by Geert Vanden Bossche, Voice For Science And Solidarity:
Is the bird flu panzootic expediting the end of the SARS-CoV-2 immune escape pandemic?
SUMMARY
Scientifically speaking, it cannot be ruled out that the bird flu panzootic is currently accelerating the evolutionary dynamics of the SARS-CoV-2 (SC-2) immune escape pandemic and expediting its final hyperacute stage. Public health authorities should therefore be on high pandemic alert for a new coronavirus (CoV) rather than bird flu! This article further explains why the end of the SC-2 pandemic would automatically result in the end of the bird flu panzootic.
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1. Introduction
There is currently a growing concern among public health officials and experts that enhanced spread of avian Influenza virus to immunologically naïve humans could result in the next flu pandemic and prompt the WHO to declare another health emergency of international concern. The potentially (!) highly pathogenic strain of avian influenza (HPAI), named H5N1, is causing a global animal pandemic (aka panzootic); it has already inflicted serious damage on various bird populations and has meanwhile also claimed victims among several mammalian species (a list of significant outbreaks, including in mammals, can be found at:
https://www.cdc.gov/flu/avianflu/timeline/avian-timeline-2020s.htm).
Up to now, public health authorities have qualified the risk of these viruses spreading from birds to people as low and essentially limited to individuals with work or recreational exposures to H5N1 virus-infected animals. Although the case fatality rate from H5N1 infection is considered relatively high, all fatalities reported so far have occurred after direct exposure to sick or dead infected poultry. However, the widespread presence of bird flu in dairy cows and milk has recently put public health authorities on high alert, as it is considered the first instance of likely mammal-to-human transmission. Consequently, many are questioning whether direct contact with infected cows or drinking untreated (or insufficiently treated) cow’s milk could increase the risk of deadly infection and whether the increasing presence of the virus in domesticated animals could facilitate viral adaptation to the host species (i.e., via adaptation in the hemagglutinin surface protein that influences cleavage by furin-like proteases).
2. There is no scientific rationale for vaccination of mammalian populations (including humans) against bird flu (H5N1).
As usual, public health authorities resort to testing when they are in the dark about causal relationships. Testing of both humans and animals (via reverse-transcription polymerase chain reaction [RT-PCR] assay) has meanwhile clearly shown that both can become infected more often without developing severe disease symptoms. This raises even more questions, particularly regarding the ‘obligate pathogenic’ nature of the virus and the role of the immune system in controlling viral replication in the body. Indeed, one cannot assume that the avian flu virus (AFV) only transmits through direct contact. Just as birds move through the air, so does the bird flu virus. Therefore, the virus can undoubtedly infect both humans and animals through the air. It is reasonable to assume that in such cases, exposed individuals are infected with a lower viral load, most of which can be eliminated by the first line of immune defense (i.e., our innate immune system). This could explain why many airborne infections with bird flu are mild or even asymptomatic and cause only moderate or no seroconversion.
There are solid immunological arguments to suggest that natural killer (NK) cells, recognizing and killing host cells at an early stage of Sars-CoV-2 (SC-2) infection (or more generally, coronavirus [CoV] infection), could also eliminate cells infected with influenza virus, regardless of the specific type of flu virus. I therefore have little doubt that the portion of the population that has not been vaccinated with Covid-19 (C-19) vaccines and has consequently strongly trained their cell-mediated innate immunity (CMII) over the course of this C-19 pandemic, enjoys additional protection against a range of other viruses, including seasonal flu virus (sFV) and AFV. I also tend to believe that even the C-19 vaccinated portion of the population is equally capable of avoiding the risk of severe disease after contracting avian flu. Their defense, however, is based on the strong activation of T cells that – at a later stage of SC-2 infection – recognize a highly conserved, self-mimicking T cell epitope presented on MHC class I molecules and thus target and kill CoV-infected host cells that present this peptide epitope on their membrane (see fig. 1). This conserved epitope shows a high degree of homology with a similar epitope that is presented on the membrane of cells infected with influenza virus (including AFV). It is therefore reasonable to assume that activation of these universal cytotoxic T lymphocytes (CTLs) by SC-2 can also abrogate productive infection of influenza virus (including AFV) and thereby prevent severe bird flu disease.
In other words, it seems completely unnecessary to vaccinate people in highly C-19 vaccinated countries with a bird flu vaccine. Given the widespread presence of bird flu, there is even a risk that vaccinating people against this disease, as well as against seasonal flu, will have a counterproductive effect, regardless of whether their CMII was previously trained. Here is how this could happen: When vaccinating against bird flu, it should be noted that – as with all non-replicating vaccines – a period of 2-3 weeks elapses before vaccinated individuals acquire a sufficiently high concentration of specific antibodies (Abs) that bind with high enough affinity to the virus to neutralize it. However, if a vaccinated individual becomes exposed to a sufficient amount of AFV, i.e., before the vaccine-induced Abs recognize the virus with sufficient affinity to effectively neutralize it, then this individual may be at risk of contracting Ab-dependent enhancement of disease (ADED). Given the current, widespread dissemination of the AFV, there would be a significant risk for a freshly vaccinated individual to become exposed to this virus in the early stages after vaccination and hence, to develop ADED.
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