AIDS cases going down in USA, not up. So is HIV infection. 
Once again you need to source your contentions because the things you say are just simply not true.
Posted on 12/11/2008 8:11:08 AM PST by GodGunsGuts
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2291054
The common response to stopping anti-HIV treatment is an increase of HIV-RNA load and decrease in CD4+ (helper T-cells)
Doctors regularly track the progression of the disease of AIDS by HIV titer count or the abundance of HIV mRNA in the patient. This is basic stuff, if you don't even know this I despair at the state of your “knowledge” on the subject.
1) HIV enters helper T-cells
True
2) HIV reproduces inside helper T-cells
Briefly, but it is soon checked by the immune system.
3) HIV infection leads to reduced counts of helper T-cells.
XXX Wrong! If this is so, why is it that they find less than 1 in 500 cells infected even with patients who are dying of AIDS? And why is HIV such a fast immunogen, but such a slow pathogen? And how is it that the number of HIV-positives remained flatlined while the number of AIDS cases continued to rise sharply. I could go on and on.
4) Low levels of helper T-cells leads to immune deficiency.
Tell me Allmendream, if AIDS is caused by illicit drugs and/or AIDS chemotherapy drugs, would a low T-cell count be the cause or an effect?
Way to not answer my questions. Here they are again:
If HIV your contention is that HIV leads to a lower T-cell count, then why do they find less than 1 in 500 cells infected even with patients who are dying of AIDS? And why is HIV such a fast immunogen, but such a slow pathogen? And how is it that the number of HIV-positives remained flatlined while the number of AIDS cases continued to rise sharply? Do you have any answers, or do you just ignore questions that are inconvenient to the status quo?
Also, if AIDS is caused by illicit drugs and/or AIDS chemotherapy drugs, would a low T-cell count be the cause of immunodeficiency or the effect of immunosuppressive behavior.
==Reduction in helper T-cell count is one of the hallmarks of HIV infection, as would make perfect sense seeings as how it is the cell that HIV infects.
Are you really so unaware as to not know that low T-cell counts are associated with a variety of conditions, to include drug abuse?
==Indeed the correlation between decreasing HIV titer or mRNA and increasing helper T-cell count is the hallmark of efficacy in anti-retroviral treatment.
Has it ever occured to you that the T-cell count might go up in response to ARV drug toxicity?
How is HIV different than SIV other than its host species?
Where is your source that says only 1/500 helper t-cells is infected with HIV?
Where is your source for the contention that T-cell count is lower in drug abusers?
“Briefly, but it is soon checked by the immune system.” GGG
And how do you suppose the immune system “checks” the infection? It stands up and says “HIV infection be gone”? No, the only way the body can deal with viral infected cells is to KILL the INFECTED CELLS.
So how would the immune system hold HIV infection in check without killing HIV infected helper T-cells? Indeed immune system killing of HIV infected helper T-cells might go a long way towards explaining why the majority of those helper T-cells we do see in someone with a low helper T-cell count who is HIV positive are not infected (assuming your unsourced statement is factual), the infected ones are the ones that were killed resulting in the low helper T-cell count.
If the immune system is killing infected T-helper cells in order to check the infection that would lead directly to ...
3) HIV infection leads to reduced counts of helper T-cells
and then ...
4) Low levels of helper T-cells leads to immune deficiency.
Can you answer MY QUESTIONS now???
==So where is the chain broken GGG?
The chain is broken at #3. HIV does not destroy T-cells directly or indirectly.
==You have a lot of gall to say I’m not answering your questions.
I don’t know how else to put it. Should I say you’re avoiding my questions? That you’re dodging my questions? That you’re hiding from inconvenient data? That you are not living up to your end of the debate?
==How is HIV different than SIV other than its host species?
I haven’t looked into SIV in some time. Last thing I remember is that the claims that SIV causes Simian AIDS were being hotly challenged by AIDS Rethinkers. Do you have evidence that suggest SIV causes monkey AIDS?
==Where is your source that says only 1/500 helper t-cells is infected with HIV?
That’s less than 1/500 T-cells. And the fact that you don’t know that means you don’t know the first thing about the position of Rethinking AIDS scientists. By the way you have been talking, one would think that you thoroughly researched the Rethinker position and rejected it based on the evidence. But the fact that you have no knowledge that they continually point this out suggests you’re flying blind (as usual). Nevertheless, here are a few citations I dug up. Next time do your homework before challenging the work of scientists you obviously know nothing (or next to nothing) about.
Blattner W A, Gallo R C and Temin H M 1988 HIV causes
AIDS; Science 241 514–515
Harper M E, Marselle L M, Gallo R C and Wong-Staal F 1986
Detection of lymphocytes expressing human T-lymphotropic
virus type III in lymph nodes and peripheral blood from
infected individuals by in situ hybridization; Proc. Natl.
Acad. Sci. USA 83 772–776
Schnittman S M, Psallidopoulos M C, Lane H C, Thompson L,
Baseler M, Massari F, Fox C H, Salzman N P and Fauci A
1989 The reservoir for HIV-1 in human peripheral blood is a
T cell that maintains expression of CD4; Science 245 305–308
Hazenberg M D, Hamann D, Schuitemaker H and Miedema F
2000 T cell depletion in HIV-1 infection: how CD4+ T cells
go out of stock; Nature Immunol. 1 285–289
==Where is your source for the contention that T-cell count is lower in drug abusers?
Continued drug injection was associated with the rate of CD4 cell loss... While it is not possible to distinguish the mechanism underlying the relationship between continued drug injection and CD4 cell loss, seropositive IV drug users should be warned that continued injections may lead to increased HIV-related immunosuppression.
—Des Jarlais DC, Friedman SR, Marmor M et al. (1987, July). Development of AIDS, HIV seroconversion, and potential cofactors for CD4 cell loss in a cohort of intravenous drug users. AIDS 1(2): 105-111.
The CD4/CD8 ratio decreased with age in the drug-exposed infants compared with control infants (P less than 0.005). ... Our data demonstrate that infants of intravenous drug-using mothers have distinct immunologic differences at birth compared with non-drug-exposed infants and that these persist throughout the first year of life. The cause appears unrelated to intrauterine viral infection, suggesting a direct toxic effect of the drugs on fetal immunologic development.
—Culver KW, Ammann AJ, Partridge JC, Wong DF, Wara DW, Cowan MJ (1987, August). Lymphocyte abnormalities in infants born to drug-abusing mothers. J Pediatr;111(2):230-5.
Since most street heroin addiction involves polydrug use including chronic use of marijuana, barbiturates, hallucinogens, and other illicit substances, the hypothesis can be proposed that the depression of T-lymphocyte percentage was caused by another drug or combination of drugs, or by the effect of drug use on the addict’s general physical health and nutrition, i.e., the addict milieu.
—McDonough RJ, Madden JJ, Falek A, et al. (1980). Alteration of T and null lymphocyte frequencies in the peripheral blood of human opiate addicts: In Vivo evidence for opiate receptor sites on T lymphocytes. J Immunol: 125(6); 2539-43.
How would the immune system “check” HIV infection of helper T-cells other than by killing helper T-cells? What mechanism that doesn't involve killing infected cells does the immune system have for holding an infection “in check”?
So how does the immune system “check” HIV infection in helper T-cells GGG?
Use of the recreational drugs, cannabis, cocaine, poppers, or amphetamines, does not adversely affect the number or percentage of CD4 or CD8 cells in either HIV-positive or HIV-negative gay men, according to data from the Multicenter AIDS Cohort Study (MACS) published online on January 3rd in the journal Drug and Alcohol Dependence. However, the investigators did not measure the quality or function of these cells.
Animal and test tube studies have previously shown that recreational drugs such as cannabis (smoked as marijuana), cocaine, poppers, and amphetamines may adversely affect animal and human T cell responses.
Notably, cocaine given to HIV-infected mice greatly increased HIV levels and reduced CD4 cell counts to one ninth of the levels of the mice in the control group.
However, studies examining the impact of these recreational drugs on CD4 and CD8 T-cells in real life have reported inconsistent and conflicting findings, possibly due to confounding factors such as antiretroviral drug use, injecting drug use, and differences in the level and frequency of recreational drugs used over time.
Consequently, Dr Chun Chao of the University of California at Los Angeles, and her colleagues, sought to assess the association between cannabis, cocaine, poppers, and amphetamine use and CD4 and CD8 counts by examining survey data and medical records from HIV-positive and HIV-negative gay men and other men who have sex with men enrolled in the Multicenter AIDS Cohort Study (MACS).
In particular, they wanted to calculate the rate of CD4 and CD8 change as a function of drug use both at baseline and throughout the study period. In order to explore possible dose-response relationships, they looked specifically at frequency and duration of self-reported recreational drug use.
A total of 3236 HIV-negative men were included in the analysis (which included men enrolled from between April 1984 and April 2003). The average follow-up time for HIV-negative men was ten years.
A further 481 HIV-positive men were included in the analysis. These men were HIV-negative at MACS enrolment and acquired HIV before a cut-off date of December 31st1995, chosen to avoid any confounding effects of highly active antiretroviral therapy (HAART). The average follow-up time for HIV-positive men was five years.
Recreational drug use at baseline was high both for men who remained HIV-negative and those who became HIV-positive during the study.
Of the men who remained HIV-negative, 59% used cannabis, 27% used cocaine, 58% used poppers, and 16% used amphetamines at baseline.
Of the men who seroconverted during the study, 61% used cannabis, 30% used cocaine, 58% used poppers, and 17% used amphetamines at baseline.
Surprisingly, however, the investigators found that fater controlling for smoking (which can raise CD4 cell counts) and other factors known to affect CD4 cell levels, the men who said they used any of the four drugs either at baseline, or any time during the study, had a (non-statistically significant) higher average CD4 cell count throughout the follow-up period, compared to those men who said they did not use any of the drugs.
Consequently, they write, “we did not find any clinically meaningful associations, adverse or otherwise, between use of marijuana, cocaine, poppers, or amphetamines and T cell counts and percentages in either HIV-uninfected or HIV-infected men.”
They add that they “also did not observe any threshold effect by frequency of use or duration of use (at least not with weekly or more frequent use or continuous use in the past year).”
They note that although their study found that the use of poppers was significantly associated with a lower CD4 cell count, “the size of the effect was tiny, even the strongest effect (for weekly or more frequent use) amounting to only a 4% reduction relative to [men] who did not use poppers.”
They also say that although other studies have suggested that cocaine use had an adverse effect on CD4 cell counts “this association was not observed in our study, even in those who used cocaine weekly or more frequently.”
The investigators also looked at the effect of tobacco smoking, and found that “tobacco smoking was associated with approximately 6% (p < 0.01) and 7% increase (p = 0.04) in mean CD4 cell count in HIV-uninfected and HIV-infected men.”
However, in their conclusion, the investigators concede that “although the circulating numbers of CD4 and CD8 T cells do not appear to be significantly affected by use of these substances, these findings do not preclude the possibility that substance use may adversely affect the functional properties of T cells.”
They also fail to point out that recreational drug use can affect sexual risk-taking; that use of poppers was significantly correlated with seroconversion during gay men’s unprotected sexual encounters; that amphetamine use can affect adherence to HAART; and that smoking may undermine the benefits of HAART.
Reference
Chao C, et al. Recreational drug use and T lymphocyte subpopulations in HIV-uninfected and HIV-infected men. Drug Alchol Depend doi:10.1016/j.drugalcdep.2007.11.010, 2008.
Thanks. Money quote...
“Use of the recreational drugs, cannabis, cocaine, poppers, or amphetamines, does not adversely affect the number or percentage of CD4 or CD8 cells in either HIV-positive or HIV-negative gay men”
But it’s 2008 research, not 1980 research, so it’s obviously commie propaganda.
I think it’s about time you started answering some of my questions, don’t you think? Here they are again (for the third time):
Way to not answer my questions. Here they are again:
If your contention is that HIV leads to a lower T-cell count, then why do they find less than 1 in 500 cells infected even with patients who are dying of AIDS? And why is HIV such a fast immunogen, but such a slow pathogen? And how is it that the number of HIV-positives remained flatlined while the number of AIDS cases continued to rise sharply? Do you have any answers, or do you just ignore questions that are inconvenient to the status quo?
Also, if AIDS is caused by illicit drugs and/or AIDS chemotherapy drugs, would a low T-cell count be the cause of immunodeficiency or the effect of immunosuppressive behavior.
==Reduction in helper T-cell count is one of the hallmarks of HIV infection, as would make perfect sense seeings as how it is the cell that HIV infects.
Are you really so unaware as to not know that low T-cell counts are associated with a variety of conditions, to include drug abuse?
==Indeed the correlation between decreasing HIV titer or mRNA and increasing helper T-cell count is the hallmark of efficacy in anti-retroviral treatment.
Has it ever occured to you that the T-cell count might go up in response to ARV drug toxicity?
“If your contention is that HIV leads to a lower T-cell count, then why do they find less than 1 in 500 cells infected even with patients who are dying of AIDS?”
Easy, because the infected cells get killed by the immune system, thus there is a lower count, and among the population of cells that survive only a few are actually infected.
“why is HIV such a fast immunogen, but such a slow pathogen?”
The two are in no way related. Anything non self, pathogen or not, can elicit an immune response.
“how is it the the number of HIV positives remains flatlined while the number of AIDS cases continued to rise sharply”
I think you have this backwards GGG, once again you need to source your contentions.
“Also, if AIDS is caused by illicit drugs and/or AIDS chemotherapy drugs, would a low T-cell count be the cause of immunodeficiency or the effect of immunosuppressive behavior.”
It most certainly could, but what immunosuppresive behavior does illicit drug use or AIDS drugs have? Why would they target the specific cell type that HIV infects more prevalently than other cell types? Why would it not be an ‘across the board’ immunosuppression associated with drug use rather than a specific loss of helper T-cells associated with HIV positive status?
Ok. All done.
Now answer my question please GGG (because you really stuck your foot in it), how does the immune system “check” HIV infection of helper T-cells besides by KILLING infected helper T-cells?
Heck, how does the immune system deal with ANY viral infected cell other than by killing the infected cell?
AIDS cases going down in USA, not up. So is HIV infection. Once again you need to source your contentions because the things you say are just simply not true.
The fact is that contraction of AIDS through blood transfusions has gone down to about zero after widespread application of the HIV marker test to the blood supply. Therefore, even if the test doesn’t detect AIDS itself, it detects something at least closely related. Also, anti-virals have led to much longer life expectancy for AIDS patients, so again there has been a medical benefit.
Ding! We have a winner!
Me: If your contention is that HIV leads to a lower T-cell count, then why do they find less than 1 in 500 cells infected even with patients who are dying of AIDS?
You: Easy, because the infected cells get killed by the immune system, thus there is a lower count, and among the population of cells that survive only a few are actually infected.
Me: Once again, you display your ignorance. The 1 in 500 cells are latent virus that the immune system does not act on. In the vast majority of cases, they can’t find any virus at all...only the antibodies to the same, which, until the advent of AIDS, had always been understood to confer immunity. And in the RARE cases where they do find active HIV, it can only be found in about 1 in 10,000 cells—even in AIDS patients who are on their deathbeds, dying of AIDS defining diseases! These are the cells that the immune system eliminates. Thus, even in the rare cases that HIV can be found making coat proteins that the immune system acts against, there are 9,999 cells, a tiny fraction of which that are latently infected, happily dividing with no adverse immune response whatsoever. Given this glaring paradox, how is it you propose that HIV depletes T-cells again?
Me: why is HIV such a fast immunogen, but such a slow pathogen?”
You: The two are in no way related. Anything non self, pathogen or not, can elicit an immune response.
Me: What kind of answer is that? The point is, the immune systems quickly checks HIV, thus iliminating active virus. All that is left is dormant virus, and on rare occasion, active HIV in a tiny fraction of cells, but even then, only in patients with severely compromised immune systems.
You say that a retrovirus—a class of virus that are known for being harmless—causes T-cell depletion, despite the fact that in almost all cases they can’t find active virus. And when they do find active virus, they can only find it in 1 in 10,000 T-cells in severely immune deficient AIDS patients. Given this data, I must once again ask, how can a virus that lies harmlessly dormant in 1 in 500 cells, and on rare occasion, active in 1 in 10,000 cells, cause the T-cell depletion we see in AIDS patients? Don’t you think it is about time we started at least considering other causes???
HOW does the immune system “quickly check HIV infection” without killing infected helper T-cells?
Cells infected. Cells killed. Low helper T-cells. Immune deficiency.
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