[NRC] AIDS epidemie in Afrika is bedrog

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Op dinsdag 16 september 2008 23:26 schreef Monolith het volgende:

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Het gaat niet om personen, het gaat om ideeen. Ze leveren net als jij kritiek op HIV, maar het is blijkbaar onzin als je dat doet vanuit een creationistisch perspectief?
Maar je negeert weer vakkundig elke poging van mij om je een inhoudelijke reactie te ontlokken. Ga eens in op het "onderzoek" van Snelling dat ik hierboven postte. Ga eens in op het feit dat Zapruder een onderzoek ten eerste verkeerd citeert en vervolgens er een uit de lucht gegrepen conclusie aan verbindt. Of nog leuker, geef eens aan wat er precies mis is met de voorgestelde mechanismen voor de afname van CD4⁺ bij chronische HIV infectie.

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Op dinsdag 16 september 2008 23:26 schreef Lambiekje het volgende:

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Jy moet met bewijs komen dat het er wel is. Beetje omgekeerde wereld he.

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Op dinsdag 16 september 2008 23:26 schreef Lambiekje het volgende:

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Jy moet met bewijs komen dat het er wel is. Beetje omgekeerde wereld he.

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Op dinsdag 16 september 2008 23:27 schreef Lambiekje het volgende:

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Daar heb ik op geregeerd met CD4

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Op dinsdag 16 september 2008 23:33 schreef Lambiekje het volgende:

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Jij verdedigd de orthodoxiewaanzin.

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Op dinsdag 16 september 2008 23:32 schreef Lambiekje het volgende:

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Op dinsdag 16 september 2008 23:35 schreef One_of_the_few het volgende:

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ik weet niet wat triester is. dat je hier om moet lachen of dat je aan het plaatje zag uit welk deel het komt

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Op dinsdag 16 september 2008 23:33 schreef Lambiekje het volgende:

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Jij verdedigd de orthodoxiewaanzin.

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Op dinsdag 16 september 2008 23:29 schreef Lord_Vetinari het volgende:

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Weinig kaas gegeten van de academische manier van discussiëren, zeker? JIJ poneert een stelling, dus JIJ dient die te bewijzen.

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Op dinsdag 16 september 2008 23:37 schreef One_of_the_few het volgende:

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In kaas zitten stoffen, express ingebracht zodat je niet meer helder kan denken en meer kaas wilt. Daarom vinden mensen pizza ook zo lekker en de Mac. zitten allemaal verslavende stoffen in, door de NWO ingespoten. Maar dat weet verder niemand, dus niet verder vertellen.

maar daarom eet hij bijna geen kaas. al moet je dan wel oppassen voor ondervoeding

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August 2, 2007, over six months ago, I wrote an essay on the evolution of a cool new gene/protein in HIV-1 called 'Vpu'. To quickly summarize, Vpu first emerged in chimpanzees version of HIV, SIV. After chimpanzees transmitted SIV to humans, Vpu acquired new properties to deal with the environment of a new host. As time progressed, HIV-1 split into multiple subtypes, and the Vpus of different subtypes started to evolve different characteristics as well. Thus SIVcpz Vpu, HIVSubtype B Vpu, and HIVSubtype C Vpu are genetically and biochemically distinct proteins.

Quite the opposite of Behes claims about HIV-1 in 'Edge of Evolution', "the story of Vpu is turning into a beautiful example of how evolution works in the real world, the continual evolutionary struggle between host and disease producing a novel function, formation of an active ion channel, from a simple protein. It also nicely illustrates and how scientists use evolution to explore our universe and produce improvements in medical practice." (to quote an email from Ian Musgrave)

This didnt happen a billion years ago. It didnt take a billion years to occur. This is real evolution happening in real time with real consequences.

While that was enough to put Behes ridiculous claims about the evolution of HIV-1 to rest, there is still more to Vpus story. Six months ago, science only had a 'just so story' explanation for Vpu:
So theoretically, ion channel formation evolved in HIV-1 when it infected humans to overcome a species specific and cell specific host factor.
Why did Vpu evolve the way it did? Well, it had to overcome something in human cells. There was something about human cells that were different from chimpanzee cells that HIV-1 needed to evolve around. Whats that something? Um... something. But thats what happened! Thats why Vpu forms a viroporin!

It was one of those 'just so stories' that Creationists love to dismiss.

But that was six months ago. And, you see, scientists arent like 'Creationist' scientists. They dont see a black box, declare a deity made the box, and take the rest of the week off. Scientists see problems and demand answers. Several weeks ago, a paper was published in Nature that turned Vpus 'just so story' into just another 'so?' story for evolution:

Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu
Human cells possess an antiviral activity that inhibits the release of retrovirus particles, and other enveloped virus particles, and is antagonized by the HIV-1 accessory protein, Vpu. This antiviral activity can be constitutively expressed or induced by interferon-alpha and it consists of protein-based tethers, which we term 'tetherins', that cause retention of fully formed virions on infected cell surfaces. Using deductive constraints and gene expression analyses, we identify CD317 (also called BST2 or HM1.24), a membrane protein of previously unknown function, as a tetherin. Specifically, CD317 expression correlated with, and induced, a requirement for Vpu during HIV-1 and murine leukaemia virus particle release. Furthermore, in cells where HIV-1 virion release requires Vpu expression, depletion of CD317 abolished this requirement. CD317 caused retention of virions on cell surfaces and, after endocytosis, in CD317-positive compartments. Vpu co-localized with CD317 and inhibited these effects. Inhibition of Vpu function and consequent mobilization of tetherin's antiviral activity is a potential therapeutic strategy in HIV/AIDS.

These researchers used Vpus 'just so story' to discover a new component of the human innate immune system. When most people think of their immune system, they think of antibodies. But there are lots of ways your body can defend itself against viruses without the adaptive immune system. It can be something as simple as your skin (keeps em out!), or something really general like Toll-Like Receptor 3, or pH changes within a cell. So because there are a lot of ways the innate immune system can help get rid of viruses, and there is a very distinct pattern of need/no need for Vpu in different cell lines, these authors thought 'maybe' Vpu was countering one of those innate mechanisms. Here is their initial logic:

Some kinds of cells cant be infected well unless you use an HIV that has Vpu.

Other kinds of cells dont care if Vpu is there or not-- they produce lots of viruses.

Whats different about the protein expression in these two cells?

They used a microarray to identify proteins that were upregulated in cell #1, and not expressed very much in cell #2. This gave them a list of putative proteins that could be interfering with HIV-1 particle release. Then they asked:

Vpu seems to act at the cell membrane, where viruses are budding off. That means that the putative protein should be either in the cell membrane, or secreted.

So they kicked everyone off the list that wasnt a membrane bound protein or secreted. This left them with one possibility-- 'CD317'. So then they asked:

The cells from #2 dont express CD317. If we make them express CD317, do they act like cells from #1?

The cells from #1 express CD317. If we knock down its expression with siRNA, do they act like cells from #2?

The answers to both of those questions is 'YES!!!'

They renamed CD317 'tetherin' and concluded that tetherin is a component of the innate immune system activated by interferon-alpha which interferes with the release of HIV-1 viruses in certain human cells, BUT this inhibition can be overcome by HIV-1 Vpu.

On top of Vpu down-regulating CD4.

On top of Vpu forming super sweet viroporins.

Now its important to note that tetherin is joining lot of other innate anti-viral systems like APOBEC3G (found using the HIV-1 protein Vif) and TRIM5alpha. Its also important to stress that like the APOBEC and TRIM, tetherin isnt a feature unique to humans-- lots of organisms have APOBEC proteins, lots of mammals have TRIM proteins. But, each species particular set of variants, each species restriction abilities, are unique. Comparing different species APOBECs and TRIMs has turned into a fruitful avenue of research.

The publishers at NATURE hope for the same with tetherin-- From a Nature News and Views on this paper:

Because the amino-acid sequence of tetherin differs considerably among mammals, some HIV-1-related animal viruses might find it difficult to overcome human tetherin, preventing them from becoming human viruses. Conversely, it is worth investigating whether tetherin contributes to the inability of HIV-1 to efficiently escape from most rodent cells, which has hampered efforts to develop small-animal models of HIV-1 infection. Even in human cells, Vpu might not always be able to overcome the powerful effect of tetherin, as the release of infectious Vpu-positive HIV-1 can be inhibited with high doses of interferon-. Thus, an understanding of how tetherin works, and how Vpu fends it off, could lead to strategies to limit the spread of HIV-1 and other viruses that target humans.

In six months, evolutions 'just so story' led to new drug targets for new HIV/AIDS therapies, and a brand new avenue of research for immunologists and virologists all over the world.

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Op dinsdag 16 september 2008 23:46 schreef Lambiekje het volgende:

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Zoals je weet worden alle acedemic (in spé) ERNSTIG geindoctrineerd vanuit de industrie. Er is geen objectieve kijk opzaken.

Elke flutwetenschappers praten elkaar na. Als je wel ECHT bezig bent dan kom je er al HEEL snel achter dat het bullshit is wat je aan het doen bent. Maar ja als je dissidente geluiden laat horen dan wordt je carrieredood gemaakt. Dus je houd je mond en pruts maar wat aan.

Vaccines die als de sodemieter van de markt gehaald moesten worden. Ach ja. Lekker in de rondte prutsen.

Woekersubsidies moeten kosten wat kosten geïnt worden voor een MINOR aandoening. Waar maar een paar popper-homos aanleiden. Maar gelukkig is dat nu dan aangekaart dat dat de enige motieven zijn om de leugen in stand te houden.

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Op dinsdag 16 september 2008 23:50 schreef Bommenlegger het volgende:

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Ik weet dat het verspilde moeite is, maar kom jij eens met de namen van de ECHTE wetenschappers.
Ook wist ik niet dat je Lord_Vetinari persoonlijk kent, gezien je uitspraak.

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Op dinsdag 16 september 2008 23:57 schreef Monolith het volgende:

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Namen zijn niet erg relevant. Laat Lambiekje eens komen met een definitie van wat gedegen uitgevoerd wetenschappelijk onderzoek is. Een dergelijke definitie dient uiteraard volkomen los te staan van eventuele conclusies.