=4th Generation Photodynamic Therapy==
How to kill viruses in the body by shining light on the situation
http://www.cytoluminator.com/virus.html
The scientific community has known for at least 12 years that the HIV virus can be completely destroyed with a very simple PDT protocol. In fact, it has been law in Europe for that long that all blood for transusion MUST be treated with PDT to eliminate the chance of tranfection during transfusion. So if we know it is easy to kill in blood bags with PDT, what keeps us from being able to do it in a living human being?
No one has attempted it because of factors which we will discuss later, but we have overcome those limitations.
The diagram below is the construct of the HIV virus. It looks pretty here, but in the real world it is ugly.
So, Let's Try to Kill the HIV Virus!
Aluminum phthalocyanine (AIPc) is a dye.
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Inactivation of viruses in red cell and platelet concentrates with aluminum phthalocyanine (AIPc) sulfonates.
https://www.ncbi.nlm.nih.gov/pubmed/1617188
Abstract
Aluminum phthalocyanine tetrasulfonates (AIPcS) are photoactive compounds with absorption maxima at 665-675 nm. The inactivation of viruses (vesicular stomatitis virus, VSV; human immunodeficiency virus, HIV) added to either whole blood or red blood cell concentrates (RBCC) and platelet concentrates (PC) on treatment with tetrasulfonated AIPc (AIPcS4) was evaluated. Treatment of RBCC with 10 microM AIPcS4 and 44 J/cm2 visible light resulted in the inactivation of greater than or equal to 10(5.5) infectious doses (TCID50) of cell-free VSV, greater than or equal to 10(5.6) TCID50 of cell-associated VSV, and greater than or equal to 10(4.7) TCID50 of cell-free sindbis virus. Both greater than or equal to 10(4.2) TCID50 of cell-free and greater than or equal to 10(3.6) TCID50 of cell-associated forms of HIV were also shown to be inactivated. Encephalomyocarditis virus, used as a model for nonenveloped viruses, was not inactivated. Equivalent virus kill with Photofrin II required a substantially higher concentration of dye and longer exposure to visible light. Following AIPcS4 treatment, red cell integrity was well maintained as judged by the low level (less than 2%) of hemoglobin release immediately following treatment and on subsequent storage, by measurements of erythrocyte osmotic fragility, and by the normal recovery and circulatory survival on infusion of treated, autologous red blood cells in baboons. Treatment of PC with 10 microM AIPcS4 and 44 J/cm2 visible light also resulted in effective virus kill (greater than or equal to 10(5.5) TCID50) of VSV; however, both the rate and extent of platelet aggregation in response to collagen addition declined by at least 50%. Based on these results, further characterization of AIPcS4-treated RBCC is justified.