https://en.wikipedia.org/wiki/Yersinia_pestisIn humans and other susceptible hosts[edit]Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors, including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Is the Coronae Viriae a "natural AI complex" ? An e-game figure ,selflearning and self-decisive ?
Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses a
plasmin activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate systematic invasion.
[20] Many of the bacteria's
virulence factors are antiphagocytic in nature. Two important antiphagocytic
antigens, named F1 (fraction 1) and V or
LcrV, are both important for
virulence.
[14] These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as
monocytes, but not in
neutrophils. Natural or induced
immunity is achieved by the production of specific
opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.
[35]In addition, the type-III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins, called Yersinia outer proteins (Yops), include Yop B/D, which form pores in the host cell membrane and have been linked to
cytolysis. The YopO,
YopH, YopM, YopT, YopJ, and YopE are injected into the
cytoplasm of host cells by T3SS into the pore created in part by YopB and YopD.
[36] The injected Yops limit phagocytosis and cell signaling pathways important in the
innate immune system, as discussed below. In addition, some Y. pestis strains are capable of interfering with immune signaling (e.g., by preventing the release of some
cytokines).[/font][/size]
Y. pestis
proliferates inside
lymph nodes, where it is able to avoid destruction by cells of the immune system such as
macrophages. The ability of Y. pestis to inhibit phagocytosis allows it to grow in lymph nodes and cause
lymphadenopathy. YopH is a
protein tyrosine phosphatase that contributes to the ability of Y. pestis to evade immune system cells.
[37] In macrophages, YopH has been shown to
dephosphorylate p130Cas,
Fyb (
Fyn binding protein)
SKAP-HOM and
Pyk, a
tyrosine kinase homologous to
FAK. YopH also binds the p85 subunit of
phosphoinositide 3-kinase, the
Gab1, the
Gab2 adapter proteins, and the
Vav guanine nucleotide exchange factor.
YopE functions as a
GTPase-activating protein for members of the
Rho family of GTPases such as
RAC1. YopT is a
cysteine protease that inhibits
RhoA by removing the
isoprenyl group, which is important for localizing the protein to the
cell membrane. YopE and YopT has been proposed to function to limit YopB/D-induced cytolysis.
[38] This might limit the function of YopB/D to create the pores used for Yop insertion into host cells and prevent YopB/D-induced rupture of host cells and release of cell contents that would attract and stimulate immune system responses.
YopJ is an
acetyltransferase that binds to a conserved
α-helix of
MAPK kinases.
[39] YopJ acetylates MAPK kinases at
serines and
threonines that are normally phosphorylated during activation of the
MAP kinase cascade.
[40][41] YopJ is activated in eukaryotic cells by interaction with target cell
phytic acid (IP6).
[42] This disruption of host cell protein kinase activity causes
apoptosis of macrophages, and this is proposed to be important for the establishment of infection and for evasion of the host immune response. YopO is a protein kinase also known as Yersinia protein kinase A (YpkA). YopO is a potent inducer of human macrophage apoptosis.
[43]Depending on which form of the plague with which the individual becomes infected, the plague develops a different illness; however, the plague overall affects the host cell’s ability to communicate with the immune system, hindering the body to bring phagocytic cells to the area of infection.
Y. pestis is a versatile killer. In addition to rodents and humans, it is known to have killed dogs, cats, camels, chickens, and pigs.
[44]A bio-circuit
,the blood becomes "informated by plasmon" :
Vector
[
edit]The transmission of Y. pestis by fleas is well characterized.
[31] Initial acquisition of Y. pestis by the
vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage system and Yersinia
murine toxin (Ymt). Although Ymt is highly toxic to rodents and was once thought to be produced to ensure reinfection of new hosts, it is important for the survival of Y. pestis in fleas.
[19]The hemin storage system plays an important role in the transmission of Y. pestis back to a mammalian host.
[32] While in the insect vector, proteins encoded by hemin storage system genetic loci induce
biofilm formation in the
proventriculus, a valve connecting the
midgut to the
esophagus.
[33] Aggregation in the biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" after entomologist
A.W. Bacot, the first to describe this phenomenon).
[34] Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria lodged in the proventriculus, which is regurgitated back into the host circulatory system.
[34]https://translate.google.com/translate?hl=de&sl=auto&tl=en&u=https%3A%2F%2Fwww.stiftung-gesundheitswissen.de%2Fgesundes-leben%2Fkoerper-wissen%2Fviren-oder-bakterien-wo-ist-der-unterschiedKnowing the process negative symptoms neutralizing medicine/healing bio-alimentation( acids) can change !
