[NRC] AIDS epidemie in Afrika is bedrog

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Op dinsdag 16 september 2008 13:29 schreef Lambiekje het volgende:

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Yo wat een blaaskaak ben je

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Op dinsdag 16 september 2008 13:29 schreef Lambiekje het volgende:

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Yo wat een blaaskaak ben je

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Op maandag 15 september 2008 16:22 schreef DiRadical het volgende:
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Kan ik ook zo'n verhaal verwachten over Global Warming en het IPCC.
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Op dinsdag 16 september 2008 15:08 schreef One_of_the_few het volgende:
Lambiekje is zo figuur voor wie de wereld niet spannend genoeg is zonder doemscenario's en wereldwijde complotten.

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Op dinsdag 16 september 2008 10:51 schreef Monolith het volgende:

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Leuk zo'n linkje, heb je enig benul wat er daadwerkelijk staat? Voornamelijk onzin eigenlijk. Ze beginnen met het citeren van een onderzoek van Yates et al. Daarbij halen ze resultaten en conclusies even door elkaar, maar dat zien we dan nog maar even door de vingers. Hier de abstract waaruit ze citeren:
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Ze citeren de 'Findings' uit bovenstaande abstract en stellen "Vrij vertaald: HIV is niet verantwoordelijk voor AIDS, er moet iets anders zijn dat de instorting van het immuunsysteem veroorzaakt.". Vrij vertaald is erg zacht uitgedrukt. Hier is weer duidelijk de parallel tussen dit soort idioten en creationisten te zien. Men heeft geen flauw benul van de materie, dus de gangbare methode 'Dit lijkt kritiek te leveren op HIV / AIDS, dus het zal wel aantonen dat HIV / AIDS niet bestaat' wordt gehanteerd. Dat doen creationisten ook vaak. "Deze publicatie levert kritiek op een specifieke klein punt in de moderne evolutionaire synthese, dus evolutie zal wel onzin zijn". Maar goed, als men op zapruder nou eens gewoon alleen al de conclusie in bovenstaande abstract had gelezen, dan had men het volgende kunnen lezen in de conclusie:
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Op dinsdag 16 september 2008 15:25 schreef Monidique het volgende:

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En alles heeft altijd met elkaar te maken. Het is niet zo dat iemand denkt dat AIDS een samenzwering is. Nee, zwarte helikopters, 9/11, de Reptilians, verarmd uranium, oliepijpleidingen, wereldregeringen, Bush (alle vijf incarnaties), de NAVO, de VN, de EU, graancirkels, ze hebben er allemaal mee te maken...

...en natuurlijk bouwden aliens de pyramiden, die by the way geheimzinnige krachten bezitten. Ze bouwden andere gebouwen. Van steen. Nu zijn er ook nog aliens, ontvoeringen, heeft ook weer overal mee te maken. Grootschalig geheim experiment.

En wie weet, voor veel van hen is inderdaad de CO2-HOAX!!!1 ook een middel om de wereldbevolking te indoctrineren en controleren.

Lees meer over deze ultrageheime, topsecret eeuwenoude vrijmetselaarssamenzwering op www.geocities.com/TheRealTruthDisclosed.

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Op maandag 15 september 2008 19:57 schreef Lambiekje het volgende:

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Bestaat wel, is alleen buitensporig en oncontroleerbaar geworden door verplichte polio vaccinatie programma en pokken vaccinatie

Dus kort door de bocht gezegd, kanker is express uitgezet.

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Op maandag 15 september 2008 19:47 schreef Lambiekje het volgende:

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+ westerse homo

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Op dinsdag 16 september 2008 19:00 schreef Lambiekje het volgende:

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Dat van Monolith dat slaat noch wal noch kant. Zo blabla in de rondte.

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We have used a simple and robust model to reject a mechanism for CD4⁺ T cell decline in chronic HIV infection. However, the model has two key limitations. First, while it distinguishes between quiescent and proliferating memory CD4⁺ T cells, it neglects other potential sources of phenotypic heterogeneity within this population with respect to activation, proliferation, and death. Second, it assumes that cells’ replicative capacity remains intact after repeated rounds of stimulation. Chronically stimulated cells may become senescent and progressively lose their ability to proliferate or survive. With these caveats in mind, we can still use the model to frame alternative hypotheses for the mechanism driving the set point in the chronic phase of infection slowly towards an AIDS state. Many hypotheses have been discussed in the literature, all of which involve proposing an additional slow process in T cell population dynamics. We summarise them below in the context of T cell homeostasis.

Exhaustion of CD4⁺ subpopulations. Chronic stimulation
may drive the accumulation of a heterogeneous population of T cells exhibiting a nonresponsive or exhausted phenotype, with higher susceptibility to apoptosis and reduced proliferative capacity [50]. This phenomenon is observed among responding T cells in other persistent viral infections, but may also occur among nonspecific (bystander-activated) CD4⁺ T cell populations in HIV infection. In Text S1 we show how an extension to the model of a low constant rate of differentiation of stimulated cells into an exhausted state can generate a slow decline in total T cell numbers.

Virus evolution.
Increasing the efficiency of infection, p, lowers the memory CD4⁺ set point in our model (Figures 3 and 6), suggesting a mechanism of decline in which progression is driven by slow adaptation of the virus, as has been proposed previously [51]. The infectivity p is a compound parameter representing at least two distinct quantities: the probability of productive infection upon encounter between a virion and a susceptible T cell, and (ii) the dependence of plasma virion density on infected cell numbers. The first may change over the course of an infection through a switch in coreceptor usage [52,53] or perhaps changes in receptor expression of chronically stimulated populations. The second may be influenced by virus adaptation (e.g., increases in the numbers of virions produced per infected cell) or the rate of clearance of free virions by antibodies, which may fall as new mutants emerge and/or the availability of T cell help wanes. These processes could be distinguished by assessing whether virus in patients in the chronic phase of infection shows an increasing capacity to infect host CD4⁺ T cells ex vivo over time. We note that this measure of fitness is not necessarily related to virus diversity. Clinical evidence is conflicting in this regard, and the association between diversity and progression is unclear [54–56]. A further possibility is that within-host virus evolution causes a progressive increase in the per capita rate of immune or bystander activation. As can be seen in Figure 7, our model predicts that increasing this rate will lower the steady-state number of memory CD4⁺ T cells.

Failure of immune surveillance.
Impaired T cell help and/ or CTL exhaustion may decrease the rate of recognition and killing of infected cells by CTLs (contained in the rate constant v in the model above) over time [57]. Thus despite the low frequency of infected cells, changes in the efficiency with which they are removed can produce an impact on the T cell compartment as a whole. CTL killing can now be quantified directly in vivo [58] and longitudinal measurements of killing rates may help us to assess whether declining CTL function drives progression. However, this potential mechanism shifts the problem to explaining the slow rate of CTL exhaustion in HIV infection, which is faster in other chronic infections [59].

Attrition of homeostatic resources.
Homeostasis may be impaired in HIV infection due to damage to lymphoid architecture [3,60]. Thus chronic inflammation may progressively lower the homeostatic set point by diminishing the availability of T cell proliferation or survival signals. Our model predicts that in the absence of HIV infection, CD4⁺ memory numbers increase with the activation rate a— however, they fall with increasing a and a* in the presence of HIV, as activation renders more cells susceptible to infection and destruction. This prediction implies that if destruction of lymphatic infrastructure is the source of memory CD4⁺ T cell decline in HIV, its dominant effect on T cell dynamics must be to increase the death rate of activated cells l. The dynamics of activated cells strongly dictate the dynamics of the pool as a whole; the model predicts that increases in the average death rate of activated cells l by as little as a factor of two above healthy levels can lead rapidly to profound depletion in the steady state memory T cell numbers.

Immune hyperactivation.
As we have shown, IA in the presence of HIV can cause a reduction in the set point memory CD4⁺ cell numbers, but the set point for a given level of IA is attained too rapidly to explain the slow depletion of these cells. However, our model predicts that a slow, progressive increase in the per capita rate of activation could cause a downward drift of the set point. Alternatively, and perhaps more plausibly, the immune hyperactivation and heightened homeostatic proliferation may drive a slow increase in the average death rate in the memory population through senescence or exhaustion, as described above [50,61].

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Additional information, however, comes from the phenomenon of viral rebound—after cessation of ART, the rapid increase of viral load and decline of CD4þ counts in peripheral blood to approximately pretreatment levels [62]. Assume that treatment drives the infectivity parameter p from an initial value p0 to a value close to zero, and markedly reduces levels of IA (a* in the models above), which is likely to be an increasing function of the viral load and/or p. If reservoirs of latently infected cells persist during treatment, retaining a representative memory of the pretreatment virus population, the virus adaptation model predicts that allowing viral replication to restart will drive the memory CD4þ numbers quickly—on a time scale of weeks—to the pretreatment set point determined by p0, a*, and the remaining (constant) homeostatic parameters. Other models predict the rapid return to the previous set point only if the homeostatic parameters remain constant during treatment— that is, if there is not significant recovery of CTL function or repair of lymphoid architecture or T cell regenerative capacity while virus replication is suppressed.
Clearly the virus adaptation model is not the whole story. Assuming treatment effectively abrogates the production of virus, this model predicts the full reconstitution of the T cell memory compartment during sustained treatment, which is not usually observed. This discrepancy between the virus adaptation model and the observations implies an additional role for lasting impairment to homeostatic mechanisms in HIV infection, perhaps from attrition of homeostatic resources or through differentiation (senescence or exhaustion).