'Professor Sucharit Bhakdi MD is a retired Professor Emeritus of Medical Microbiology and Immunology, Former Chair, Institute of Medical Microbiology and Hygiene, Johannes Gutenberg University of Mainz.

Sucharit Bhakdi was born in Washington, DC, and educated at schools in Switzerland, Egypt, and Thailand. He studied medicine at the University of Bonn in Germany, where he received his MD in 1970. Professor of immunology from Germany. He was a post-doctoral researcher at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg from 1972 to 1976, and at The Protein Laboratory in Copenhagen from 1976 to 1977. He joined the Institute of Medical Microbiology at Giessen University in 1977 and was appointed associate professor in 1982. He was named chair of Medical Microbiology at the University of Mainz in 1990, where he remained until his retirement in 2012. Dr. Bhakdi has published over three hundred articles in the fields of immunology, bacteriology, virology, and parasitology, for which he has received numerous awards and the Order of Merit of Rhineland-Palatinate. Sucharit Bhakdi and his wife, Karina Reiss, live with their three-year-old son, Jonathan Atsadjan, in a small village near the city of Kiel.'

Karina Reiss Ph.D.
Karina Reiss was born in Germany and studied biology at the University of Kiel where she received her PhD in 2001. She became assistant professor in 2006 and associate professor in 2008 at the University of Kiel. She has published over sixty articles in the fields of cell biology, biochemistry, inflammation, and infection, which have gained international recognition and received prestigious honors and awards.

'Dr. Michael Palmer is an Associate Professor of Biochemistry at the University of Waterloo (Canada) teaching Pharmacology and Toxicology. Dr. Palmer's advanced research in biochemistry focuses on the interaction of peptides and proteins with biological membranes. One current area of interest is the action mode of lipopeptide antibiotic daptomycin, as well as the mechanism of bacterial resistance to it.'

Bizarro thought....

'Immunity to respiratory viruses: systemic versus mucosal immunity
We now turn to an important fact regarding the protection of the respiratory tract against infections: it is mediated by cells of the immune system which reside within and beneath our respiratory mucous membranes, and these cells function quite independently from those immune cells which protect our internal organs.

A key aspect of this functional separation between mucosal and systemic immunity concerns the nature of antibodies produced by plasma cells located directly beneath the mucous membranes. These antibodies—secretory immunoglobulin A (sIgA)—are secreted across the mucous membranes to their surface. They are thus on site to meet airborne viruses, and they may be able to prevent them from binding and infecting the cells within those mucous membranes. The same mode of protection pertains to the digestive tract as well.
In contrast, IgG and circulating IgA are the main antibodies found in the bloodstream. They cannot prevent the entry of viruses into the cells that line the airways or the gut, and they may at best counteract their spread if they gain entry to the circulation. Crucially, vaccines that are injected into the muscle—i.e., the interior of the body—will only induce IgG and circulating IgA, but not secretory IgA. The antibodies induced by such vaccines therefore cannot and will not effectively protect the cells of the respiratory tract against infection by airborne viruses. This realization is neither contentious nor new. As long as 30 years ago, McGhee et al. concluded:

It is surprising that despite our current level of understanding of the common mucosal immune system, almost all current vaccines are given to humans by the parenteral route [i.e. by injection]. Systemic immunization is essentially ineffective for induction of mucosal immune responses. Since the majority of infectious microorganisms are encountered through mucosal surface areas, it is logical to consider the induction of protective antibodies and T cell responses in mucosal tissues.'

The failure of intramuscular injection to induce secretory IgA has been confirmed in a study on Middle East Respiratory Syndrome (MERS). Like COVID-19, this disease is caused by a coronavirus, and the experimental vaccine used in the study was gene-based, like all of the major vaccines currently deployed against COVID-19. More recently, another study has shown that the mRNA COVID-vaccines also do not stimulate substantive production of secretory IgA. For this simple reason, one cannot expect that vaccination will inhibit airway infection. Indeed, the utter failure of the vaccines to prevent SARS-CoV-2 infection is today solidly documented.

It is general knowledge that secretory IgA antibodies (sIgA) are produced in response to naturally occurring airway infections. The mucous membranes of healthy individuals are consequently coated with antibodies directed against common respiratory viruses. However, the capacity of these antibodies to prevent infections is limited. The outcome of an encounter with a virus is not “black or white”—numbers are all-important. A wall of protective antibodies may ward off a small-scale attack, but it will be breached at higher viral loads. This is why infections with airborne viruses occur repeatedly throughout life, a fact that will not even be altered by the use of intranasal vaccines in order to stimulate sIgA-production, even though intranasal vaccine application does induce stronger mucosal immune responses than does intramuscular injection.