MA believes that in the very near future the HIV virus, which has been continually evolving to a higher level of virulence, will develop the ability to move from lung to lung.
Once in the lung, the new HIV mutant will create a cytokine storm that will quickly overwhelm the patient and the time from infection to death will be sudden and dramatic.
The virus has now defeated all of modern medicine and can be found in every geographical region and in every culture on our little rock.
The weakness of this very diabolical bug is it's lack of an effective transmission method.
HIV is one of the most mutanagenic life forms on earth. The numbers of mutants created daily is an almost unbelievable number.
The change necessary to allow it to ride water droplets in a cough from one lung to another is really quite achievable considering the massive mutation rate.
That is why the rising virus count of patients is worrisome. The denser the infection the more likely airborne transmission might be possible.
Her fixation on the use of neuriminidase inhibitors on HIV patients with the flu is based on the known science that neuriminidase increase HIV mutation. Which in a sick patient with coughing, sneezing etc. seems, to MA, insane.
So, sorry for all the words, your summation is spot on. The method of transmission changes the long time from infection to death to something much more akin to the Spanish Flu.
Well...COLONIC RELEASE AVALANCHE PHENOMENA!(or CRAP for short!)
So it is like a “Masque of the Red Death” scenario as written of by Poe.
I am an RN by trade working in an ICU. If something like this broke out, I might be faced with an untenable dilemma; especially since I have family!
So it is like a “Masque of the Red Death” scenario as written of by Poe.
I am an RN by trade working in an ICU. If something like this broke out, I might be faced with an untenable dilemma; especially since I have family!
Sounds like the viral equivalent of pneumonic plague. << shudder >>
It is not just the increase in mutation, but the neuraminidase inhibitors would not be in use if the flu virus wasn't present. Both the HIV and Flu variant together with increased mutation rates in the HIV present an opportunity for the sort of recombinant development which would present a 'superbug', an HIV variant which would be more contagious, and could cause the cytokine storms she describes.
Why out of Egypt?
Not just the flu, but the sexual attitudes toward young men in islam, and the 'silent' HIV progress through that population increase the chance of both being in the same patient at the same time...
This is a frightening prospect, if it occurs.
A commentary from Niman today, about Egypt. (BTW I am an ignoramous and can’t grasp deep scientific stuff, I keep trying to get the gist of stuff anyway.)
Commentary
H1N1pdm09 Recombination In Egypt H5N1 Raises Concerns
Recombinomics Commentary 21:00
January 25, 2012
http://www.recombinomics.com/News/01251203/H5_Transmission_H1N1pdm09.html
The recently released H5N1 sequences from Egypt contain H1N1pdm09 sequences in the PB1 and PB2 gene segments. The recent comments by Yoshihiro Kawaoka on the data in the censored Nature paper indicate H5 on an H1N1pdm09 genetic background transmits in ferrets. Although the paper remains censored, the comments suggest H5 was added to 7 gene segments from H1N1pdm11. However, an earlier study suggested that the H1N1pdm09 M gene was critical for the jump from swine to humans, so it is unclear if the other six gene segments are required for transmission.
However, the presence of H1N1pdm09 gene sequences in the H5N1 isolates raise concerns that additional combinations are likely and the status of such combinations are far from clear. The most recent human H5N1 sequence from Egypt are from cases in March 2010. More recently, clusters in Egypt have been confirmed and an increased case fatality rate has been noted, raising concerns that H1N1pdm09 internal genes may be present in human cases in Egypt.
NAMRU-3 typically generates H5 and N1 sequences for human cases in Egypt, while samples are frequently sent to the CDC in Atlanta for further analysis. These sequences should be released immediately. The presence of such sequences may signal and enhanced transmission in humans and may be related to the confirmation of clusters.
Although the H5 transmission in ferrets in the Kawaoka study did not produce a lethal H5N1 in the ferret model, the wide circulation of such sequences in human populations could have significant implications, as has been demonstrated for the H1N1pdm09 M gene in trH3N2 (H3N2v) and trH1N1 (H1N1v) cases in the United States in 2011.
The Kawaoka Nature paper highlights the need for full sequences from cases in Egypt. This need applies to other recent cases, such as the clusters in Indonesia. Only HA and NA sequences were released from the Bali cluster, which also had clear evidence of recombination. Similarly, no sequence data has been released for the cluster in North Jakarta.
The censored papers at Nature and Science highlight the dangers of a transmitting H5N1 and demand more timely and transparent release of H5N1 sequences.