Date:   9/13/2012 3:09:41 PM ( 13 y ago)
Hits:   1,427
URL:   https://www.curezone.org/forums/fm.asp?i=1984939

No, I never got a biopsy because so many people here said it turned up nothing, I didn't want to expose myself to infection, and didn't want scarring. But after nearly 6 years I'm reconsidering getting one to rule out or prove the chronic infection hypothesis.

I don't want to sound pedantic, but let's clarify some things here. When we talk about inflammation, we are talking about either acute or chronic inflammation. Inflammation symptoms (heat, redness, swelling, pain, loss of function) normally denote an immune response to a pathogen, and involve plasma with white blood cells rushing to the site, releasing cytokines, attracting other cells to attack the abnormal cells with hydrogen peroxide, and phagocytes to engulf and digest the cells. Then signals end the inflammatory response. Many people here have chronic inflammation and peeling of the lips, i.e. exfoliative cheilitis. Chronic inflammation can be a sign that normal immunomodulating systems are not working and the tissue itself is being attacked.

At most, I can remember redness and minor burning directly following trauma to my lips from rough kissing and directly following obsessively peeling my chapped lips, but all other inflammation since then has been a direct result of different experimental topicals or consuming acidic foods and drinks. So if there is a virus, fungus, or bacteria at work on my lips, it seems like my immune system indeed doesn't recognize it or doesn't have the resources to fight it. I'm not sure which is worse, chronic inflammation or chronic persistence of a localized pathogen. Depends on the virulence of the pathogen and level of inflammation, I guess.

Different viruses act in different ways, and create different immune responses, from what I can gather. For example, in high-risk HPV, which is the predominant causes of oral-HPV related cancers, the virus alter keratinocytes in the basal layer of the epithelium, below the epidermis. (Low-risk visible warts affect the epidermis). The virus is pretty sneaky as far as the immune system is concerned, only replicating its DNA and expressing its proteins after the keratinocyte has started to move up toward the stratum corneum, where it eventually becomes our well-known corneocyte (skin cell with no nucleus) and sheds off the host, us.

The key point though is that there is no inflammation due to the virus. The body resolves the problem in 80-90% of cases through other means:
"In this infectious cycle, the virus is basically a hitchhiker-joining the keratinocyte at the start of its journey as a primitive basal cell in the epithelium through to its end as a terminally differentiated squame. It is a replication strategy in which viral DNA replication and virus assembly occur in a cell that will terminally differentiate and die by natural causes. Thus, there is no viral-induced cytolysis or necrosis, and therefore no inflammation. For most of the duration of the HPV infectious cycle, there is little or no release into the local milieu of proinflammatory cytokines, which is important for antigen presenting cell (APC) activation and migration. The central signals to kick start the immune responses in squamous epithelia are absent."
Source: http://red.9thunder.com/pdf/gwdt-pdf/9.pdf


Now, a herpes outbreak if left untreated could more easily invite secondary infection which would invite inflammation and the release of cytokines. If you have HPV and HSV, and control the herpes outbreak with acyclovir, maybe the body stops fighting the HPV. The question remains, do we want inflammation to end the persistence of the pathogen, or do we want the inflammation to stop attacking healthy cells, as in the case of psoriasis.

Finally, I think I should mention that the effect of Protopic is to inhibit cytokine production (interleukin-2), and the effect of Imiquimod is to induce cytokine production (interferon-α, interleukin-6, and tumor necrosis factor-α). However, it seems to me that both carry substantial risks based on the existing trauma and permeability of the area, and depending on the constitution of your immune system and your body's ability to regulate the all-out-attack or lack thereof ... as there's no way to know how your body will react, it's a simple game of roulette.

Peace,
C.S.
 

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