2009: Scientists now know how smallpox kills

This stuff is way over my head but given that the JHU “event 201” simulation from oct 2019 involved a new strain of coronavirus, and the JHU “dark winter” simulation predicted the 2001 anthrax attacks and also a future release of smallpox, https://unlimitedhangout.com/2020/04/investigative-series/all-roads-lead-to-dark-winter/ https://soundcloud.com/guns-and-butter-1/connecting-the-anthrax-attacks-to-911-graeme-macqueen-234 maybe someone could look into finding a source of “Rec type I IFN bp”.   It seems to be an effective vaccine against smallpox and probably less dangerous than the attenuated virus.

Also see this from 2018: http://thoughtcrimeradio.net/2018/04/fearmongering-by-gates-raises-question-of-staged-bioattack-in-usa/

From science daily in 2009:

A team of researchers working in a high containment laboratory at the Centers for Disease Control and Prevention in Atlanta, GA, have solved a fundamental mystery about smallpox that has puzzled scientists long after the natural disease was eradicated by vaccination.: they know how it kills us. In a new research report appearing online in The FASEB Journal, researchers describe how the virus cripples immune systems by attacking molecules made by our bodies to block viral replication.

This discovery fills a major gap in the scientific understanding of pox diseases and lays the foundation for the development of antiviral treatments, should smallpox or related viruses re-emerge through accident, viral evolution, or terrorist action.

“These studies demonstrate the production of an interferon binding protein by variola virus and monkeypox virus, and point at this viral anti-interferon protein as a target to develop new therapeutics and protect people from smallpox and related viruses,” said Antonio Alcami, Ph.D., a collaborator on the study from Madrid, Spain. “A better understanding of how variola virus, one of the most virulent viruses known to humans, evades host defenses will help up to understand the molecular mechanisms that cause disease in other viral infections.”

In a high containment laboratory at the Centers for Disease Control and Prevention in Atlanta, scientists produced the recombinant proteins from the variola virus and a similar virus that affects monkeys, causing monkeypox. The researchers then showed that cells infected with variola and monkeypox produced a protein that blocks a wide range of human interferons, which are molecules produced by our immune systems meant to stop viral replication….

Journal Reference:

  1. del Mar Fernandez de Marco et al. The highly virulent variola and monkeypox viruses express secreted inhibitors of type I interferonThe FASEB Journal, 2009; DOI: 10.1096/fj.09-144733


The doi resolves to https://faseb.onlinelibrary.wiley.com/doi/epdf/10.1096/fj.09-144733
… Uniquely among IFN receptors, and indica-
tive of their potential host range, the poxvirus-encoded
IFN decoy receptors bind IFNs from a broad range of
host species (19). Deletion of the IFN/BP gene from
the VACV WR genome attenuates the virus in a mouse
model of infection (19, 24), and it has been recently
demonstrated that the IFN/BP is also essential for
ectromelia virus (ECTV) virulence and that vaccination
with the IFN/BP induces protective immunity (25)….


25. Xu, R. H., Cohen, M., Tang, Y., Lazear, E., Whitbeck, J. C.,
Eisenberg, R. J., Cohen, G. H., and Sigal, L. J. (2008) The
orthopoxvirus type I IFN binding protein is essential for viru-
lence and an effective target for vaccination. J. Exp. Med. 205,


The orthopoxvirus type I IFN binding protein is essential for virulence and an effective target for vaccination

Nonliving antiviral vaccines traditionally target proteins expressed at the surface of the virion with the hope of inducing neutralizing antibodies. Orthopoxviruses (OPVs), such as the human smallpox virus and the mouse-equivalent ectromelia virus (ECTV; an agent of mousepox), encode immune response modifi ers (IRMs) that can increase virulence by decreasing the host immune response. We show that one of these IRMs, the type I interferon (IFN) binding protein (bp) of ECTV, is essential for ECTV virulence and is a natural target of the antibody response. More strikingly, we demonstrate that immunization with recombinant type I IFN bp protects mice from lethal mousepox. Collectively, our experiments have important implications for our understanding of the role of IRMs in OPV virulence and of type I IFNs in OPV infections. Furthermore, our work provides proof of concept that effective antiviral vaccines can be made to prevent disease by targeting virulence factors as an alternative to the traditional approach that attempts to prevent infection by virus neutralization.


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