Heat Shock Protein 70 - Protect Yourself!
The human immune system is complex, sophisticated, and sensitive. Nature has built many physiological mechanisms that become activated when our bodies sense a foreign invader, such as COVID-19, also known as CoronaVirus.
Working automatically and tirelessly our Lymphocytes hunt down and attack these invaders until our body returns to balance. These Killer cells are activated when our bodies core temperature rises above normal. We all know this as a “fever”.
It is well known and documented in Health Science, that a fever is our bodies front line defense against invaders. In essence, our brain senses an invader, it turns off our internal thermostat and our core body temperature begins to rise. As our temperature reaches 101 degrees F to 102.5 degrees F there is a natural die-off of bacteria and viral invaders. At the same time, our Killer cells are activated and sent out to attack and engulf the virus. Our bodies mechanism or “GPS” targeting system sent in to tag the invaders, so the Killer cell knows what and where to attack, is called a Heat Shock Protein, or HSP for short. HSP’s are deployed when a fever is present. A hot bath, a hot tub, steam or dry sauna, or a very efficient method of Infrared sauna can be used to create hyperthermia (or false fever) to initiate this primal immune response. To make this discussion even more interesting HSP70 is a specialized Heat Shock Protein designed to disable the Viral Replicating System. Essentially, the real danger of a viral infection is when the virus attacks and multiplies faster than your immune system can eradicate it. Hyperthermia can be a helpful natural tool, to initiate HSP70 weaken the advancement of COVID-19 and reduce the harmful effects.
NOX2-dependent oxidant production inhibits TLR7 signaling
In light of worldwide concern regarding the recent outbreak of a deadly novel strain of coronavirus in China, it is fortuitous that two recent discoveries point the way to effective nutraceutical measures for potentiating the type 1 interferon response to RNA viruses.
Activation of toll-like receptor 7 (TLR7) by single-stranded viral RNA trapped within endosomes provides a key stimulus to type 1 interferon induction by RNA viruses.1 Selemidis and colleagues have recently demonstrated that, within the endosomes of human alveolar macrophages, such viruses evoke superoxide production by NOX2-dependent NADPH oxidase complexes; the presence of TLR7 is required for this effect.2 This phenomenon was demonstrated with a wide range of RNA viruses, including rhinovirus, respiratory syncytial virus, human parainfluenza virus, human metapneumonia virus, Sendai virus, Dengue virus, and HIV. Furthermore, the subsequent generation of hydrogen peroxide within these endosomes leads to an oxidation of Cys98 on TLR7 that blocks the ability of this receptor to transmit a signal boosting type 1 interferon production. In macrophages deficient in NOX2 activity, either genetically or owing to administration of a targeted NOX2 inhibitor (gp91ds-TAT), the production of type 1 interferon was markedly higher in response to RNA virus infection. When genetically normal or NOX2 knockout mice were exposed to an inactive strain of influenza virus, the interferon-beta response and the antibody response evoked by this virus were markedly higher in the NOX2 knockout mice. Continue Reading Here....
- Melody Besner