Tuesday, March 14, 2017

Hervs, viruses, demethylation, and methylation: is this how cancer viruses turn on embryotic genes?

Noticed patterns which still need to be understood:

Nuclear viruses use demethylation or  methylation which may be how viruses turn on dormant embryo Herv genes

Zygote - demethylation- Blastocyte- methylation- Epiblast (pluripotent cells)
       awakens Herv K                                Herv H

Epiblast  -demethylation  - PGCs  -  methylation -Fetus
                    Herv E                              Herv W

viruses: HPV/flavivirus    Herpes/ polyomaviruses/retroviruses
                   demethylation                     methylation

Herpes viruses as part of their cycle use methylation of the host DNA which awakens the herv-H and herv-W

(exception herv-k18 which is stimulated by IFN alpha not demethylation)

epstein barr and methylation
https://www.ncbi.nlm.nih.gov/pubmed/23567077

epstein barr with herv-H and herv-W
https://www.ncbi.nlm.nih.gov/pubmed/22608883
https://www.ncbi.nlm.nih.gov/pubmed/18566025

Retroviruses, like HIV, as part of their cycle use demethylation of the host DNA which awakens herv-K and herv-E.

Retrovirus infection and host demethylation
https://www.ncbi.nlm.nih.gov/pubmed/14623319

HIV and Herv-K
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311604/

HIV and Herv-E
http://jvi.asm.org/content/85/14/6977.full

HPV (human papilloma virus is not a retrovirus, infects using cannabinoid receptors) has been linked to cervical cancer

global demethylation during cervical cancer (which means demethylation for HPV)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1291396/

cervical cancer and herv-K
http://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-13-4

HPV and Herv-K
http://onlinelibrary.wiley.com/store/10.1002/ijc.29003/asset/ijc29003.pdf?v=1&t=j0a6z1qh&s=d0dde9b76c7e1a8c7bd22fee34bb4a6597b34104

HPV causes cervical and pancreatic cancer

HPV might cause kidney cancer
https://www.ncbi.nlm.nih.gov/pubmed/22237219

herv-E and kidney cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775266/

Melanoma (flavivirus) is herv-k (demethylation)
https://www.ncbi.nlm.nih.gov/pubmed/19167380

(earlier hypothesis on blog that some flaviviruses can use MCR1 and end up in the nucleus)

merkel cell carcinoma and polyomavirus
https://www.ncbi.nlm.nih.gov/pubmed/23387356

herv-w and JC polyomavirus
https://www.researchgate.net/publication/296208262_Activation_of_HERV-W_human_endogenous_retroviruses_by_JC_polyomavirus_in_human_astrocytes_a_novel_effect_that_could_contribute_to_neurodegeneration

polyomaviruses go through the ER

Further thoughts Hervs are named for the amino acid tRNA that binds to the primer-binding-site of the viral RNA  (tRNA are what match the amino acids to the RNA in ribosomes)

Herv-E is lysine
Herv-K is glutamic acid

these amino acids of the tRNA are both zwitterions (can be bipolar)

Herv-H is histidine
Herv-F is phenylalanine
Herv-W is tryptophan

These amino acids are not just zwitterions but they have imidazole rings (stronger charges)

How is this significant for methylation during embryogenesis?  is it because the carboxyl groups are methylated and the imidazole rings are amphoteric? (the rings can be bipolar) so the tRNAs can function even with all the methylation

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