Posted June 24, 2017, 2 PM Eastern Time:
So, multiple bacteriophages from OspC (which would come from ONE bacteriophage), transfer genetic material to the OspA gene product, a lipoprotein, Pam3Cys (so now the lipoprotein has somewhere to house DNA – this is surely novel, but go on…), causing a recombinant DNA (which is to say, OspA is also a laboratory that does gene splicing). THAT IS fascinating, I must say.
Connection to ambers? You mean like the aliens you met while visiting the Planet Egypton in the Pleiadian’s Michael Jackson Galaxy?
Question, Do these Ambers have blood like humans or more like snowshoe crabs?
On this next one, No one ever says they understand Mayday’s Brainscramble if you look at her page and read the comments.
First of all there is no “Lipoprotein 54” of OspA, since OspA alone, singular, is a lipoprotein. A lipoprotein, singular. It’s molecular type is pam3cys. There are many other lipoproteins in Borrelia, *** Use your google machine to look up the word lipoprotein.***
“Phage terminase” – a bacteriophage is a thing, a virus that only attacks bacteria and not humans or mammals. A terminase would be an enzyme. A phage terminase is what the virus uses to cut and splice itself into bacterial DNA. In Lyme, these phages remain as independent plasmids (say Barbour and Burgdorfer, Casjens et al).
A portal protein is just where/how the phage enters its target bacteria. These concepts are not at all related.
The Osps are thought to be phage vectored GENE PRODUCTS (single molecules, not DNA, but a DNA product) and they, as fungal antigens shed by Borrelia, cause immunosuppression or a post-sepsis outcome.
She’s never even looked up the word, “protein.”
Does not know lateral means the same thing as horizontal:
Remember, OspA is Pam3Cys… Cant be a phage doing all the damage if the OspA GENE PRODUCT causes the same disease:
Ann N Y Acad Sci. 1988;539:65-79.
Clinical pathologic correlations of Lyme disease by stage.
”….Soon after the onset of ECM, the organism disseminates hematogenously, with what appears to be random dispersal throughout the body. The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells. Others look like typical immunoblasts (FIG. 1). In one example, cervical lymph nodes show cell degeneration with karyorrhexis and nuclear debris of lymphoid elements. This patient had repeated high fevers and marked discomfort of neck nodes. Large atypical immunoblasts can also be seen in the spleen and bone marrow. The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis. Spirochetes can be demonstrated in the lymph nodes, spleen and bone marrow and liver. There is a transient hepatitis reflected by elevated liver cell enzymes such as SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal triaditis all the way to liver cell derangement that simulates acute viral hepatitis. The cells at this stage appear swollen with clear cytoplasm and microvesicles of fat (FIG. 2). Numerous leukocytes are seen in the sinusoids, and there is Kupffer cell hyperplasia…”
J Immunol. 2005 Jun 1;174(11):6639-47.
Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2.
AbstractThe role of TLR4 in mature B cell activation is well characterized. However, little is known about TLR4 role in B cell development. Here, we analyzed the effects of TLR4 and TLR2 agonists on B cell development using an in vitro model of B cell maturation. Highly purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were cultured for 72 h, and B cell maturation in the presence of the TLR agonists was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS or lipid A resulted in a marked increase in the percentage of CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the increase of CD23(+) B cell population induced by lipid A or LPS. The TLR4-induced expression of CD23 is not accompanied by full activation of the lymphocyte, as suggested by the absence of activation Ag CD69. Experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2. We studied the effects of TLR-agonists on early steps of B cell differentiation by analyzing IL-7 responsiveness and phenotype of early B cell precursors: we found that both lipid A and Pam3Cys impaired IL-7-dependent proliferation; however, while lipid A up-regulates B220 surface marker, consistent with a more mature phenotype of the IgM(-) precursors, Pam3Cys keeps the precursors on a more immature stage. Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.