Is lichen planus autoimmune cross-targeting of HPV16 and trichophyton?

Autoimmune cross-targeting hypothesis

The layering of 2 different infections on one target triggering autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria infection marking the outside.

Is lichen planus autoimmune cross-targeting of HPV16 and trichophyton? 

Lichen planus and trichophyton schoenleinii
https://www.researchgate.net/publication/234085237_Pitfall_scarring_alopecia_Favus_closely_mimicking_lichen_planus

Lichen planus and HPV
http://www.pasteur.fr/en/institut-pasteur/press/press-documents/human-papillomavirus-linked-auto-immune-disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075460/
http://www.ncbi.nlm.nih.gov/pubmed/25256345
http://www.ncbi.nlm.nih.gov/pubmed/21528036

How does tinea captis overlap with lichen planus? Just location? when the fungus causes loss of hair on the head?

tinea capitis and trichophyton schoenleinii
http://www.ncbi.nlm.nih.gov/pubmed/17992453

tinea captis and trichophyton tonsurans
https://www.researchgate.net/publication/16724647_Lupus_Erythematosus_like_Tinea_Capitis_caused_by_Trichophyton_Tonsurans

note that tinea captis is the specific type of alopecia (hair loss) that is caused by fungus?

Previously i had looked at alopecia as an autoimmune disease cross-targing of trichophyton and flaviviruses (west nile or hepatitis C)
http://angelabiggs.blogspot.com/2015/05/updated-alopecia-as-autoimmune-disease.html

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 Nobel prize for HPV work)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135410/

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen  inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications done by the virus. 

There are DNA polymerases and RNA polymerases. Think of DNA as the cookbook and RNA as recipes...one polymerase copies the entire cookbook, one makes repairs, and one polymerase copies just a recipe.

If the viral polymerases are inhibited by the carcinogen instead of the host's polymerase then the cancer "stem" cell could be created.  The host's polymerases have access to and can make unlimited copies.

Oral cancers:  HPV and alcohol/tobacco

http://www.ncbi.nlm.nih.gov/pubmed/21330164

connection between lichen planus and oral cancer could be the HPV
http://www.ncbi.nlm.nih.gov/pubmed/10527601