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Medical Forum / Diseases and Disorders / Herpes / November 2003Where, when asymptomatic shedding, viruses are located in the body?
does anyone know? In the mucus and stuff like that? Where about? Perl Molson If "viruses are located in the body", then they aren't "shedding". In the body, they're dormant. Once they begin replicating (from the nerve center that's infected), they can travel to the surface of the skin and then be 'shed'. This can occur anywhere within the area served by the nerve center where the virus hibernates. People with genital herpes have tested positive for shedding all through the boxer shorts area at times. This shedding can most easily occur at thinly skinned areas such as the sexual organs, anus, etc. Orally located shedding is mostly around the chin just below the lips, lips, nose area...again, "thinly skinned" areas. But can happen on cheeks, point of chin, etc. Herpes virus being shed can be found in saliva (for oral) and sexual secretions (for genital) also but the researchers think this is caused by these secretions passing over a shedding location and picking it up as it goes by. Once in these secretions, the virus has a limited lifespan and limited ability to be transferred. They THINK this to be the case anyway... Hang in -G > does anyone know? > In the mucus and stuff like that? Where about? > > Perl Molson > If "viruses are located in the body", then they aren't "shedding". In the > body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 20 lines] > > > > Perl Molson It seems we did not discussed the issues related to the surface of skin/mucosa too much in here. I'd like to learn more about it. http://www-ermm.cbcu.cam.ac.uk/99000393h.htm Schematic representation of genes/proteins involved in herpes simplex virus infection - animated > If "viruses are located in the body", then they aren't "shedding". In the > body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 20 lines] > > > > Perl Molson It seems we did not discussed the issues related to the surface of skin/mucosa too much in here. I'd like to learn more about it. http://www-ermm.cbcu.cam.ac.uk/99000393h.htm Schematic representation of genes/proteins involved in herpes simplex virus infection - animated. From the animation it's easy to figure out, that, THE SKIN-MUCOSA IS A MEDIUM THROUGH WHICH THE EPITHELIUM CELLS CANNOT BE INFECTED OR REINFECTED BOTH WAYS. it results that an OB cannot exist without viruses being able to overpass the skin-mucosa areas. Who is responsible for the defence in the skin-mucosa? The immune system and other factors. Also, the health of the skin seems to be a key factor in offering the defence mechanisms an environment where the viruses can be defeated. It is my current assumption that if the skin mucosa can be made extremely efficient in killing the viruses, at one point in time, from the cell body of the sensory ganglion cell, the viruses will, at one point in time, not be able to either FIND THE TRACK THEY USUALLY FOLLOW TO THE MUCOSA - THEY WILL LOSE THE TRACK OR THEY WILL NOT BE CARRIED BY THE TRANSPORTING MECHANISMS CARRIER, or, the ammount of the viruses that the ganglion cell will produce will stop at one point; the ganglion cell virus mechanism cannot be perfect to be able to provide, forever, the new born viruses/genes. It is hard to imagine that, in the ganglion responsible for the producing of viruses, the mechanism will function perfectly forever without becomining otherwise. Even a swiss clock will perish sooner or latter. Imagine an extremelly efficient defence mechanism of the skin/mucosa. No matter how much the ganglia is stressed into producing new viruses, by the triggering factors, the defence mechanism will not colapse. It is hard to believe, that, without any traces that can be found in the skin/mucosa, related to the mechanism of the virus, the virus will keep going as in the animation from the above link. Something from the skin/mucus, must attract the viruses from the ganglia, to it. It EVENTUALLY is something of an electrical nature, as some ions or such, that, provided from the skin/mucosa, will cause the viruses to be transported from through the neuron. I cannot see an independent process, neurons independently to work the viruses way out of the ganglia, independent from the skin/mucosa itself. Like the magnet ideea. It is required some opposite charge to attract the viruses out. Viruses HAVE NO INTELLIGENCE and the genes are not such programmed to provide viruses with such capability of transporting themselves in such a diverse environments such as from skin/mucus to neuronal pathways to the ganglia. Or an I wrong and is it like an earthquake of the body, that will cause the lava of viruses to exit the magma - ganglia towards the surface - mucosa/skin? The magma will exit through the only path that it can exit, because it just there is no other path? Probably not, because initially, the same path was been used in the reverse process. You see the analogy? In the first place, the herpes virus had find its way towards the NEURON dependently of the factors such as the trigerring factors - enzymes, hormons, other substances or in excess or in the lack of it. There was the need for the triggering factors to allow the virus to travel all along the path. The triggering factors "HAVE TO BE", THEN, RESPONSIBLE FOR the transportation. The hijacking of the neuron is dependent of the triggering factors that will cause a reverse proccess. So, in order to exit the ganglia and find their way to the skin/mucosa, the viruses will have the existing viruses from the skin/mucosa as an propulsion factor BY THE SPECIFIC ENVIRONMENT CAUSED BY VIRUSES' ACTIVITY IN THE BODY. My final argument is that the viruses themselves are creating a special environment in the body that will allow the new viruses to born from the genetic material in the ganglia and transported to the skin/mucosa. The special environment made of such enzymes, hormones, etc that allows a certain conductivity or movement mechanisms to be taken place in the body in most likely relevant to the continuity of the viruses' activity. Whether the viruses that cause such an environment are part of the asymptomathic shedding, or they came from the outside the body ( if you receive them from the shedding of your partner, or from your tooth brush etc), these particular viruses will be at the origins of the cause of the environment that will allow the viruses from the ganglia to become active on the skin/mucose areas. Yeah, folks, herpes viruses have neither intelligence nor memory. It is all about the specific environment produced by the same viruses to reactivate old viruses - the later once much more uncontrolable because the long term of the environment goes beyond the lifetime of the causal skin/mucosa viruses. An environment produces by the herpes virus in our bodies persist even after the viruses themselves perish- I repeat, that is eventually sufficient for the genes and such of herpes reminiscences from the ganglia to find their path to the skin/mucosa. These are my speculations, Cheers, Perl Molson. P.S. Comments are obviously welcome > > If "viruses are located in the body", then they aren't "shedding". In the > > body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 33 lines] > THE SKIN-MUCOSA IS A MEDIUM THROUGH WHICH THE EPITHELIUM CELLS > CANNOT BE INFECTED OR REINFECTED BOTH WAYS. I have to make a correction. I have made a mistake: I've intended to write: THE SKIN-MUCOSA IS A MEDIUM THROUGH WHICH the herpes viruses must go to reach THE EPITHELIUM CELLS and consequently, the epithelium cells CANNOT BE REINFECTED and the viruses cannot return to the ganglia to stay there dormant. In other words, the skin-mucosa seems to be the intermediate passageway for the viruses both ways towards the ganglia from the epithelium and from the ganglia towards the epithelium. The skin-mucosa is a "must be 100% protected" area. Perl Molson > it results that an OB cannot exist without viruses being able to > overpass the skin-mucosa areas. [quoted text clipped - 122 lines] > > P.S. Comments are obviously welcome > > If "viruses are located in the body", then they aren't "shedding". In the > > body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 33 lines] > THE SKIN-MUCOSA IS A MEDIUM THROUGH WHICH THE EPITHELIUM CELLS > CANNOT BE INFECTED OR REINFECTED BOTH WAYS. <<<<<< I have to make a correction. I have made a mistake: I've intended to write: THE SKIN-MUCOSA IS A MEDIUM THROUGH WHICH the herpes viruses must go to reach THE EPITHELIUM CELLS and consequently, the epithelium cells CANNOT BE REINFECTED and the viruses cannot return to the ganglia to stay there dormant. In other words, the skin-mucosa seems to be the intermediate passageway for the viruses both ways towards the ganglia from the epithelium and from the ganglia towards the epithelium. The skin-mucosa is a "must be 100% protected" area. Perl Molson <<<<<< Boy, another mistake! Actually, in conformity with the animation at http://www-ermm.cbcu.cam.ac.uk/99000393h.htm we can see clearly that, from "React" to "Epithelium" area, as in below the description left from the "Play" button, following the animation, that the ephitelial cells can be infected directly from the ganglia and then neuron, using its transport mechanism. But still, THERE IS ALWAYS AN AREA WHERE THE VIRUS IS COMPLETELY OUTSIDE THE NEURON AND GANGLIA. That means, that the viruses can be destroyed ALWAYS without the need of the virus killer to reach the neuron! How the viruses can be distroyed before they get to return to the neurons? Through the immune system activity, even including increased oxigen levels, why not, skin-mucus protection using a variety of protective methods: build your skin stronger, more resistant to the disease and use antivirals like pure oils etc, discussed in A.S.H. Yes, folks, the virus must have no escape once it exits the neuron! Perl Molson > it results that an OB cannot exist without viruses being able to > overpass the skin-mucosa areas. [quoted text clipped - 122 lines] > > P.S. Comments are obviously welcome > If "viruses are located in the body", then they aren't "shedding". In the > body, they're dormant. Once they begin replicating (from the nerve center > that's infected), they can travel to the surface of the skin and then be > 'shed'. That's something not very clear yet for me. I've read somewhere that the virus will shed only a few days at a time. The virus eventually will get reactivated in the neuron and travel and shade again. Does the virus return to the ganglia or it can multiply where it sheds (skin, boxers areas, lips). The multiplication must be clearer; where exactly does the multiplication takes place? That is from the neuron to the skin area all included. If they multiply in both neuron and skin locations, is the virus fully developed in both situations? Perl Molson This can occur anywhere within the area served by the nerve center > where the virus hibernates. People with genital herpes have tested positive > for shedding all through the boxer shorts area at times. This shedding can [quoted text clipped - 16 lines] > > > > Perl Molson >> If "viruses are located in the body", then they aren't "shedding". In the >> body, they're dormant. Once they begin replicating (from the nerve center >> that's infected), they can travel to the surface of the skin and then be >> 'shed'. >That's something not very clear yet for me. Along with everything else. >I've read somewhere that the virus will shed only a few days at a time. The trouble with simple people like you is that they have completely simple views of the things they read. "The virus" in the sense you use it is not a monolith. "The virus" is actually thousands of discrete viruses, each of which is quite capable of acting individually. In the average HSV infected person it is likely that *some* virus is active at any given moment, but it is only when sufficient numbers of viruses to be detected get active that we refer to the condition as "shedding". >The virus eventually will get reactivated in the neuron and >travel and shade again. >Does the virus return to the ganglia or it can multiply where it sheds (skin, >boxers areas, lips). After the hundreds of articles you've posted, Perl, how can you not know that? Individual viruses don't "return" anywhere. Individual viruses hijack cellular machinery to make thousands of copies of themselves, but like the cells they commandeer they don't survive the process. Some of the copies, however, can and will go back to the ganglia. >The multiplication must be clearer; where exactly does the multiplication >takes place? If you had the slightest inkling of basic viral morphology you wouldn't be asking that question. >That is from the neuron to the skin area all included. >If they multiply in both neuron and skin locations, >is the virus fully developed in both situations? I think you need to heat up some wooden spoons and stick them in your ears. Mike > >> If "viruses are located in the body", then they aren't "shedding". In the > >> body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 16 lines] > when sufficient numbers of viruses to be detected get active that we > refer to the condition as "shedding". > >The virus eventually will get reactivated in the neuron and > >travel and shade again. [quoted text clipped - 3 lines] > After the hundreds of articles you've posted, Perl, how can you not > know that? Some times I am focussing on a particular issue about the virus and I am ommiting some basic things. > Individual viruses don't "return" anywhere. Individual viruses hijack > cellular machinery to make thousands of copies of themselves, but like > the cells they commandeer they don't survive the process. In this case how is it possible for viruses to survive on a towel or tooth brush for several hours? Is that because on the towel, tooth brush etc, there are INFECTED SKIN CELLS that contain viruses (still alive?). Some of the > copies, however, can and will go back to the ganglia. > [quoted text clipped - 3 lines] > If you had the slightest inkling of basic viral morphology you > wouldn't be asking that question. Eventually these are some of the currently unknown areas. http://darwin.bio.uci.edu/~faculty/wagner/movieindex.html Perl Molson > >That is from the neuron to the skin area all included. > [quoted text clipped - 5 lines] > > Mike >> >The virus eventually will get reactivated in the neuron and >> >travel and shade again. >> >Does the virus return to the ganglia or it can multiply where it sheds (skin, >> >boxers areas, lips). >> After the hundreds of articles you've posted, Perl, how can you not >> know that? >Some times I am focussing on a particular issue about the virus >and I am ommiting some basic things. Perl, truthfully, I haven't seen you understand a single thing, no matter what you're focusing on. >> Individual viruses don't "return" anywhere. Individual viruses hijack >> cellular machinery to make thousands of copies of themselves, but like >> the cells they commandeer they don't survive the process. >In this case how is it possible for viruses to survive on a towel or >tooth brush for several hours? By exactly the same method by which you would survive if somebody drove you out to the desert and left you there. You would still have the ability to function (relatively speaking) for a few hours until your constituent components had degenerated to the point where you could no longer function. A virus is nothing more than a very tiny, very complex machine. Let's say it's like a toaster, comprende? When the toaster is in the kitchen it can make toast if someone plugs it in, adds bread, and pushes the button. If you take the toaster and put it out in the yard, it's still a toaster (even though it's not making toast) until such rain and snow and other junk has fallen on it to the point where it no longer will function as a toaster. These aren't difficult concepts for most people to master, Perl, but I appreciate the fact that you are having trouble. >Is that because on the towel, tooth brush etc, there >are INFECTED SKIN CELLS that contain viruses (still alive?). No, it's because the particles of the submicroscopic atmosphere haven't yet fully degraded or sucked off the outer coating of the viral structure. Mike > If "viruses are located in the body", then they aren't "shedding". In the > body, they're dormant. Once they begin replicating (from the nerve center [quoted text clipped - 20 lines] > > > > Perl Molson I think I've found the part of the answer myself. Following the animation, http://www-ermm.cbcu.cam.ac.uk/99000393h.htm it says that the neuronal cell is less permissive to HSV replication you can see that when the green line at the bottom is reaching the "cell body" triangle on that graphic. I would like a bit more details, though, then just "less permissive". Perl Molson >I think I've found the part of the answer myself. Sure you have, Perl, sure you have. >Following the animation, >http://www-ermm.cbcu.cam.ac.uk/99000393h.htm >it says that >the neuronal cell is less permissive to HSV replication >you can see that when the green line at the bottom >is reaching the "cell body" triangle on that graphic. Okay, now how do we get those little triangles out of our bodies??? Maybe if we rub little circles on our skins?!? Mike > >I think I've found the part of the answer myself. > [quoted text clipped - 12 lines] > > Mike You, dumb a.s! Perl Molson > does anyone know? > In the mucus and stuff like that? Where about? IIRC its mostly at the mucocutaneous junctions that it gets shed. Though that isnt automatic (probably where the early ideas of skin latency came from they were spotting shedding virus not latent). It hasn't been completely investigated as far as I know - swabs ued to test for this experimentally will likely be quite wide ranging to get the most accurate Yes/No answer for an individual. Try plugging a few keywords into pubmed and see what comes back Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568 > > does anyone know? > > In the mucus and stuff like that? Where about? [quoted text clipped - 10 lines] > > Tim http://jvi.asm.org/cgi/content/full/75/2/821 Herpes Simplex Virus gE/gI Sorts Nascent Virions to Epithelial Cell Junctions, Promoting Virus Spread the page has lots of illustrations > > > does anyone know? > > > In the mucus and stuff like that? Where about? [quoted text clipped - 16 lines] > > the page has lots of illustrations More on "asymptomatic shedding" or "subclinical" shedding: Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons. Wald A, Zeh J, Selke S, Warren T, Ryncarz AJ, Ashley R, Krieger JN, Corey L. Department of Medicine, University of Washington, Seattle 98122, USA. annawald@u.washington.edu BACKGROUND: Most persons who have serologic evidence of infection with herpes simplex virus (HSV) type 2 (HSV-2) are asymptomatic. Historically, it has been assumed that these persons have less frequent viral reactivation than those with symptomatic infection. METHODS: We conducted a prospective study to investigate genital shedding of HSV among 53 subjects who had antibodies to HSV-2 but who reported having no history of genital herpes, and we compared their patterns of viral shedding with those in a similar cohort of 90 subjects with symptomatic HSV-2 infection. Genital secretions of the subjects in both groups were sampled daily and cultured for HSV for a median of 94 days. RESULTS: HSV was isolated from the genital mucosa in 38 of the 53 HSV-2-seropositive subjects (72 percent) who reported no history of genital herpes, and HSV DNA was detected by the polymerase-chain-reaction assay in cultures prepared from genital mucosal swabs in 6 additional subjects. The rate of subclinical shedding of HSV in the subjects with no reported history of genital herpes was similar to that in the subjects with such a history (3.0 percent vs. 2.7 percent). Of the 53 subjects who had no reported history of genital herpes, 33 (62 percent) subsequently reported having typical herpetic lesions; the duration of their recurrences in these subjects was shorter (median, three days vs. five days; P<0.001) and the frequency lower (median, 3.0 per year vs. 8.2 per year; P<0.001) than in the 90 subjects with previously diagnosed symptomatic infection. Only 1 of these 53 subjects had no clinical or virologic evidence of HSV infection. CONCLUSIONS: Seropositivity for HSV-2 is associated with viral shedding in the genital tract, even in subjects with no reported history of genital herpes. http://content.nejm.org/cgi/content/abstract/342/12/844 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 0727588&dopt=Abstract&holding=f1000 > > > does anyone know? > > > In the mucus and stuff like that? Where about? [quoted text clipped - 16 lines] > > the page has lots of illustrations http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Link&db=PubMed&dbFrom=PubMed&f rom_uid=10727588 > > IIRC its mostly at the mucocutaneous junctions that it gets shed. Though > > that isnt automatic (probably where the early ideas of skin latency came [quoted text clipped - 3 lines] > Herpes Simplex Virus gE/gI Sorts Nascent Virions to Epithelial Cell > Junctions, Promoting Virus Spread I think you are mixing junctions - these junctions are not the gross anatomy junction I was talking about. Thats glycoproteins and how they organise cell-cell spreading you are linking rather than anatomic areas of shedding. Skin and mucous membranes are both epithelial structures. Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568 mucocutaneous junction The site of transition from epidermis to the epithelium of a mucous membrane. http://cancerweb.ncl.ac.uk/cgi-bin/omd?mucocutaneous+junction OK a syntax, semantic error. How I see it, all the blisters, lesions, ulcers etc develop OUTSIDE THE NEURON. Even though the virus may escape in neuron, those that are outside the neuron can be destroyed by our immune system and through various methods presented here at A.S.H. Until recently, I wasn't aware of it. What's hiding in the neuron, can be made sort of not able to become active. It seems to me that no significant damage can be produced BUT outside the neurons. Am I correct here, Tim? Perl Molson On 31 Oct 2003, Perl Molson wrote: > Tim Fitzmaurice <tjf11@cus.cam.ac.uk> wrote in message news:<Pine.SOL.3.96.1031031140427.1431A-100000@draco.cus.cam.ac.uk>... > > [quoted text clipped - 5 lines] > Herpes Simplex Virus gE/gI Sorts Nascent Virions to Epithelial Cell > Junctions, Promoting Virus Spread I think you are mixing junctions - these junctions are not the gross anatomy junction I was talking about. Thats glycoproteins and how they organise cell-cell spreading you are linking rather than anatomic areas of shedding. Skin and mucous membranes are both epithelial structures. Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568 > mucocutaneous junction > The site of transition from epidermis to the epithelium of a mucous membrane. [snip] > Am I correct here, Tim? Sticking just to the junction bit here not the rest of it which Ill come back to (been off net for a while lots to wade through). I didn't have a problem with the word junction. However the glycoproteins will be shuttling things to cell junctions according to that abstract. Cell junctions are structures in the cell membranes like 'tight junctions' and 'gap junctions' and a whole host of weird bits only membrane chemists really understand....the virus would use these cellular structures to moe fom cell to cell Thats an entirely different scale to muco-cutaneous junctions which is an anatomic description. I think you were mixing the two..... Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568 And tot he rest of this post.... > How I see it, all the blisters, lesions, ulcers etc develop > OUTSIDE THE NEURON. Yes. Well, for the moment. Targeting the DNA circle in the neuron is a potential target but we need much more information on latency. And there are people doing just this sort of work. > Even though the virus may escape in neuron, those > that are outside the neuron can be destroyed by our immune system and > through various methods presented here at A.S.H. For the moment. Yes this is what the topicals do...some by interfering with the DNA replication ACV etc) some by interfering with virus movement (Abreva is one of thoseIIRC) > What's hiding in the neuron, can be made sort of not > able to become active. Theoretically. And yes people are trying to do this. If you can't remove it can you control thelatent state sufficiently to make it stay there > It seems to me that no significant damage can be produced > BUT outside the neurons. > > Am I correct here, Tim? Yes, pretty much. The virus has developed to not take out the neuron and to make sure it doesn't do anything to make the body take the neuron out (difficult enough anyway) as part of its survival mechanism. Tim -- When playing rugby, its not the winning that counts, but the taking apart ICQ: 5178568 |
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