I am a writer and not a medical professional but here is what MA says about the Cy. storm.
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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.
Neutralizing antibody responses are induced very late by HIV in humans - Zinkernagel
While for most acute cytopathic classical childhood infections, tetanus, diphtheria, measles, polio or small pox, our usual in vitro assays ELISA, ?-IFN producing T cells or T cell proliferation correlate reasonably well with the immunological memory, neutralizing antibody responses are induced very late by HIV in humans (or by LCMV in mice), observed Nobel Laureate Dr. Rolf M. Zinkernagel.
Delivering Public Lecture on 'Why do we not have a vaccine against HIV or TB', Zinkernagel said this common feature applies to several human persisting viral infections, including HBV, HCV, HIV (and many parasitic infections) even as HIV-1 infections induce quick and very good ELISA positive responses. If a neutralizing antibody arises and viraemia re-emerges, then often neutralizing antibody escape mutant viruses get selected. This indicates that only a multi-specific type of vaccine may eventually control such infections. Since this may include up to 10,000 or 100,000 variations for HIV (or 1,000 for influenza virus), such a vaccine will be very difficult to develop, he said.
The Nobel laureate said there is good evidence that only persisting and re-encountered antigen maintains the specific neutralizing antibody. This antigen-dependent protection is a far cry from the immunological memory and its relationship to vaccine mediated protection to become plasma cells. Therefore impact of antigen dependent protection via activation of B cells or effector T cells impinges on our understanding of protective vaccines, particularly against chronic persistent types of infections, he maintained.
Zinkernagel who got the Nobel Prize in Physiology or Medicine for 1996 along with Peter C Doherty said vaccine strains that tend to persist, such as BCG, loose protective capacity once the vaccine strain has been eliminated by the host.
On the other hand attenuated vaccine strains may regain virulence under certain circumstances (e.g. HIV-1 or SHIV) suggesting that development of sufficiently attenuated but not too much attenuated vaccine strains
may be either extremely difficult or impossible.
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