Posted on 12/14/2011 4:59:02 AM PST by James Oscar
MA: Do you read the many threads that have to do with pandemic preparedness and all the reports of exotic diseases that pop up worldwide?
Q: From time to time.
MA: Well they are watching. Not only those fine folks but there is a survivalist movement in our country that grows steadily with new converts.
In fairness, they will all tell you they are watching for something different. Some are looking for financial collapse, some are looking for totalitarian government movements, and some are looking for plagues, earthquakes, and the end of time.
But many are those who are watching.
I am not the only person with the nagging feeling that there is something very dark on the horizon.
Q: But your interpretation of these dark clouds is tied into your vocation. Could it be that the reason you fear an outbreak - is because that is the subject you know best?
MA: Of course it is possible, anything is possible. I suppose the smart money would be betting on me just being the crazy lady in the big house. But that does not change the story that I am telling you. These events are my understanding of our immediate future and are not the result of any external influence.
Q: Fair enough. You say that because the HIV virus is already pandemic there is little we can do to stop the “coming wave”. How can that be true?
MA: We have fought against the HIV virus for over thirty years and yet it continues to march forward - were this organism to change its virulence the sheer scope of that event would be overwhelming.
Q: And you fully believe that transformation is coming?
MA: It is imminent.
You are quite welcome. I started to write about the origin of the flu blogs, but the history was so compelling that I ended up writing something far different.
Art has a mind of it’s own.
You are welcome,
Don’t I recognize your name from the SARS threads?
Ron
Plus if James just posted a link and an except, you’d be calling him a blog pimp.
No I would not...I don’t care who blogs or not. So you’ve jumped the gun here.
Ok, sorry for jumping the gun. Others on this forum would with out a doubt.
Yep..I agree...like stiring a pot of sludge and all the crap comes to the surface. No "Spring" about it....it's a cesspool of the likes the world has yet to see. Again there was a reason God kept the Arab nations isolated/contained for centuries.
This whole idea of international trade and "universal" appraoch to life worldwide is more than concerning. Reminds me of the Tower of Babel where the nations leaders now think they can build a one world system of distribution, and or not distributing as they see fit.
God seperated the people for a reason.... "distinctions" of cultures is a good thing. Trying to have every nation "westernized" in all ways is playing with dynamite.
Not only are the diseases crossing borders, but religious practices, all being incorporated into the communities as "partners" one to the other. It's a dangerous thing to attempt to undo what God established...and there will surely be the price to pay as this "thing" gains more and more momentum on the International stage and here at home.
As for blog pimps...I really have no problem with them...as long as the articles are interesting....and I think we need them, for some news we need to know will only get to us thru them.
MA’s thesis is not that HIV will mix with H5N1, but rather that HIV has been permeating all cultures and regions and is trying to break out (become airborne).
HIV is one of the most mutanaginic bugs on earth and soon one of those mutations will be able to be expelled by an infected person and ride the cough to another's lungs - a very deadly event.
Her point is that because of all the eyes watching for the H5N1 virus in Egypt - it will be the first place where we will notice the outbreak (because of the similarity of symptoms it will misdiagnosed as H5N1)
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Page #62
Q: Ma if you are not sure how it changes then how can you be so certain it will be dangerous?
MA: Well, it is not so black and white as you make it. What I believe is that it will change. It will go airborne and it will become quick and deadly. When it makes that magic mutation that gives it the ability to ride the water droplets expelled in a cough or sneeze to the lungs of a healthy person - not only will it have found the mechanism for rapid transmission but the mutation will also set in motion a very different chain of events from what we know now.
When the new HIV virus arrives in the lungs of a new patient there is the great potential for a positive feedback loop to be established between the new invader and the host's immune system. At the arrival of the new pathogen, cytokine will signal the body to send T Cells to fight the infection. The T cells, upon being stimulated by the cytokine will begin to produce even more cytokine.
This is the normal reaction and happens all the time. But we have a real problem don't we?
Q: HIV lives on T cells?
MA: Yes of course. So now we have the feedback loop. T cells rushing to the lungs where they are infected with new virus and more and more cytokine being produced by the body. The result is called a “Cytokine Storm”. The lungs begin to fill with fluids and immune cells. The result is sudden death. When this event takes place in the lungs, it can kill a healthy young person in less than 48 hours. We learned this lesson in the 1918 flu outbreak.
Q: So the hardy virus can jump from lungs to lungs and once there put in motion a very serious reaction that will kill you rather quickly. Is that about it?
MA: Just about, the only addition I would add is that once the new bug creates this “soup” in the lungs - with each cough or sneeze this deadly pathogen is sent on an airborne journey looking for a healthy lung to infect.
The HIV virus has crossed all borders and lies buried in the bodies of millions of humans in every region on earth.
As you say containment is not an option.
Great post. I will try to pretend to understand give a reasonable answer.
There is a bit of confusion about the flu and HIV (I hope it is not in my writing).
There is no part of her thesis that hypothesizes that influenza and HIV will join or swap genes.
Her concern is that under no circumstances should we be messing with the nerumindase in a HIV infected patient.
Boosting, inhibiting - nothing!
She explains that neuraminidase is a known mutanagenic enhancer for HIV and it is stupid to be messing with it in a patient who is HIV positive.
HIV is already a mutant producing machine, making zillions of variations daily trying to break out.
And to purposefully administer any drug that disrupts neuraminidase regulation in a HIV carrier is suicide.
I can understand what you mean as the night the Global Warming e-mails were dumped I was on line and in the heat of it as bloggers and scientists came together in the dead of night. I followed it all as they wanted confirmation...shared what was coming out...etc. I'll never forget it and didn't sleep at all that night.
That's why I am not opposed to bloggers etc. Although some can muddy the waters in a crisis most are very good at attracting people of brillant minds who can filter the false from the real. In a crisis they have little time to give the bogus stuff any mind so those fall off the speed the internet takes in getting the facts out as the information comes in. In no time the sites where the truth of the matter is and dilogue about rises to the top.
Though of course a pandemic is another story altogether as dealing with life matters and something which one can't necessarily see to fight.
You say the HIV virus has already infiltrated every nation and thus many who are carriers. I thought one could be tested for this? I know surgeons who require such a test before they will do surgery.
“I do wonder about these virus’s coming into our nation from other countries.”
I do chuckle at that. It’s been like that always, however now as with everything, things happen much much quicker and it’s much easier for things to get here and there.
Thanks for the clarification on this. So what we should be watching for is events where it looks like flu but tests aren't positive for flu.
However, he tested negative for H5N1 in a polymerase chain reaction test conducted by the hospital.
Precognition? Dunno, but females are fraught with what they deem intuition. I'll concede there's something there that needs discovery.
First off the bat:
I'm going to toss this out there, as the issue of "superinfection" was broached:
ABSTRACTSecondly, despite the purported avian intestinal tissue-philic nature of avian influenza, avian influenza is not restrictive to such with respect to the scope of its tropism. Researching influenza specific tropism stumbled me upon the following:
Enveloped viruses use multiple mechanisms to inhibit infection of a target cell by more than one virion. These mechanisms may be of particular importance for the evolution of segmented viruses, because superinfection exclusion may limit the frequency of reassortment of viral genes. Here, we show that cellular expression of influenza A virus neuraminidase (NA), but not hemagglutinin (HA) or the M2 proton pump, inhibits entry of HA-pseudotyped retroviruses. Cells infected with H1N1 or H3N2 influenza A virus were similarly refractory to HA-mediated infection and to superinfection with a second influenza A virus. Both HA-mediated entry and viral superinfection were rescued by the neuraminidase inhibitors oseltamivir carboxylate and zanamivir. These inhibitors also prevented the removal of α-2,3- and α-2,6-linked sialic acid observed in cells expressing NA or infected with influenza A viruses. Our data indicate that NA alone among viral proteins limits influenza A virus superinfection.1
Poor human-to-human transmission of influenza A H5N1 virus has been attributed to the paucity of putative sialic acid α2-3 virus receptors in the epithelium of the human upper respiratory tract, and thus to the presumed inability of the virus to replicate efficiently at this site. We now demonstrate that ex vivo cultures of human nasopharyngeal, adenoid and tonsillar tissues can be infected with H5N1 viruses in spite of an apparent lack of these receptors.2Background
Avian influenza virus H5N1 is a major concern as a potential global pandemic. It is thought that multiple key events must take place before efficient human-to-human transmission of the virus occurs. The first step in overcoming host restriction is viral entry which is mediated by HA, responsible for both viral attachment and viral/host membrane fusion. HA binds to glycans-containing receptors with terminal sialic acid (SA). It has been shown that avian influenza viruses preferentially bind to α2,3-linked SAs, while human influenza A viruses exhibit a preference for α2,6-linked SAs. Thus it is believed the precise linkage of SAs on the target cells dictate host tropism of the viruses.Results
We demonstrate that H5N1 HA/HIV pseudovirus can efficiently transduce several human cell lines including human lung cells. Interestingly, using a lectin binding assay we show that the presence of both α2,6-linked and α2,3-linked SAs on the target cells does not always correlate with efficient transduction. Further, HA substitutions of the residues implicated in switching SA-binding between avian and human species did not drastically affect HA-mediated transduction of the target cells or target cell binding.Conclusion
Our results suggest that a host factor(s), which is yet to be identified, is required for H5N1 entry in the host cells.3In the Results section of the paper cited above, it is stated "H5N1 HA can mediate HIV pseudoviral infection", QED.
To alleviate the safety concerns in characterizing the entry mechanism of highly pathogenic avian influenza virus H5N1, we sought to develop an human immunodeficiency virus (HIV)-based entry assay, a surrogate system widely used for entry studies of other highly pathogenic enveloped viruses such as Ebola virus. To generate the HIV pseudovirions, a mammalian expression vector pcDNA-3 containing the hemagglutinin (HA) gene which was derived from a highly pathogenic H5N1 from dead birds in Qinghai Lake, China, referred to as HA(QH) in this report, was co-transfected with an env-deficient HIV vector, pNL4-3-Luc-R--E-, in 293T producer cells. Western blotting analysis of the media collected from the 293T cells 48-hours post-transfection indicated that HA(QH) was efficiently incorporated into the HIV viral particles...That notwithstanding, the foregoing should be set aside to consider the following:...[The] results indicate that this highly pathogenic H5N1 virus can enter numerous human cells including those derived from human lungs more efficiently than that in the two avian cell lines, suggesting that the HA protein of H5N1 can effectively interact with the cognate cellular receptor(s) on human cells to initiate viral infection. Furthermore it appears that other viral and/or human determinants, rather than HA, restrict efficient transmission of H5N1 to humans in a sustained manner. Therefore we believe that while the H5N1 virus still needs to acquire the ability, either through mutations or genomic re-assortment or both, to produce sustained infection in humans, it appears that this final step for the virus to overcome is at the post-entry level...4
"...Human flu virus has the capacity to interact with and infect human macrophages and lymphocytes, two mononuclear cell types known to harbor HIV-1. In patients infected with flu virus, viral replication is occurring on the mucosal surface of respiratory tracts and virions are also found in mucosa-associated lymphoid tissue that is also one of the natural reservoir of HIV-1, therefore suggesting the possible co-localization of both pathogens at the same site. Although previous studies have indicated that influenza vaccination could increase HIV-1 viral loads, a recent study has indicated that influenza infection did not alter HIV-1 viral load or the rate of CD4+ T cell decline or clinical progression. However, no study has directly addressed the role of flu-derived NA on the HIV-1 replicative cycle. In the present work, we provide evidence suggesting that flu NA either as purified enzymes or as virus-associated augments the processes of HIV-1-mediated syncytium formation and virus infection..."5
For some readers the immediately following may prove illuminating before considering the findings of the above researchers presented thereafter:
HIV infects CD4+ T cells and makes the cell produce viral proteins, including fusion proteins. Then, the cell begins to display surface HIV glycoproteins, which are antigenic. Normally, a cytotoxic T cell will immediately come to "inject" lymphotoxins, such as perforin or granzyme, that will kill the infected T helper cell. However, if there are nearby T helper cells, the gp41 HIV receptors displayed on the surface of the T helper cell will bind to other similar lymphocytes. This makes dozens of T helper cells fuse cell membranes into a giant, nonfunctional syncytium, which allows the HIV virion to kill many T helper cells by infecting only one. - Syncytium (from the Wiki)"...In this report, we have initially tested the modulatory role of purified flu NA on HIV-1-mediated syncytium formation and cell-free virus infection. We showed that treating cells with flu-derived NAs remarkably augmented the initial cell-cell interaction and thereby promoted HIV-1-mediated cytopathic effect (i.e. syncytium formation). We have also noticed that desialylation of target cells increased susceptibility of target cells to infection with cell-free HIV-1 particles. Here, we demonstrate for the first time that virion-associated flu NA exhibits a similar enhancing effect on HIV-1-mediated syncytium formation and cell-free virus infection.
In our in vitro experimental systems, studied target cells, including freshly isolated PBMCs, were more prone to HIV-1-mediated syncytium formation in the presence of either purified flu NA enzyme or different strains of UV-inactivated flu virus that bear NA activity. The flu NA-dependent up-regulating effect on HIV-1-induced syncytium formation is likely to occur through a mechanism involving the removal of sialic acids from the cell surface as zanamivir, a specific flu NA inhibitor, suppressed the observed up-regulation. Sialic acid content is one of the key elements regulating cell-to-cell contact and desialylation caused by flu NA enzymatic activity results most likely in a higher rate of intercellular interaction, which eventually increases HIV-1-mediated syncytium formation. Given that our results demonstrate that flu NA treatment increases the intercellular interaction of a number of cells including PBMCs and T cells, the presence of NA-producing microorganisms in local lymph tissues could increase the stability of cell-cell interactions, thereby promoting transmission of HIV-1 between susceptible cells.
Besides HIV-1-mediated syncytium formation, purified flu NA was also found to affect the process of cell-free HIV-1 infection in several different cell source, an increase in infection which was zanamivir-sensitive. Because transcriptional activity of HIV-1 LTR region in 1G5 cells was not modulated by purified NA, it can be postulated that NA is primarily affecting the early steps of the HIV-1 replication cycle. Experiments conducted with single-cycle luciferase reporter viruses supports the idea that flu NA is most likely affecting the initial events in HIV-1 life cycle. It should be noted that desialylation by bacterial-derived NA has also been observed to promote HIV-1 attachment and entry (15, 17). Such a modified interaction between target cells and HIV-1 particles in the presence of secreted NA by surrounding NA-producing pathogens might have a profound impact on HIV-1 spreading and infection. For example, a more rapid and stable binding of virions to susceptible cells under in vivo conditions will likely positively affect the HIV-1 attachment process.
Most studies, which were aimed at defining the effect of NA on HIV-1 biology, were using purified soluble NA derived from various pathogens of bacterial origin. It can therefore be questioned whether the amount of NA released by or associated with such microorganisms are in the same order of magnitude as the concentrations of purified NA used in these experimental studies. Besides, NAs of several pathogens, including human flu virus A and B, are membrane-associated. Thus, the validity of the data obtained with purified soluble NA remains questionable and might not be representative enough to deduce the exact role played by membrane-bound NA on the biology of HIV-1 in patients dually infected with HIV-1 and NA-bearing pathogens. We therefore assessed whether flu-anchored NA would exhibit a similar positive effect on HIV-1 replication. This specific issue was addressed by using several flu virus isolates that were inactivated by UV treatment to eliminate possible expression of flu-encoded protein(s) within studied cells. This is founded on a previous report showing that expression of flu virus hemagglutinin in mammalian cells induces activation of NF-κB, a transcription factor recognized as a powerful activator of HIV-1 transcription. Whole UV-inactivated flu viruses were first confirmed to harbor NA enzymatic activity on their surface but importantly were also capable of potentiating HIV-1-dependent giant cell formation and HIV-1 replication in both T cell lines and PBMCs. Both of these events were furthermore positively modulated by flu viruses in a zanamivir-sensitive fashion.
On the basis of these latter results, it could be postulated that an effective treatment against flu infection in HIV-1-positive individuals might be beneficial for such patients. However, previous observations have reported that flu infection in HIV-1-positive individuals did not alter HIV-1 viral load or clinical progression. In fact, because the flu virus is mainly localized in the upper respiratory tract, such interaction between this virus and HIV-1 target cells might not be sufficiently predominant. However, one important related issue concerns the safety and risk-benefit ratio of flu vaccination of HIV-1-infected adults, which is still a matter of debate because of the controversy surrounding putative changes in plasma levels of HIV-1 RNA following vaccination of HIV-1-infected patients against flu. It is plausible that this risk could be even higher with the use of live-attenuated flu vaccines in light of our results..."6
The money summary is this
Our results thus offer a model by which the interactions of NA-bearing pathogens with HIV-1 can be studied. Although in vivo, such interactions between flu viruses and HIV-1 are less likely to occur, other pathogens, which represent opportunistic infectious agents and which are NA-positive, could be tested in our cell lines model for their effect on HIV-1 replication and virus-mediated syncytium formation. In addition, the in vitro activity of zanamivir against flu NA-mediated positive modulation of the HIV-1 life cycle in our system calls for discovery and potential use of NA inhibitors of other NA-producing pathogens known to be frequently detected in HIV-1-infected individuals.Furthermore (and finally)8:In summary, our findings indicate that human flu virus through the enzymatic activity of NA, one of the two surface glycoproteins of this virus, accentuates syncytium formation and infection by HIV-1. A specific inhibitor of flu NA (i.e. zanamivir) was used to successfully block flu NA-mediated enhancing effect on HIV-1 life cycle. These findings should provide a new model, which has direct physiological relevance because microbial pathogens that produce NAs as virulence factors may affect HIV-1 pathogenesis via desialylating effect of these enzymes. In addition, we are presently studying the use of the ex vivo tonsil fragment model to study the impact of NA-bearing pathogens on HIV-1 replication. Through the results from the presented flu virus model, potent specific inhibitors of NA might be considered for the treatment of patients suffering from infection with HIV-1 and NA-encoding pathogens.7
OBJECTIVE:
To characterize the clinical presentation, course and mortality of pandemic influenza in HIV-1-infected patients in Santiago, Chile.
METHODS:
Prospective observational study.
RESULTS:
Thirty patients were included (three hospitalized), 93% were on HAART, mean CD4(+) cell count was 423 cells/μl and viral load was undetectable in 77% of patients. All patients had fever, 90% had cough, 80% had myalgias, 70% had pharyngeal congestion, 47% had coryza, 47% had odynophagia, 37% had headache and 23% had vomiting. Four patients developed pneumonia. All patients received antiviral therapy and no patient died.
CONCLUSIONS:
HIV patients infected by the new influenza A pandemic (H1N1) virus behave similarly to the general population.
Affiliation
Department of Medicine, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile. cape@med.puc.cl
======================================== Notes:
1) Influenza A Virus Neuraminidase Limits Viral Superinfection, by Chueh Huang, Wenhui Li, Jianhua Sui, Wayne Marasco, Hyeryun Choe, and Michael Farzan; First published March 2008, doi: 10.1128/JVI.00079-08 J. Virol. May 2008 vol. 82 no. 10 4834-4843
2) Tropism of avian influenza A (H5N1) in the upper and lower respiratory tract, J M Nicholls, M C W Chan, W Y Chan, H K Wong, C Y Cheung, D L W Kwong, M P Wong, W H Chui, L L M Poon, S W Tsao, Y Guan & J S M Peiris; Nature Medicine 13, 147 - 149 (2007) Published online: 7 January 2007 | doi:10.1038/nm1529
3) Analysis of hemagglutinin-mediated entry tropism of H5N1 avian influenza, Copyright © 2009 Ying Guo, Emily Rumschlag-Booms, Jizhen Wang, Haixia Xiao, Jia Yu, Jianwei Wang, Li Guo, George F Gao, Youjia Cao, Michael Caffrey, and Lijun Rong (licensee BioMed Central Ltd.)
4) ibid., Guo, et. ali.
5) Syncytium Formation and HIV-1 Replication Are Both Accentuated by Purified Influenza and Virus-associated Neuraminidase, by Jiangfeng Sun, Benoit Barbeau, Sachiko Sato, Guy Boivin, Nathalie Goyette and Michel J. Tremblay; First Published on January 7, 2002, doi: 10.1074/jbc.M110764200 March 22, 2002 The Journal of Biological Chemistry, 277, 9825-9833.
6) ibid, Jiangfeng Sun, et. al.
7) ibid, Jiangfeng Sun, et. al. [emphasis mine]
8) Pandemic influenza A (H1N1) in HIV-1-infected patients (PMID:20802295[PubMed - indexed for MEDLINE]) Emphasis: mine.
Yes, I was on the early threads when Mother Abigail began posting.
That notwithstanding, I'm unaware of any passages alluding to an near-exinction event prior to then. In fact, the 7 plagues described in Revelation of John make no implication; nor can such inference be made.
Truly the latter half of the Tribulation will be dreary, but not even the 7th plague describes what is being purported. Come on, an earthquake felt round the world, and hailstones of dinner plate-diameter, that's some radical carnage.
However, that notwithstanding, the threat of extinction to ALL life on this planet - the inference by extension risk of human extinction - won't occur until after the Millenial Kingdom, i.e., Battle in the Plains of Meggido.
I'm takin' the Lord at His Word when He stated He'd never again deliver another "flood" type punishment.
The link to footnote #2 of my previous post s/b:
Tropism of avian influenza A (H5N1) in the upper and lower respiratory tract, J M Nicholls, M C W Chan, W Y Chan, H K Wong, C Y Cheung, D L W Kwong, M P Wong, W H Chui, L L M Poon, S W Tsao, Y Guan & J S M Peiris; Nature Medicine 13, 147 - 149 (2007) Published online: 7 January 2007 | doi:10.1038/nm1529
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