The recent finding by Penn state supports the prediction that Flaviviruses like Zika use melanocortin receptors. Melanocortin receptors are inhibited by clatherin inhibitors.
Zika use melanocortin receptors: specifically ACTH
http://angelabiggs.blogspot.com/2016/03/acth-and-placenta.html
Melanocortin receptors are sensitive to clatherin endocytosis inhibitors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2547351/
ACTH receptor specifically
https://www.ncbi.nlm.nih.gov/pubmed/12530627
Penn state found that: nanochangmycin inhibits Zika infection through clatherin endocytosis inhibiting
http://www.news-medical.net/news/20170117/Penn-researchers-discover-antimicrobial-that-thwarts-Zika-viral-entry-into-human-cells.aspx
The drug amantidine might work against Zika too
http://angelabiggs.blogspot.com/2016/05/can-we-use-amantidine-against-zika.html
Guillian Barre and autoimmune cross-targeting
http://angelabiggs.blogspot.com/2016/01/is-guillian-barre-caused-by-autoimmune.html
I have been dividing up the flaviviruses with the melanocortin receptor they could use:
mcr1 Tick borne encephalitis virus/ hepatitis C (Thrombocytopenia due to red blood cells with mcr1)
mcr2 (ACTH receptor) Zika (placenta, developing brain)
mcr3 West nile (kidneys)
mcr3 and mcr1 Japanese encephalitis
mcr4 Yellow fever (liver)
mcr5 Dengue (immune system T cells) (which explains the second exposure response)
I am thinking they open the door into cells using this receptor most of the time and the other melacortin receptors less well.
Addressing which receptors other researchers suspect zika to be using.
AXL is expressed by tons of cell types and is also considered one of the three macrophage "hands" called TAMs. When a cell is infected with a virus it wears a protein that the macrophages TAMs bind....thus destroying the infected cell. Viruses evolve to bind these "macrophage hands" as a way to slow the immune system reaction down. Understanding this relationship between TAMs and viruses: AXL is not the primary receptor of Zika.
http://angelabiggs.blogspot.com/2017/02/tam-receptors-and-ifns.html
update April 24 : TAMs not required for zika infections
http://www.cell.com/cell-reports/pdfExtended/S2211-1247(17)30419-9
TLR3 is an immune system net and is suppose to catch cytosolic viruses....in the cytosol. Which means if Zika binds TLR3 then Zika is already in the cytosol.
Here is the link that covers the specific HLAs grabbing specific viruses and the TLRs for the same regions grabbing all Viruses non specifically.
http://angelabiggs.blogspot.com/2016/12/updating-hla-location-hypothesis.html
Zika use melanocortin receptors: specifically ACTH
http://angelabiggs.blogspot.com/2016/03/acth-and-placenta.html
Melanocortin receptors are sensitive to clatherin endocytosis inhibitors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2547351/
ACTH receptor specifically
https://www.ncbi.nlm.nih.gov/pubmed/12530627
Penn state found that: nanochangmycin inhibits Zika infection through clatherin endocytosis inhibiting
http://www.news-medical.net/news/20170117/Penn-researchers-discover-antimicrobial-that-thwarts-Zika-viral-entry-into-human-cells.aspx
The drug amantidine might work against Zika too
http://angelabiggs.blogspot.com/2016/05/can-we-use-amantidine-against-zika.html
Guillian Barre and autoimmune cross-targeting
http://angelabiggs.blogspot.com/2016/01/is-guillian-barre-caused-by-autoimmune.html
I have been dividing up the flaviviruses with the melanocortin receptor they could use:
mcr1 Tick borne encephalitis virus/ hepatitis C (Thrombocytopenia due to red blood cells with mcr1)
mcr2 (ACTH receptor) Zika (placenta, developing brain)
mcr3 West nile (kidneys)
mcr3 and mcr1 Japanese encephalitis
mcr4 Yellow fever (liver)
mcr5 Dengue (immune system T cells) (which explains the second exposure response)
I am thinking they open the door into cells using this receptor most of the time and the other melacortin receptors less well.
Addressing which receptors other researchers suspect zika to be using.
AXL is expressed by tons of cell types and is also considered one of the three macrophage "hands" called TAMs. When a cell is infected with a virus it wears a protein that the macrophages TAMs bind....thus destroying the infected cell. Viruses evolve to bind these "macrophage hands" as a way to slow the immune system reaction down. Understanding this relationship between TAMs and viruses: AXL is not the primary receptor of Zika.
http://angelabiggs.blogspot.com/2017/02/tam-receptors-and-ifns.html
update April 24 : TAMs not required for zika infections
http://www.cell.com/cell-reports/pdfExtended/S2211-1247(17)30419-9
TLR3 is an immune system net and is suppose to catch cytosolic viruses....in the cytosol. Which means if Zika binds TLR3 then Zika is already in the cytosol.
Here is the link that covers the specific HLAs grabbing specific viruses and the TLRs for the same regions grabbing all Viruses non specifically.
http://angelabiggs.blogspot.com/2016/12/updating-hla-location-hypothesis.html
This comment has been removed by a blog administrator.
ReplyDeleteThis comment has been removed by the author.
Delete