Portajon, do you realize that most of those quotes are either of anti-HIV quacks or taken completely out of context? Yes there are people who don’t believe HIV=AIDS.
Many of the people you quoted believe HIV=AIDS, but are taken out of context. For instance, the Sabin quote. All he’s saying is that it is possible to be HIV+ and but not infectious. You can be HIV+ and have a very low virus count…low to the point of undetectability. Such people probably wouldn’t transmit the virus. Or the Baggaley quote. She said that people never officially die of AIDS…the deaths are always attributed to something else without a social stigmata. Other quotes might be accurate but taken from much earlier during the epidemic.
Others are journalists who have no more credentials than you or I do who simply repeat the lies of others. Others are frauds. Others are simply idiots. Others are true believers, but are wrong.
But, you won’t be convinced by anything like “evidence”, will you? Your kind are always the same.
portajon:
It is nice that you can copy and paste web pages. The simple fact of the matter is that the vast majority of scientists sign on to the fact that HIV causes AIDS. The Durban Declaration was signed by 4900 scientists, who pledged their names to a document affirming that HIV causes AIDS. This carries more weight IMHO than several quotes from a few dozen people, some of which may be taken out of context.
Viral culture is performed with HIV-1 all of the time. I don’t understand what this article is getting at – the technique is rather well defined, and can be used to infect new cells, get new virus out, and sequence genomes.
Genotyping by sequencing of HIV is routinely done. In fact, care is often given based on a specific genotype detected by sequencing. This genotype has been correlated with drug resistance, and further clinical course.
Here is an example of an article:
I just don’t understand what the HIV isolation prize is looking for aside from this. It seems to me to be kind of like that $10,000 creationist challenge to unequivocally demonstrate evolution. Every time that one of their goals is neared or met, they just move the goalposts back. Show microevolution, no microevolution does not constitute evolution. This HIV challenge seems to be the same – unless very stringent, exact goals are met, they will not accept that HIV has been “isolated”, even though in reality it has. In all reality, the complete “isolation” of the virus will actually prove nothing, and is not necessary for showing that it causes infection. We detect its genome, we detect its proteins (which can be predicted from the genome), we see the particles, only those people who have the particles and genome and proteins get the disease, none of the people without the genome and proteins and particles don’t get the disease. Open. Shut.
In a quick search, I found a paper that demonstrates HIV particles, infectivity, and the presence of the genome in semen during symptomatic primary HIV-1 disease. The paper is from 1992, so I don’t know what else it doesn’t show:
Ya know, in terms of viruses, HIV isn’t by far the hardest to work with. It is pretty amenable to ex vivo manipulation. Hepatitis B Virus can’t be cultured yet. Nobody is running around claiming that HBV doesn’t cause hepatitis. I wonder what all of the controversy is really about.
Yes my kind are always the same. That is what the word “kind” indicates. Therefore, my “kind” share similar characteristics. I don’t claim that HIV does or does not cause AIDS. My statement was that no one has proven isolation of HIV. From what I understand, isolation is one of the most important steps of truely understanding the nature of a given pathogen. Remember the guys who claimed to have created life (amino acids) in a sterile atmosphere? Everyone jumped on that wagon too. Then it could not be replicated. Just seems to me that someone would replicate the isolation of HIV, collect the reward and put this to bed.
Erm…I don’t want to get off topic here, but cite? Are you talking about the Miller-Urey experiment?
Next, according to your above link, no one has demonstrated isolation of HIV. It was isolated almost simulataneously in the US and in France, by Gallo and Montagier, in 1983, as posted by andros above. I don’t know from which this replication which you speak of.
Erm…I don’t want to get off topic here, but cite? Are you talking about the Miller-Urey experiment?
Next, according to your above link, no one has demonstrated isolation of HIV. It was isolated almost simulataneously in the US and in France, by Gallo and Montagier, in 1983, as posted by andros above. I don’t know from which this replication which you speak of. **
[/QUOTE]
The last time someone asked for cites I was criticized for posting them. “Nice that you can cut and paste web pages”. As for the isolations in '83 and '84, folks on both sides of the argument agree that the isolation did not meet all of the accepted requirements.
Main Entry: ci·ta·tion
Pronunciation: sI-'tA-sh&n
Function: noun
Date: 13th century
1 : an official summons to appear (as before a court)
2 a : an act of quoting; especially : the citing of a previously settled case at law b : EXCERPT, QUOTE
3 : MENTION: as a : a formal statement of the achievements of a person receiving an academic honor b : specific reference in a military dispatch to meritorious performance of duty
synonym see ENCOMIUM
I wouldn’t claim that HBV coesn’t cause hepatitis. I would claim exactly that which you state; “Hepatitis B virus can’t be cultured yet”. Same goes for HIV. It has not been properly isolated. If you belive otherwise prove it.(it is worth alot of money)
Yeah, I wondered about that, too, but I eventually figured out that Willner must have known the press might be checking, so since he already had Almandoz’s permission to pull off this stunt and use his name, he (or Almandoz) probably just gave the receptionist instructions to “tell all” to any members of the press who called, asking for more information.
Well, I won’t adress everything, but here’s a start:
This is false. False false false false false.
It’s been too many years for me to remember the names and details involved, but a virus can lie dormant for years; its genetic material is inserted in the host DNA, and copied whenever the host cell divides. It can then be expressed many times over–budding hundreds of copies from the cell and destroying it.
This is an absurd level of proof, regardless of whether it has in fact been isolated. I can go into the lab and–off the top of my head–whip up ten compounds that cannot be isolated given current techniques. OTOH, I can use a million other methods–NMR, IR, UV-Vis, GC-MS, intermediate trapping reactions, etc–to show what I have. And everyone will believe me, unless the topic is politically charged, and someone has something to gain from telling me I’m wrong.
Hi, welcome to the SDMB! When we ask for a “citation” or a “cite”, we don’t mean just copy and pasting a web page–we mean a link. You can copy and paste the URL of the web page from the address window and vBulletin will automatically make it into a link.
It isn’t enough to just copy and paste text–you also have to show us where you got it from, so we can go look at it for ourselves.
For anyone who wasn’t there, this has been discussed before. Perhaps some of what was brought up there, including the links, might be useful here as well.
OK, I’m gonna take this isolation post apart as best as I can. Lemme know if this is all wasted bandwidth. At least it is a nice review for me.
A retrovirus is a virus which can reverse transcribe its genome from RNA to DNA, and thus cause infection. This sentence does not make sense – no researcher has isolated any particle proven to be a retrovirus because it can replicate itself? I can replicate myself, I am a particle in the scientific sense, yet I am not a retrovirus. We stick HIV into a culture medium, it can infect non-infected cells. Both Gallo and Montagnier infected cord blood lymphocytes in 1983 and 1984. The particle was a demonstrated retrovirus by relation to a number of previously characterized retroviruses, the HTLV family. HIV was shown to replicate its genome, an RNA sequence, through a DNA intermediate in its host cells. The only way known to do this is through a reverse transcriptase, which HIV contains and its genome encodes. The Gallo/Montagnier experiment has been repeated numerous times, and in fact is one of the diagnostic tests for HIV infection used currently (viral culture).
I would like clarification of this because none of my sources on HIV or retroviruses give these criteria for retroviral isolation. The first retrovirus was identified and isolated in 1911, and in 1950 Gross showed that it could cause cancer.
Why? As mentioned before, there are many chemical and biological entities which defy absolute isolation. Everything has contaminants to some degree or another. We can still do experiments though – we can PCR genome fragments, we can isolate proteins, we can evaluate immune reactions. These are all consistent – the infected hosts react to a set of HIV proteins (which ones are particular to the hosts’ immune systems). These proteins are found in HIV isolation. Genomic sequencing reveals ORFs which encode said proteins. By taking the system apart, we have been able to show mechanistically how the proteins interact to cause disease, and by designing drugs against these steps, we can reverse the disease.
But it is specific for reverse transcriptase, which are only found in retroviruses…
I’m sorry but IMHO this is nonsense. The polyclonal response is detected by ELISA rather reliably – in fact it is the primary test for HIV infection. More on this test below. The genes encoding the HIV proteins are consistently PCRed from the HIV genome in infected patients and not in non-infected patients (the viral load test is a quantitative rtPCR count of copies of the HIV genome). In fact, we can now even predict drug resistance based on specific mutations in the reverse transcriptase enzyme. gp41 is a complicated protein with extensive post-translational modification, and a predicted weight means nothing due to this.
This confuses an issue terribly. What I think the issue is here is that everybody’s immune system is different, due to a well-researched process of immune development which is unique in every person. Everyone forms different antibodies, which have different avidities and affinities for specific antigens. Thus, every immune response is different. One of the ways to detect the immune response to HIV is by Western blot. Therefore, it is to be expected that the Western blot results are non-homogenous. In fact, the tests to detect HIV are not really optimal – the ELISA, the first line test is highly sensitive but not specific. This means you will catch a HIV+ person, but you will get many false positives. The Western blot has a complicated readout because of heterogenous immune response, but basically the result is negative or positive or a large range of indeterminate. It is highly specific – a Western blot positive nearly assures HIV+ – but can be quite indeterminate. There are many protocols based on biostatistics for getting around this common phenomenon of ELISA+ and Western blot negative/indeterminate.
Basically, you run an ELISA first. If negative, you can most probably rule oout HIV unless it is in a 3 month window after primary infection. If ELISA positive, you must confirm by Western blot to get rid of false negatives. If Western blot negative, the ELISA was false positive. If Western blot indeterminate, repeat in 1 month or go to another test (p24 antigen capture or RNA assay or HIV DNA PCR). Got it?
Yeah, but it has since been isolated from the HIV particle through PCR. Obtaining enough virus to do high-throughput sequencing would be phenomenally hard, but IIRC it has been done with dental samples. If requested, I can provide cites.
This is also misleading. The HIV genome is relatively complex, with overlaying open reading frames (ORFs) which have only recently been characterized. The genes further encode many proteins. The genes, as I see it are gag, pol, env, tax/rex (1 message, so I am calling it 1 gene, others have called it 2), tat, rev, nef, vif, and vpr. I count 9 genes. Counting genes is hard, as the genes are overlain and the messages are polycistronic and alternatively spliced to hell and back.
The core parts of HIV stay the same in any infection-capable virus. One of HIV’s tricks, though, is that its reverse transcriptase which it uses to replicate its genome is very very error prone. Therefore, there are many serotypes in every infected person. Not all of these are infection-compotent. High mutation rate speeds the process of drug resistance tremendously. Missing only a few doses of anti-retrovirals can lead to the long-term development of drug resistance in several key genes. Saying something varies 40% also doesn’t tell which part varies 40% – the 20% sequenced of open reading frame could be 100% conserved, while the other 80% of spacer sequenced could vary 50%. This wouldn’t affect the virus’s performance at all.
As I have said above, the key parts of the virus are untouched. Many of these parts are what our antibodies detect – the env proteins which bind to human cells, the replication machinery, the cell entry machinery. This stuff has to stay constant in order to work, so much of the immune response outside of individual variation, like I talked about above, is relatively constant. Therefore, we can use ELISA and Western blot. I would like to remind the author that there is no such thing as one “human DNA” or one “human genome” so it is not surprising that there are so many HIVs out there.
I don’t know what the last sentence means. All molecular cloning refers to is the copying of a segment of DNA into a form which can be easily replicated, for instance plasmid or bacteriophage. Since sequencing generally requires cloning, detecting a unique stretch of cDNA generally requires cloning.
I have grown tired of doing this. If there is significant interest in me debunking the rest of the post, I will do so. FWIW, though, most of the rest of the post deals with specific detection errors in different HIV tests. These mean absolutely, positively nothing, as I have demonstrated above:
Each HIV test is imperfect. Some have high sensitivity but low specificity, meaning that they can catch nearly every case of the disease but also get tons of false positives. Others have low sensitivity but high specificity, meaning that they may miss many cases of infection but if they are positive, there are almost no false positives. SpIN (Specificity to rule a disease IN), SnOUT (sensitivity to rule a disease OUT). This is why we follow clinical algorithms – we first aim to rule a disease out, although we get many false positives, and then move to weed out the false positives.
OK portajon, in following what andros said, let’s try to keep the discussion going, cause I’m afraid that my last post may very well kill the thread.
Can you define “virus isolation” for me?
Can you define “virus culture” for me?
How do the two differ? What needs to still be done in order to show a good “virus isolation”?
Thank you for your time and explanation Edwino. I understand a good deal of this but some of it is over my head. I would like to hear more about the contaminents and how they may affect testing and the actual cultures. Is it not possible that without pure isolated HIV that the results could be adversely affected by the contaminents within? And you fail to cite any other viruses that defy isolation, cite? Moreover, I can study the credentials of the biologist who refute the isolation, and therefore the assunptions about cultures etc., while I have no idea who you are. Why should your jargon be anymore appealing to my sense of credibility than theirs?