Continued from post above.
MYTH 3: HIV has never been reliably identified
This myth is perhaps the most easily debunked. There are multitude of electron micrographs in the public domain showing HIV. Here are a few: [8], [9],
[10]. Perhaps the most interesting of these three pictures (in my opinion, at least), is the third. It shows a mature HIV particle budding from a
human lymphocyte, which is clearly distinguishable by the nature of the granules inside the cell plasma. This picture not only provides a glimpse into
the microstructure of the virus, but it clearly demonstrates the virus's ability to infect and reproduce within lymphocytes. This reproduction is a
common mechanism used among virsues, and often leads to the destruction of the host cell, which in this case is usually a CD4 Helper T-cell. This
destruction is the reason AIDS is defined as a CD4-count below 200. The virus targets CD4 cells for destruction (as demonstrated in this picture, as
well as in the studies accompanying those pictures), which eventually leads to a immunodeficient state, or AIDS.
MYTH 4: ANTIVIRAL THERAPY CAUSES AIDS, NOT HIV
This section, unfortunately, I have to use my drug reference manual as a reference. I'm unable to find a resource as thorough and accesible online.
If you have any issue with the information provided, PLEASE reply or send a U2U, and I will do my best to find an online source for you, I promise!
Examining the nature of antiretroviral drugs (those specifically given for HIV) very clearly demonstrates that such an adverse effect is simply not
possible. There are several classes of these drugs [11], and I'll do my best to explain each one succintly, as well as why it could not produce an
immunodeficient state:
(1) Nucleoside reverse transcriptase inhibitors (NRTIs): nucleosides are DNa bases that lack the functional group necessary for elongation. The NRTIs
are made specific to the sequence of the HIV genome, thus they can incorporate into the newly synthesized DNA, made while HIV is trying to integrate
into C4 T-cells, and interrupt the elongation of that DNA. As the HIV genome sequence does not exist in human genomes in any form, cross-reaction
between human DNA and the nucleosides is unlikely.
(2)Non-nucleoside reverse transcriptase inhibitors (NNRTIs): rather than inserting into the viral DNA and preventing elongation, these drugs bind
specifically to the viral reverse transcriptase enzyme and stop it's function. This enzyme does not exist in the human genome, nor does any
homologous enzyme, so cross-reaction is impossible and cannot cause immunodeficiency.
(3)Protease Inhibitors (PIs): protease inhibitors target the viral machinery used to clip and shape proteins (specifically, glycoproteins) into the
form used to create the viral capsid. Without protease, mature HIV cannot be formed, and spread of infection is not possible. The proteases are
specific to HIV, and thus, cross-reaction with human proteases is not possible.
(4)Fusion Inhibitors (FIs): fusion inhibitors interfere with the proteins/receptors used by HIV to fuse to CD4 cells prior to entry into the cell.
These receptors are specific to HIv and do not interefere with normal CD4 or CD8 function, thus no immunodeficiency is possible due to this drug
class's action.
(5)Integrase inhibitors: integrase inibitors target the viral machinery (other than reverse transcriptase) that allows the viral cDNA to insert into
the host cell's genomic DNA. Preventing this integration stalls the replication of the virus. As there is no machinery for such an integration in the
native human cell, no cross-reaction is possible.
In addition to these, there are a few lesser-used classes that are rarely used alone, more often being supplmental to the classes above.
Now, as a final note about these drugs, I think it should be noted that HIV is now considered a chronic disease by medical professionals. It is viewed
in the same way as diabetes: through careful management, you can live a long and (relatively) healthy life. The life expectancy for HIV patients has
SKY-ROCKETED since the intoduction of combination anti-retroviral therapy. If these drugs were the cause of AIDS, wouldn't we see the opposite?
Wouldn't HIV patients be seeing a constant DECREASE in life span as new drugs are produced and higher/tougher regimens are prescibed? The fact is, we
don't see this effect, so suggesting these drugs cause AIDS is illogical and without merit.
Closing Remarks
I apologize for a post (or two) of such length, but as you can see, I've put quite a bit of time, effort, and research into this topic, partially
from a person/professional interest, and partially because I am absolutely exhausted from repeating this information ad infinitum on these boards in
piece-meal format. I have saved the entirety of these two posts, and will use them as constant references in future threads on the topic.
If anyone has ANY questions regarding the information in these posts, or if a reference is broken/missing, please post a reply or send a U2U. I will
be more than happy to answer anything that is not a personal attack on myself or my profession. Any such attack will warrant an immediate ALERT as a
violation of the ATS terms and conditions. I've done it before, and I'll do it again, I promise you.
Source
[edit on 4/9/2010 by VneZonyDostupa]
[edit on 5/11/2010 by Sinter Klaas]