I know an old lady who swallowed a germ
That managed to hide out a very long term
She swallowed the germ to match the lie
But I don’t know why she swallowed the lie
Perhaps she’ll die

I know an old lady who swallowed a pill
What a thrill to swallow a pill
She swallowed the pill to kill the germ
That managed to hide out a very long term
She swallowed the germ to match the lie
But I don’t know why she swallowed the lie
Perhaps she’ll die

I know an old lady who swallowed more pills
Made her ill. To swallow more pills.
She swallowed the pills to aid the pill
She swallowed the pill to kill the germ
That managed to hide out a very long term
She swallowed the germ to match the lie
But I don’t know why she swallowed that lie
Perhaps she’ll die

I know an old lady who swallowed ad hoc
What a crock to swallow ad hoc!
She swallowed ad hoc to match the pills
She swallowed the pills to aid the pill
She swallowed the pill to kill the germ
That managed to hide out a very long term
She swallowed the germ to match the lie
But I don’t know why she swallowed that lie
She’s going to die

I know an old lady who dismissed the horse(sh*t)
She’s alive and well of course!

The absolutely first thing you must do is take care at all times to distinguish clearly between infection and disease/clinical symptom. HIV is ranked as a co-factor not in infection but in the clinical manifestation of KS. Not long ago, it was thought that HIV was a primary, possibly sufficient, cause of KS. That view has reluctantly been abandoned because KS tumors didn’t yield any traces of the HIV molecular signature despite Roman efforts by Gallo and others to tease it out.

But since the First Cause of all things MUST be a virus, they kept hunting and found that KS tumors reliably express at least fragments of the HHV-8 molecular signature. Post hoc(us pocus), there’s surely the cause of KS! Unfortunately, it has also proved impossible to establish HHV-8 as a sufficent cause of KS, so, just as with HIV, everything becomes a co-factor to preserve the core myth of Viral Causation.

Regardless of whether the scientists are on the right track or not — who can tell in each case? — this is the inevitable pattern the narrative will follow each and every time. But with the advent of the lenti-viruses and immune-deficiency viruses, something was added: viruses are now each other’s co-factors. So for example herpes facilitates HIV, and HIV facilitates herpes. HIV even facilitates itself; its mere presence creates the conditions that facilitate its presence. It is a perfect viral Ouroboros myth, and as with all myths, it holds a core of truth clothed in multiple layers of superstition.

The reason i ask what if not HIV, is because it is the mainstream view, im sorry, but i happen to hold the belief that HIV causes AIDS.

How do you mean viruses are mentioned as co-factors? Do you mean what are the co-factors to the infections?

As for why the discrepancy in rates, first of all, it is arguable to say RSA has been the hardest hit, certainly one of the hardest, but it may be down to several key issue. Quality of data handling and correct diagnosis. I accept that if there was a significant enough discrepancy in the figures it may reduce the efficacy of the argument.

It could also be that HHV8 infections were more prevalent in RSA to start with, and less common in in the other countries although im sure there is plenty of data in the literature to back up or falsify. I’d try to find it, but im away from my network computer at the minute, and i only have a basic access to journals, mostly on fungus

The aetiology of KS is an interesting topic. Although it may not be central to Prof. Bauer’s general line of argument, it is certainly pertinent. but I think we would all be more inclined to concern ourselves with your questions if you could be persuaded to stick to one topic at a time and put a little more work and thought into it than simply Googling and throwing bits and pieces at us in the form described by Prof. Bauer above:

“But if HIV doesn’t cause AIDS, how do you explain…?”

As you will know, it’s A LOT less work asking such a quesion than answering it, so let’s restrict ourselves a bit, shall we? The general familiarity with the HIV/AIDS topic demonstrated in your mails suggests that you are quite capable of this.

But let me give you an example of what I mean. You write

“This article describes a 3 fold increase in an already prevalent disease from 1988-1996 and suggests that this figure is still rising.

F Sitas. Kaposi’s Sarcoma in South Africa. Journal of the National Cancer Institute Monographs, No. 28, 1-4, 2000

References a 20 fold increase in KS in uganda and zimbabwe in the past 10-15 years.

If we can already assume these diseases were already endemic and and infection rates of KSHV were stable, then what can explain the sudden rise in infection rate other than AIDS caused by HIV?”

Evelcyclops, here is what the CDC says about KS, KSHV and HIV:

“The etiology of KS is complex, but infection with human herpesvirus 8 (HHV-8 ) appears to be the primary and necessary event for development of the tumor (6). The sequence of the HHV-8 genome suggests several ways the virus might promote uncontrolled cellular proliferation. The virus encodes for several genes, incorporated from its human host, that are homologous to human oncoproteins, including a cyclin that regulates the G1-to-S phase of the cell cycle, and a Bcl-2 like protein that prevents apoptosis (6). In addition, HHV-8 encodes for functional chemokines that may promote angiogenesis and inhibit immune type I helper-T-cell responses. Early in the development of a KS lesion, large numbers of inflammatory cells are recruited to the site, and their production of pro-inflammatory cytokines such as IL-6 and TNF-alpha are thought to promote the angioproliferative inflammation that characterizes the disease.
However, HHV-8 infection alone is not sufficient for the development of KS, and epidemiologic evidence supports the contribution of other environmental, hormonal, and genetic cofactors in the pathogenesis of the condition. For instance, co-infection with HIV dramatically increases the risk for development of KS, as does the immunosuppressive therapy required by organ transplant patients. Because KS is more prevalent in men than women, sex hormones have also been postulated to act as cofactors in the pathogenesis of the disease”

In other words, nobody is really sure about anything other than there appears to be certain correlations. Viruses are mentioned as cofactors, so is the environment, hormones, genes. . . It’s all in the mix. Now I have a question for you: Which of these many cofactors would explain that KS incidence has risen only three-fold in South Africa, the country supposedly hardest hit by HIV/AIDS, while it has risen twenty-fold in Uganda and Zimbabwe?

Once you have answered this and similar questions, from the inexhaustible store of paradoxes, inconsistensies and discrepancies generated by the HIV/AIDS explain-all, maybe we can fruitfully return to your question concerning which factors other than HIV could explain the supposedly increased incidence of KS in Africa.