• Quick note - the problem with Youtube videos not embedding on the forum appears to have been fixed, thanks to ZiprHead. If you do still see problems let me know.

AIDS (hah)

JoeEllison said:
This also explains the "changing shape" you've noticed. The virus has gone from spreading rapidly/killing rapidly to spreading slowly/killing slowly.... so we can logically expect a significant shift in the way it presents.
Click to expand...

I was more referring to the shape of the human perspective of the disease than the virus itself, but I take your point - even though I'm not sure your analogy is all that accurate.

I think the changing spread of the disease is more about changing behaviour than viral mutation.

skeptigirl said:
Here are a few debunking web sites of this particular nonsense and Dabljuh's twisted logic.
Click to expand...

Extremely well put case. Thanks.

kellyb said:
The UNICEF link explains it. They've had a long drought, and a lot of war. They're dying from starvation and violence, and a small decrease in HIV prevalence isn't going to eclipse that. Also, a lot of HIV infected individuals are dying, and apparently no longer quite replacing themselves with one or more new infections there so quickly before death.
Make sense?
Click to expand...

Sure. I'm actually very well aware of the Kenyan situation. I know that AIDS education is #1 priority from birth in the parts of Kenya actually receiving education, so the message is clearly getting through. The fact that changes in sexual behaviour have resulted in immediate lowering of AIDS cases and deaths does tend to support conventional thinking.

I'm not 100% convinced by UNICEF's picture of drought and violence causing the decreasing life expectancy, either. The drought's peak effects were in 2004/5, by which time the life expectancy has shown a small upturn, which would kind of dent their theory a little. Interesting that Dabjah mentions TB, because that's a disease which has increased enormously in Kenya in the time frame under question. 30% increase between 2000 and 2002

Given that AIDS was falling at the time, I think it's reasonable to assume that the non-AIDS sector of TB may have been rising by as much as 50% in that time. That has a pretty deleterious effect on mortality rates.
 
JoeEllison said:
You're right, and I had considered this point the very moment after posting. I was immediately struck by how fast ebola acts, or how quickly necrotizing fasciitis can spread. However, it is still short compared to how the disease behaves when treated by drugs... drugs designed based on the facts of the disease that people like Dabljuh aggressively deny.
Click to expand...

Yeah...I also remember when you were considered "lucky" if you made it several years.
 
Adding to SYLVESTER1592's comments on the ways which viruses can produce illness, here are a couple of additional discussions.

Viral pathogenesis in idiopathic autoimmune diseases
Independent lines of evidence suggest a viral aetiology in autoimmune rheumatic diseases. The possibility of a viral aetiology was raised by findings of virion-like tubuloreticular structures in endothelial cells and lymphocytes as well as demonstration of increased serum concentrations of type I interferon (IFN) in lupus patients.38 Virus-like particles were also noted in RA synovium.39 Many viral infections are accompanied by production of autoantibodies and viral proteins have profound effects on both antigen presentation and effector functions of the immune system. Dysregulation of programmed cell death has been reported in HIV infected40 and lupus patients as well.41 Similar to SLE, anaemia, leucopenia, thrombocytopenia, polymyositis, and vasculitis have been widely reported in patients with AIDS.42 Direct virus isolation and transmission attempts from tissues of autoimmune patients have not been successful.43 Nevertheless, it is possible that a (retro)virus, responsible for provoking an immune response cross reactive with self antigens, has been cleared from the host, so the absence of viral particles is not conclusive. An alternative retroviral aetiology---that is, activation of endogenous retroviral sequences (ERS) was initially proposed by a study of the New Zealand mouse model of SLE.44 Endogenous retroviral envelope glycoprotein, gp 70, was found in immune complex deposits of autoimmune lupus prone NZB/NZW mice. Abnormal expression of an ERS was noted in the thymus of lupus prone mouse strains.45 More recently, expression and autoantigenicity of human ERS has been demonstrated in patients with SLE.46-50

Below, two possible mechanisms of viral pathogenesis will be discussed. The first scenario involves molecular mimicry causing abnormal self reactivity.51 Naturally, viral infections elicit potent antiviral immunity that may lead to cross reactivity against self antigens. Analysis of molecular mimicries that is delineation of autoantigenic epitopes of self antigens may provide clues to the identity of viral antigens responsible for triggering the cross reactive immune responses. Secondly, infection of genetically susceptible hosts by a potentially large number of commonly occurring viruses may lead to T and B cell dysfunction and autoimmunity. Immunoregulatory aberrations triggered by well defined viral proteins at the level of antigen presentation, modulation of cytokine activities, and disruption of cell death pathways, will be discussed.
Click to expand...

MECHANISMS OF VIRAL PATHOGENICITY
* Arthus reaction
* Cell-mediated viral hypersensitivity
* Cell-transformation
* Immune allergic mechanisms to virus infection
* Polykaryocytosis
* Pyknosis
* Syncytia
* Viral alteration of host cell membrane
* Viral induction of non-normal host-specified products
* Viral induction of structural alterations of cells
* Viral teratology
* Viral toxins
* Viral-induced cell lysis
* Viral-induced chromosome abnormalities
Click to expand...
 
The Atheist said:
I was more referring to the shape of the human perspective of the disease than the virus itself, but I take your point - even though I'm not sure your analogy is all that accurate.

I think the changing spread of the disease is more about changing behaviour than viral mutation.
Click to expand...

My point is that the change in the way we view the virus is affected directly by the way we have dealt with the virus. It is the same way that views on aging have changed as lifespans have increased. As you survive longer, the things that are likely to kill you change. Living longer has changed the sorts of diseases that we are forced to live with... it has been said that if you live long enough, everyone gets cancer. In the same way, as drugs have extended the lives of people infected with HIV, the deaths by AIDS-related illnesses have changed.
 
kellyb said:
Yeah...I also remember when you were considered "lucky" if you made it several years.
Click to expand...
If you are referring to HIV-AIDS, the usual course before anti-retrovirals was ~5 years until symptoms and ~2 years until death after symptoms. There were some rapid progressors, ~80% of infected newborns were symptomatic by age 2. Some people especially those who got large initial doses such as with a blood transfusion were often symptomatic within a year. And then there were the long term non-progressors who have gone 10-15 years without treatment and without advancing to AIDS. The CCR5 deletion is believed to have accounted for some of those cases.
 
Last edited:
kellyb said:
Yeah...I also remember when you were considered "lucky" if you made it several years.
Click to expand...
And, when you consider that fact...

In the history of humanity, there has NEVER been a situation like this. A disease appeared suddenly, was always fatal, and the causes were unknown. In ONE GENERATION, the cause was identified, treatments were developed, and "100% fatality' was converted into "chronic illness and a lifespan of possibly two decades or more." Never before has an illness been identified and treated this successfully and this quickly. It is this unprecedented success that makes the HIV/AIDS pseudo-skeptics seem so ridiculous.

Could we really have had this much success, if no one had any clue as to what caused the whole thing in the first place? It just seems stupid to think so.
 
skeptigirl said:
And then there were the long term non-progressers who have gone 10-15 years without treatment and without advancing to AIDS. The CCR5 deletion is believed to have accounted for some of those cases.
Click to expand...

Would you mind expanding on that?
 
http://en.wikipedia.org/wiki/CCR5

CCR5-Δ32
CCR5-Δ32 (or CCR5-D32) is a genetic variant of CCR5.[1] [2]

It is a deletion mutation of a gene specifically impacting the function of T cells. CCR5-D32 is widely dispersed throughout Northern Europe and in those of European descent. It has been hypothesized that this allele was favored by natural selection during the Black Death, or during smallpox outbreaks, which is unlikely, given that the frequency of CCR5-Δ32 in Bronze Age samples is similar to that seen today.[3] The allele has a negative effect upon T cell function, but appears to protect against smallpox, plague and HIV. Individuals with the Δ32 allele of CCR5 are healthy, suggesting that CCR5 is largely dispensable. However, CCR5 plays a role in mediating resistance to West Nile virus infection in humans, as CCR5Δ32 individuals are enriched in cohorts of West Nile virus symptomatic patients, indicating that all of the functions of CCR5 may not be compensated by other receptors.

While CCR5 has multiple variants in its coding region, the deletion of a 32-bp segment results in a nonfunctional receptor, thus preventing HIV R5 entry; two copies of this allele provide strong protection against HIV infection.[4] This allele is found in 5-14% of Europeans but is rare in Africans and Asians.[5] Multiple studies of HIV-infected persons have shown that presence of one copy of this allele delays progression to the condition of AIDS by about 2 years. It is possible that a person with the CCR5-Δ32 receptor allele will not be infected with HIV R5 strains.
Click to expand...
 
Yer welcome.
:)

W asked how HIV kills immune system cells.

Ok. First read his. It's pretty cool (if you think biology is neat).

Cell suicide:
http://en.wikipedia.org/wiki/Apoptosis

Here's (part of) what HIV does when it infects some immune system cells.

It even has a control group, like W asked for.

http://gateway.nlm.nih.gov/MeetingAbstracts/102271406.html

Preferential Apoptosis of HIV-1 Specific CD4+ T cells.
Click to expand...

A greater frequency of ex vivo HIV-1 specific CD4+ T cells were preferentially undergoing apoptosis compared to CMV specific CD4+ T cells, by about 5-fold (35.2% vs 6.9 % of antigen specific cells expressed activated caspase-3, respectively, p<0.05). HAART abrogated the degree of apoptosis as well as skewing towards HIV-1 specific cells, (1.3% vs 1.2% of HIV-1 and CMV-specific CD4 cells, respectively). CMV-specific CD4+ T cells showed a greater susceptibility to Fas-induced apoptosis. In untreated individuals, HIV-1 specific CD4+ T cells tended to show decreased expression of the anti-apoptotic proteins, Bcl-2 and FLIP, when compared to CMV-specific CD4+ T cells. In 3/6 individuals, overnight pre-treatment of PBMC with MnTBAP significantly enhanced the frequency of HIV-1-specific CD4+ T cells.
CONCLUSIONS: Apoptosis is an important mechanism for the preferential destruction of HIV-1-specific CD4+ T cells. Furthermore, this effect can be abolished by HAART, and supports the notion that HAART can preserve HIV-1-specific CD4 immunity.
Click to expand...

Of course,W will think this is more "junk science", I'm sure.
 
If you are not ready to read all the literature on AIDS (which is A LOT) there are some good videos that can make it more imaginable what happens at the cellular/ viral level.

I think these may be useful to you:







Sorry for the long list of videos,(forgot they come with a complete box around them)
Good luck,

SYL :)
 
Last edited:
kellyb said:
Robinson a while back located a good "logical thought experiment" that you might like.
Click to expand...

Actually I think I authored the argument, back in the 1990s. Here are some quotes, which also will link you to the original post, which is convenient because it links to another thread about this. Note to the newcomer, I was called a troll in that thread for pointing out some of the fallacies and problems with AIDS, HIV research and such. I think I can understand where you are coming from. However, consider the following ideas, which I can expand upon if needed.

robinson said:
Not everyone who has been exposed to HIV has tested positive for it, and those that have, not all of them have developed AIDS. This is not in dispute. While with enough time, some may, many still have not, even without medical treatment. It is one of those things that is being researched.
Click to expand...


robinson said:
The data from Cuba is overwhelming. Before any test was available, Cuba authorities simply stopped any chance of infection from the new disease. Based on symptoms alone. After the tests were available, they simply tested everyone, and continued to do so with any risk groups, and they isolated anybody who tested positive.

The data from Cuba is overwhelming. They are the only country with no AIDS problem.
Click to expand...

robinson said:
The controversy over HIV/AIDS is large, convoluted, and involves many many issues. That anyone would deny such controversies exist, is beyond belief. Claiming there is no debate, is dumb.

Even a quick glance at the media stories, the books published, the websites, (there a LOT), the lawsuits, and the medical studies, shows a wealth of issues, many of which involve politics, huge amounts of cash, and death. Civil liberties, employment, even the ability to travel. Health care, drug companies, and privacy issues.

In fact, there are few issues that seem to have as much controversy over them as HIV/AIDS. You might not know it from watching TV, but reading scientific journals, and looking at legal cases, there is controversy baby, and lots of it. The kind that usually makes me want to ignore it. Because it is an ugly fight, and it involves really big sums of money, and powerful special interest groups.

Not the kind of thing I like to step in, even on the best of days.

The Cuba issue is a good example. While Cuba offers the best place in the know Universe for a study of HIV/AIDS, you have to be insane to try and do it. Despite having the best health care system in the world, an ideal population for study, and extensive evidence of every AIDS case since 1983, well documented, with a small but living population of HIV infected subjects, dating back to 1983, you face a huge obstacle to doing research on it.

Just talking about it can lead to real trouble. Notice how it just isn't mentioned on any page "debating" AIDS, or HIV. Its like it doesn't exist. Nowhere has better long term scientific data on HIV and AIDS than Cuba. You can find every single person on the island that has HIV, you can check the records on every single person who has AIDS, or has died from it. It is a small number, out of a huge population.

Its a no-brainer. It is obvious. I doubt anyone who reads the data on Cuba will object to that. It is the kind of hard evidence that shows "something" detectable with HIV test can be spread, can make you sick, can kill you, and can be tested for.

While a lot of the stuff about HIV and AIDS is questionable, that there is some problem, that it can be spread, and more importantly, it can be stopped, is the lesson from Cuba. I have no doubts.

Never have.
Click to expand...

To sum up, while there are problems and politics galore with HIV/AIDS, and always have been, there is good evidence that HIV is associated with a decreased immune system, which can lead to opportunistic infections, and death.

The policy of diagnosing Africans with AIDS, without doing an HIV test, is problematic, and may well be a funding issue.

And yes, the hype about catching AIDS from unprotected sex was hype, and yes, there have been a lot of people who used AIDS to promote agendas, as well as conspiracy theories, and yes there is dispute over many of the issues around HIV.

Based on my research, AIDS has not spread or killed anywhere near what the predictions were, it hasn't spread like a sexually transmitted disease, and it certainly hasn't killed the number of people in Africa that some would have you believe.

Now before somebody jumps in demanding I back up all that with links and quotes and evidence and stuff, I would say this.

If you claim AIDS has killed the number of people that it was predicted it would, you have to show that.

If you want to claim AIDS has spread sexually, you have to show that it has.

And if you want to claim Africa has been decimated by AIDS, you have to show that this is true.

Because the onus of proof is on the person making some wild ass claim, not the person who debunks it, and tells you that they don't believe it. :wackywink:
 
robinson said:
If you want to claim AIDS has spread sexually, you have to show that it has.
Click to expand...

What do you make of the HIV/circumcision RCTs?
 
Are you implying those latter assertions have not been supported by the data, robinson? I am confused by your post.
 
Adding to what kellyb posted on CCR5 deletion, (thanks, BTW) ...CKR5 deletion and chemokine levels in long-term HIV-infected non-progressors.
Balfe P, Churcher Y, Easterbrook PJ, Goodall R, Gotch F, McKeating J.
Program Abstr 4th Conf Retrovir Oppor Infect Conf Retrovir Oppor Infect 4th 1997 Wash D C. 1997 Jan 22-26; 4th: 145 (abstract no. 439).

University of Reading.

Objectives: To examine the role of the CC-CKR-5 genotype and chemokine production on the rate of HIV disease progression in a UK Caucasian population. Methods: 168 long-term HIV-infected homosexual men (median=10 years) were enrolled into a nested case-control study of the biological determinants of long-term non-progression. Three patient groups were identified: Non-progressors (NPs), n=48; HIV-seropositive greater than or equal to 9 years, asymptomatic and current CD4 count greater than or equal to 500 cells x 10(6)/1; intermediate progressors (IPs) n=69, HIV-seropositive greater than or equal to 9 years, and current CD4 count less than 500 cells x 10(6)/1; and rapid progressors (RP) n=31, who developed AIDS within 5 years of infection. PCR analysis was used to define the two common alleles of CKR5 (+/+ wild type and delta32 deletion) in DNA samples. Levels of chemokines known to interact with CKR5 (RANTES, MIP-1alpha and MIP-1beta) were measured in serum samples from 18 NPs, 18 IPs and 18 RPs using a commercial EIA. Results: 47 (31%) of the study population were heterozygous for CKR5delta32 (+/delta32), and none were homozygous. CKR5 +/delta32 was non-significantly elevated in NPs (41%), vs IPs (28%) and RPs (25%), p=0.2, and when compared with patients carrying the wild type (+/+) allele was associated with delayed progression to a CD4 count less than 200 cells (HR=0.47, 95% CI=0.24-0.95), but not with progression to CDC stage IV disease, (HR=0.82, 95% CI=0.45-1.49), or with either initial or current viral load. Serum levels of RANTES were significantly elevated in NPs vs. IPs vs. RPs, p=0.03, but the distribution of MIP-1alpha and MIP-1beta were similar across the three groups. Conclusions: These data provide further support for a role of CKR5 +/delta32 and elevated levels of RANTES in delayed disease progression. However, the power of our study to detect a 40% reduction in progression to CD4 count or clinical endpoints, as observed by others, was approximately 50%. Large collaborative cohort studies of long-term HIV-infected individuals are required to quantify reliably the impact of the CC-CKR-5 genotype on disease progression.
Click to expand...


RANTES: A cytokine that is a member of the interleukin-8 superfamily of cytokines. RANTES is a protein. It is a selective attractant for memory T lymphocytes and monocytes. It binds to CCR5, a coreceptor of HIV. RANTES is an acronym for Regulated on Activation, Normal T Expressed and Secreted. It is also known as CCL5.
 
You must log in or register to reply here.

Back
Top Bottom