: Idiopathic CD4-T-cell Lymphopenia, ICL or ITCL: immune deficiency of unknown cause associated with low CD4 counts.
But this is precisely the original definition of AIDS before the red herring of “HIV”. Therefore AIDS Rethinkers and HIV Skeptics, given their understanding that “HIV” does not cause “AIDS”, might logically conclude that “AIDS” is indistinguishable from ICL/ITCL.
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What really matters, of course, is not names but illnesses and deaths, and the reasons for those have been thoroughly confused and obscured by several official re-definitions of “AIDS” and by corollaries of the mistaken treatment of “HIV-positive” individuals with toxic “antiretroviral drugs” instead of treatment of manifest illnesses and symptoms, typically opportunistic infections.
None of those manifest illnesses were new or unique to “AIDS”. They were brought about in different ways in the four original (early 1980s) risk groups:
(1) In drug abusers, immune deficiency is brought about directly by the drugs, resulting in “AIDS”-like diseases that were noted already in the 1960s .
(2) In Africans, immune deficiency is brought about by malnutrition and periodic infections by a multitude of endemic diseases .
(3) Haitians were soon removed from the list of risk groups to which they had been added prematurely.
(4) In gay men — in only a small proportion of gay men, it is not emphasized often enough — immune deficiency had been brought about by drug abuse as part of a blatantly unhealthy lifestyle [1, 5]. The only “AIDS disease” unique to gay men was identified, also mistakenly, as Kaposi’s sarcoma; it was not actually a sarcoma, it was damage to blood vessels caused by ingestion of volatile nitrites, “poppers” .
In absence of any known ways to strengthen immune systems, early cases of AIDS among gay men were handled by treating, or by prophylactic measures against, the specific opportunistic infections. Following the mistaken attribution of AIDS to HIV, about 150,000 deaths were then brought about by administration of the supposedly “antiretroviral” AZT . After the replacement of monotherapy by less toxic combinations of AZT-like and other types of drugs (cART or HAART), mortality declined, but it seems to have leveled off since about 1998 at roughly 15,000 annually in the USA  (15,529 in 2010 ). How much of that mortality is attributable to the drugs cannot be estimated because too many pertinent data are lacking (mortality as a function of length of time on antiretroviral drugs, type of drugs, specific causes of death).
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This factual history is a preamble to further consideration of the conundrum addressed in two recent posts : the puzzle of delayed illness in “HIV-positive” gay men. Commentaries to those postings made me realize that “AIDS” is really ICL/ITCL. When “HIV-positive” gay men who have been healthy for long periods without antiretroviral treatment then become ill and have low CD4 counts, the cause cannot be “HIV” because “HIV” does not cause illness and may not even exist; therefore the cause of “AIDS-like” illness must be idiopathic CD4-T-cell lymphopenia. Hence it is worth considering what mainstream science has to say about that condition, two decades after its discovery. If successful treatments for ICL had been found, perhaps those could also work for cases of delayed illness in “HIV-positive” gay men. Unfortunately, I have not come across reports of successful treatments for ICL. Nevertheless, some aspects of ICL may allow for a different approach to cases of delayed illness in “HIV-positive” gay men, in particular recognition of the wide range of possibly associated manifest illnesses, the good probability of recovery from those illnesses, and the occasional observation that ICL reverses itself — CD4 counts sometimes increase, for as mysterious a reason as that for their initial decline.
There are no reliable data about the population-wide prevalence of ICL, because counting CD4 is not part of routine testing. Therefore almost all cases of ICL have been identified following manifest illness later diagnosed as brought on by CD4-specific immune deficiency. Thus it is not known how many people with “low” CD4 counts never become ill. What is known, though, is that CD4 counts in themselves are not valid markers of good or bad health .
So when “HIV-positive” gay men who have long been healthy then become sick with an “AIDS-like” illness, not only is “HIV-positive” a red herring, so too is CD4 count. No doubt something specific is at the root of the newly experienced illness, but it isn’t “HIV” and it may not have anything to do with the CD4 level, and it may not be the same “something” in all such cases.
Perhaps most striking in the literature on ICL is the lack of regularities — other than that there is no identified cause for the low CD4-count. A recent review of 258 cases from all over the world  found that ICL had been diagnosed at ages ranging from 1 to 85, with a very broad distribution (standard deviation of 19 on a mean of 41). As would be expected from the manner in which cases typically come to light, most had infections “including AIDS-defining illnesses”, but about 1 in 8 were healthy despite low CD4 count. Where illness was present, it ranged over various kinds of mycobacterial and cryptococcal infections as well as candidal and herpes (Varicella zoster); nearly 1 in 5 had a malignancy, and 15% had some sort of autoimmune disease. Only 4 patients had family members who also had low CD4 counts.
Etiology (cause) of ICL remains mysterious, but it has been “hypothesized that abnormally increased microbial translocation through the intestinal wall may be an underlying etiology” — consistent with the intestinal dysbiosis hypothesis in “HIV/AIDS” . Low CD4 counts can also be caused by the manifest infections themselves.
It is encouraging that nearly 4 out of 5 of the described cases survived the manifest illness  (but for how long was not reported). Furthermore, “Transient CD4 lymphocytopenia is common and has been estimated to occur in healthy HIV-negative individuals . . . [at rates of] from 0.4-4.1%” [emphasis added], consistent with the literature that reveals CD4 and health to be independent of one another . According to one report, CD4 counts normalized spontaneously in 7 of 39 ICL patients after an average of 31 months . It is further reassuring though puzzling that “Patients with cryptococcal infection and ICL have . . . favorable prognosis . . . [despite] an increased likelihood of developing dermatomal zoster” .
There is no agreed general way to treat ICL, but some data “support IL-2 as a relatively safe and potentially effective treatment for ICL patients with opportunistic infections, especially when combined with conventional treatment regimens” .
“Adult onset” immunodeficiency  may be akin to ICL in some respects, but it is not associated with low CD4 counts. Instead, the opportunistic infections were associated with the presence of anti-interferon-γ auto-antibodies, and a hereditary or genetic predisposition was suggested. Since autoimmune conditions were also found in about 15% of ICL cases , it would seem reasonable to look into possible autoimmune conditions whenever ICL is diagnosed or suspected — including cases of “HIV-positive” gay men who have long been healthy but then become ill.
Although ICL is said to be rare, this may only be because little population-wide data on CD4 counts are available and ICL is only identified in the presence of manifest illness. It also complicates matters that “ICL lymphopenia” might actually be owing to the manifest illnesses. Similarly, cases of “HIV-positive” gay men who have long been healthy but then become ill may seem to be rare just because they become known only serendipitously through anecdotal reports when the affected individuals choose to bring their situation to wider attention.
Note that many or most of the manifest diseases associated with ICL are or could be classified as “AIDS-defining”. Therefore an “HIV-positive” gay man who has long been healthy and who then “acquires” ICL — cause unknown — would naturally suspect that HIV/AIDS theory might be correct after all, and he might infer that “HIV” had been long latent and was now making him ill, and he would likely then experiment with antiretroviral drugs. Short courses of antiretroviral drugs have indeed been effective in some instances, but an alternative might be to experiment with speculative possible treatments for ICL: IL-2, probiotics, perhaps steroids which can help against autoimmune diseases, for example Hashimoto’s encephalopathy .
In any case, it is worth knowing that nearly 80% of ICL patients recovered from their manifest illness and that in some cases the low CD4 count reversed itself after as much as 3 years.
 John Lauritsen, “CDC’s tables obscure AIDS-drug connection”, reprinted as chapter I in The AIDS War (ASKLEPIOS, 1993)
 Gallo et al.,. “Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS”, Science, 224 (1984) 500-3
 P. 103 f. in Neville Hodgkinson, AIDS: The Failure of Contemporary Science, 1996.
 Robert S. Root-Bernstein, Rethinking AIDS — The Tragic Cost of Premature Consensus, 1993; especially chapter 9
 For descriptions of that “fast-lane’ life-style, see the sources cited in section 22.214.171.124 of The Case against HIV
 John Lauritsen & Hank Wilson, Death Rush: Poppers and AIDS, 1986
 Section 5.1.5 of The Case against HIV
 Figure 3, p. 21 in Deaths Among Persons with AIDS through December 2006, HIV/AIDS Supplemental Report, 14 #3
 Statistics Overview, “Deaths of persons with an AIDS diagnosis”, updated 23 April 2013;
 The Lazarus Effect in HIV/AIDS; The Lazarus Effect and the puzzle of delayed illness in “HIV-positive” gay men
 David Crowe, “Predictability of a CD4 count”, July 2012;
 Dina S. Ahmad, Mohammad Esmadi, and William C. Steinmann, “Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections, malignancies, and autoimmune diseases”, Avicenna Journal of Medicine, 3 (#2, April-June 2013): 37-47
 See sections 126.96.36.199 & 188.8.131.52 of The Case against HIV
 Zonios et al., “Idiopathic CD4 lymphocytopenia: natural history and prognostic factors”, Blood, 112 (2008) 287-94)
 Zonios et al., “Cryptococcosis and idiopathic CD4 lymphocytopenia”, Medicine (Baltimore), 86 (#2, 2007) 78-92
 S. K. Browne et al., “Adult-Onset Immunodeficiency in Thailand and Taiwan”, New England Journal of Medicine, 367 (2012) 725-34
 When doctors can’t tell you what’s wrong (updated); Encephalitis and Hashimoto’s Encephalitis
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