Masks are politics. They do absolutely nothing to save you, them, or anyone from germs. If you are wearing a mask because you think it makes you ‘safe’ from the Cooties, you’re suffering from ignorance.
If you’re wearing a mask because you think it makes others ‘safe’ who may be immune-compromised from your potential Cooties, you’re suffering from malignant altruism, plus ignorance.
I’m no scientist, not by a long shot, but logic occasionally crosses my path. As through a swamp, I wade through information that seems logical and credible yet totally contradictory to what I hear from so many incessantly talking heads.
Here’s one such crossing, not sure exactly what to make of it, but it seems relevant to the current plandemic according to my spidey-sense.
To me it suggests inhaling your own virus-infected breath is likely more dangerous than ’catching’ another’s germs, which would provoke your own natural immune response, and vice versa. But, I’m so royally retarded, I’m sure I got that interpretation all wrong.
James G. Bedford, Giuseppe Infusini, Laura F. Dagley, Fernando Villalon-Letelier, Ming Z. M. Zheng, Vicki Bennett-Wood, Patrick C. Reading, Linda M. Wakim, Airway Exosomes Released During Influenza Virus Infection Serve as a Key Component of the Antiviral Innate Immune Response, Frontiers in Immunology, 10.3389/fimmu.2020.00887, 11, (2020). Crossref
Airway Exosomes From Influenza Virus Infected Mice Evoke Pulmonary Inflammation
We tested the capacity of exosomes recovered from the BALf of influenza virus-infected mice to trigger pulmonary inflammation. To this end, we intranasally transferred into the airways of naïve mice an equal amount of exosomes recovered from the BALf of either naïve mice, mice infected 2 days prior with influenza virus, or mice given an inflammatory agent (poly I:C). Four days following exosome delivery we assessed the level of inflammation by measuring cytokine levels in the BALf and immune cell infiltration into the lung tissue. As a positive control for pulmonary inflammation, we also included a cohort of mice directly infected with influenza virus. The delivery of exosomes recovered from the airways of influenza virus-infected mice resulted in the production of IL-6, MCP-1 and TNF, which was a very similar inflammatory profile to that observed following direct infection with influenza virus (Figures 2A–C). Widening our analysis to include assessment of a more extensive panel of inflammatory cytokines revealed that exosomes recovered from the airways of influenza virus-infected mice also resulted in the production of both type I and type II interferon (Supplementary Figure 3). In contrast, the intranasal delivery of exosomes recovered from naïve or poly I:C treated mice did not evoke the release of any cytokines (Figures 2A–C), implying that the PAMPs or potential DAMPs loaded into the exosomes generated during virus infection were essential to trigger inflammation. Exosomes derived from influenza virus infected mice did contain viral RNA which may serve as the PAMP triggering the observed inflammatory response (Supplementary Figure 4). Consistent with the capacity to trigger the release of inflammatory cytokines, the intranasal delivery of exosomes recovered from the BALf of influenza virus-infected mice, but not naïve mice also resulted in the recruitment of neutrophils while the number of CD8+ and CD4+ T cells remained stable irrespective of the treatment (Figures 2D–F). Thus, exosomes released into the airways during an influenza virus infection are inflammatory, causing the release of cytokines/chemokines and resulting in the recruitment of innate immune cells.