"Which nerve fibers does herpes infect? "

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howl (178 posts) Nov-15-02, 08:55 PM (CST) "Which nerve fibers does herpes infect? " I've been thinking about hsv and internal organs. I apologise for the really geeky questions but I'm trying to work this out in my head. Any comments are appreciated. *So if herpes is generally infecting nerve endings in mucosa and traveling to the dorsal root ganglion (DRG), it is traveling up GVA fibers (sensory fibers going to the spinal cord from the skin) to the Dorsal Root Ganglia (DRG) near its associated spinal segment. (Because those are the only nerves serving the skin). Theoretically herpes gets to the nerve cell in the ganglia and goes latent, until at some point it replicates itself. *Is it true that in most cases when it replicates the virus is traveling back down the SAME GVE fibers to the skin? Thus why most recurrences are epithelial, and close to home? *Theres some experimental evidence that herpes can cross from one cell body into another. The stuff I've read indicates it makes bridges between adjacent cell bodies, not between a cell body and an axon. That is an important distinction that could tell us exactly what HSV can and can't do in immunocompetant adults. If its only between cell bodies, HSV is limited to what is in the DRG. That is GVA cell bodies and GSA (sensory fibers from the muscles) cell bodies. If true that would effectively keeps herpes out of internal organs, since no cell bodies that directly serve internal organs are in the DRG. *So we have a DRG infected. When HSV reactivates it could travel back down the axon the way it came to the skin, or it could travel down a dendrite of that cell to wherever it ends explaining why OB can "move" somewhat. *But what if herpes can cross between an axon/dendrite and another cell body? If this is true I can see some other internal organs becoming infected with HSV becaue it can take cutoff to other highways instead of changing routes in the center of town. Sometimes GVAs synapse on neurons going to the brain. Does that lead to herpes menigitis and encephalitis? Does that mean herpes inadvertently took the "wrong path" . (It gets no reproductive advantage from heading up there or to any other organ.) Does the virus realise this and just doesn't replicate in most circumstances which is why we don't see more herpes menengitis? Or is it that the body is better at detecting HSV and mounting a response against herpes when it is outside its usual haunts within the nervous system. The virus is killed off when it starts to take the wrong path? Or is it that the virus can't travel that far b/c of the physical barriers the DRG provides? Howl   Alert Edit | Reply | Reply With Quote | Top

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Subject     Author     Message Date     ID    RE: Which nerve fibers does herpes infect? J Nov-16-02 1    RE: Which nerve fibers does herpes infect? howl (Guest) Nov-16-02 2        RE: Which nerve fibers does herpes infect? J Nov-16-02 4  RE: Which nerve fibers does herpes infect? windy Nov-16-02 3    Thanks guys. howl (Guest) Nov-17-02 5        Good discussion. - I've noticed the same thing. Rajah Nov-17-02 6            RE: Good discussion. - I've noticed the same thing... just wandering (Guest) Nov-20-02 9                RE: Good discussion. - I've noticed the same thing... windy Nov-20-02 10  RE: Which nerve fibers does herpes infect? BH (Guest) Nov-19-02 7    Yes, it helps. howl (Guest) Nov-19-02 8    RE: Which nerve fibers does herpes infect? I_amso Nov-25-02 11        RE: Which nerve fibers does herpes infect? starratt Nov-25-02 12            RE: Which nerve fibers does herpes infect? windy Nov-26-02 13                RE: Which nerve fibers does herpes infect? starratt Nov-26-02 14                    RE: Which nerve fibers does herpes infect? windy Nov-27-02 15                        windy, was it this one? msmom Nov-27-02 16                            RE: windy, was it this one? windy Nov-27-02 17

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J (1312 posts) Nov-16-02, 01:51 AM (CST) 1. "RE: Which nerve fibers does herpes infect? " Hi Howl: >*But what if herpes can cross >between an axon/dendrite and another >cell body? If this is >true I can see some >other internal organs becoming infected >with HSV becaue it can >take cutoff to other highways >instead of changing routes in >the center of town. Understaning *how* the virus spreads is interesting. However, it does happen frequently. >Sometimes GVAs synapse on neurons going >to the brain. Does that >lead to herpes menigitis and >encephalitis? Does that mean herpes >inadvertently took the "wrong path" >. (It gets no reproductive >advantage from heading up there >or to any other organ.) While we can rationalize the advantages of one path over another, it's quite possible that HSV has been successful even though it lacked this insight. Meaning, it might have evolved by spreading in multiple directions.> > >Does the virus realise this and >just doesn't replicate in most >circumstances which is why we >don't see more herpes menengitis? Howl: you keep implying the virus actually *thinks.* Meningitis is quite common -- about 30% of women and 10% of men get meningitis during a primary epsiode. HSV-2 is also the priamry cause of recurrent meningitis (Mollart's meningitis). If you look at autopsy reports, it really is quite invansive. As an example... J Pathol 2002 Jul;197(3):395-402 Related Articles, Links Herpesviruses in brain and Alzheimer's disease. Lin WR, Wozniak MA, Cooper RJ, Wilcock GK, Itzhaki RF. Department of Optometry and Neuroscience, UMIST, Manchester, UK. It has been established, using polymerase chain reaction (PCR), that herpes simplex virus type 1 (HSV1) is present in a high proportion of brains of elderly normal subjects and Alzheimer's disease (AD) patients. It was subsequently discovered that the virus confers a strong risk of AD when in brain of carriers of the type 4 allele of the apolipoprotein E gene (apoE-epsilon4). This study has now sought, using PCR, the presence of three other herpesviruses in brain: human herpesvirus 6 (HHV6)-types A and B, herpes simplex virus type 2 (HSV2) and cytomegalovirus (CMV). HHV6 is present in a much higher proportion of the AD than of age-matched normal brains (70% vs. 40%, p=0.003) and there is extensive overlap with the presence of HSV1 in AD brains, but HHV6, unlike HSV1, is not directly associated in AD with apoE-epsilon4. In 59% of the AD patients' brains harbouring HHV6, type B is present while 38% harbour both type A and type B, and 3% type A. HSV2 is present at relatively low frequency in brains of both AD patients and normals (13% and 20%), and CMV at rather higher frequencies in the two groups (36% and 35%); in neither case is the difference between the groups statistically significant. It is suggested that the striking difference in the proportion of elderly brains harbouring HSV1 and HSV2 might reflect the lower proportion of people infected with the latter, or the difference in susceptibility of the frontotemporal regions to the two viruses. In the case of HHV6, it is not possible to exclude its presence as an opportunist, but alternatively, it might enhance the damage caused by HSV1 and apoE-epsilon4 in AD; in some viral diseases it is associated with characteristic brain lesions and it also augments the damage caused by certain viruses in cell culture and in animals. Copyright 2002 John Wiley & Sons, Ltd. Keep in mind the servoprevalence of HSV-2 and the age of people with AD and matched controls (this is a UK study) -- quite invasive. > >Or is it that the body >is better at detecting HSV >and mounting a response against >herpes when it is outside >its usual haunts within the >nervous system. The virus is >killed off when it starts >to take the wrong path? > The virus appears to be successful regardless of its path. > >Or is it that the virus >can't travel that far b/c >of the physical barriers the >DRG provides? Obviously it does travel and well. J   Remove | Alert Edit | Reply | Reply With Quote | Top

howl (Guest) (288 posts) Nov-16-02, 01:11 PM (CST) 2. "RE: Which nerve fibers does herpes infect? " Hey J, I don't believe herpes *thinks* in an individual sense. Thats my shorthand for explaining why it evolved the way it did. Evolutionary biologists would decapitate me for using that word. Sorry for the sloppy wording. The whole point to life is reproduction. HSV, like any organism, is driven by the evolutionary need to reproduce itself or face extinction. Since it is well adapted to humans I think it has evolved mechanisms and pathways so it doesn't kill/severly dehabilitate immunocompetant adults. HSV is well adapted to its host (unlike AIDS). I think the key to figuring out why some people have trouble is to discover those mechanisms which generally prevent it from causing more global problems within the body. I know menigitis is common but herpes menigitis isn't often deadly, just miserable. Herpes encephalitis is rare and deadly. That bolsters my arguement that HSV generally isn't deadly and has evolved well into its ecological niche and that there are evolutionary mechanismd limiting HSVs behavior. Sorry for trotting out this line. But just because there is HSV DNA by PCR the doesn't prove that the virus is 1) present or 2) causing a problem. By analogy, there is a whole hubub over chlamydia trachomatis in arthrosclerotic plaques in coronary patients. A lot of people assume that the clamydia/associated inflammation caused the arteriosclerosis. But theres a good possibility that the macrophages of the plaque lead full lives prior to becoming part of the plaque. They may have killed some chlamydia elsewhere in the body and then gone on to form the plaque with some chlamydial remnants in it. In that senario chlamydia is totally unrelated to heart disease but we can still detect the DNA. Anywhere there are phagocytic cells in large numbers (like in Alzheimers plaques) there may be background contamination. I'm also hesitant to point to HSV1 as the smoking gun in Alzehimers because no one has ruled out prions as an etiology. I'm not sure that HSV is really present in all those tissues in immunocompetant adults. I'm not convinced that HSV travels very far with in the nervous system unless theres a specific problem in the host, because of the physical limitations, because of evolutionary pressues, & b/c of the lack of data showing HSV in organs of living healthy people. Something I'll continue to research anyway. Thank you for the thoughtful reply, J. Howl   Remove | Alert Edit | Reply | Reply With Quote | Top

J (1312 posts) Nov-16-02, 02:33 PM (CST) 4. "RE: Which nerve fibers does herpes infect? " Aha...I see what you are saying. Very interesting points that I'd like to continue to discuss. However, I will not be able to contribute any "real" time for a week or so. I hope other people chime in/continue the discussion. J   Remove | Alert Edit | Reply | Reply With Quote | Top

windy (2401 posts) Nov-16-02, 01:41 PM (CST) 3. "RE: Which nerve fibers does herpes infect? " >I've been thinking about hsv >and internal organs. I apologise >for the really geeky questions >but I'm trying to work >this out in my head. >Any comments are appreciated. > >*So if herpes is generally infecting >nerve endings in mucosa and >traveling to the dorsal root >ganglion (DRG), it is traveling >up GVA fibers (sensory fibers >going to the spinal cord >from the skin) to the >Dorsal Root Ganglia (DRG) near >its associated spinal segment. (Because >those are the only nerves >serving the skin). What about sympathetic or parasympathetic efferent fibers to blood vessels, sweat glands, and erector pilae? >*Is it true that in most >cases when it replicates the >virus is traveling back down >the SAME GVE fibers to >the skin? Thus why most >recurrences are epithelial, and close >to home? That's my understanding. The virus comes back down the same axons it went up. > . If its only >between cell bodies, HSV is >limited to what is in >the DRG. That is GVA >cell bodies and GSA (sensory >fibers from the muscles) cell >bodies. If true that would >effectively keeps herpes out of >internal organs, since no cell >bodies that directly serve internal >organs are in the DRG. There are connections to interneurons that go to adjacent ganglia, and there are sympathetics or parasympathetics in the ganglia, and these go to organs. The post-ganglionic fibers have their cell bodies in the ganglia. I don't remember the exact arrangement of all the cell bodies in the DRG to be able to say what physical barriers there are. A modern version of Gray's Anatomy would have that. > > > >*So we have a DRG infected. >When HSV reactivates it could >travel back down the axon >the way it came to >the skin, or it could >travel down a dendrite of >that cell to wherever it >ends explaining why OB can >"move" somewhat. The nervous system preserves its organization on the different levels, so the sensory cell bodies nearest to each other are the ones that terminate nearest each other on the skin. Therefore we see that herpes usually only moves a short distance. > >*But what if herpes can cross >between an axon/dendrite and another >cell body? If this is >true I can see some >other internal organs becoming infected >with HSV becaue it can >take cutoff to other highways >instead of changing routes in >the center of town. > >Sometimes GVAs synapse on neurons going >to the brain. Does that >lead to herpes menigitis and >encephalitis? Does that mean herpes >inadvertently took the "wrong path" >. (It gets no reproductive >advantage from heading up there >or to any other organ.) One known pathway to the brain is from the tip of the nose, through the greater petrosal nerve (GVE to nasal mucosa), and I guess it makes its way back to the geniculate nucleus. (If it's possible to get subclinical encephalitis, then I'm pretty sure I've experienced this route.) > > Your other questions are all good ones, but I have nothing to offer right now, except a couple more questions. When herpes jumps to adjacent nerves, is it more likely that it jumped in the ganglion, or at the zone of skin where the two nerves overlap? (My dollar is on the ganglion) How active is the immune system inside a nerve or inside the DRG? Rattus once posted something about chronic neuralgia being caused by inflammation within the nerve from the immune response. Most sources say that the nervous sytem is protected from the immune system, but I wonder if that's an over-simplification. windy   Remove | Alert Edit | Reply | Reply With Quote | Top

howl (Guest) (288 posts) Nov-17-02, 08:02 PM (CST) 5. "Thanks guys." The more I learn the more questions I have I really appreciate the feedback. Howl   Remove | Alert Edit | Reply | Reply With Quote | Top

Rajah (4635 posts) Nov-17-02, 08:42 PM (CST) 6. "Good discussion. - I've noticed the same thing." I think that is as it should be. Definitely the more we know about a subject the more clearly we can see the aspects of it that we don't understand. One way to tell that you are making progress is by the number of unanswered questions. Rajah   Remove | Alert Edit | Reply | Reply With Quote | Top

just wandering (Guest) (1 posts) Nov-20-02, 00:49 AM (CST) 9. "RE: Good discussion. - I've noticed the same thing." Everything comes back to Darwin and natural selection. This is supposed to explain every thing. No way a virus can think. We as humans have a hard time excepting that anything can think other than us. I'm not saying a virus can think. The natural selection process depends on mutations but what makes a gene change to better fit it's enviroment. How does it know to make a feather a different color or add some legs. You can't figure out why it came to be you can only figure out how to kill it. You don't have to believe it thinks but you have to except that it is intelligent.   Remove | Alert Edit | Reply | Reply With Quote | Top

windy (2401 posts) Nov-20-02, 01:02 PM (CST) 10. "RE: Good discussion. - I've noticed the same thing." Hey, even a single photon has consciousness, else it wouldn't know if there were one or two slits in the screen and whether to behave like a particle or a wave.   Remove | Alert Edit | Reply | Reply With Quote | Top

BH (Guest) (1 posts) Nov-19-02, 06:53 AM (CST) 7. "RE: Which nerve fibers does herpes infect? " Hi Howl: I have not been around lately, but M's Mom e-mailed me to ask me if if I had any input...and I do. You are correct about the trip that makes up from the skin to the sensory neurons. There is even some evidence that the virus is more likely to go latent in pain fibers, rather than other types of sensory neurons. It only takes until about 2 days after infection for the virus to reach the DRG, and there the virus immediately goes latent in neurons and replicates in other neurons (remember that this is not singular virus, bur a population of thousands of virus particles that are bombarding your nerve cells at the skin). When the virus is replicates in the sensory nerves, it can not only be carried out to the skin, but further in to the spinal cord. It is my understanding that at this step the virus is released to other nerve endings in the same DRG as well as nerve fibers that carry sensory signals to the brain. My knowledge of neuroanatomy really bites, so I cannot help you with the details of how the connections work, but you seem to be pretty knowledgeable in that area. The basic idea that I want to convey is that wihtin the nervous system HSV does not seem to spread laterally in the ganglia (i.e. not directly from cell body to cell body), but rather the virus jumps between nerves at the nerve termini....so whereever there is a connection, the virus can make the jump. In contrast, Varicella Zoster Virus (the related herpesvirus that causes chickenpox) can spread laterally within the ganglia, such that one infected neuron rapidly leads to infection of whole clusters of adjacent neurons.....this seems to account for the rapid spread of VZV throughout your peripheral nervous system and the consequent "chickenpox" lesions that you often get from head to foot. Hope that helps, Bill H.   Remove | Alert Edit | Reply | Reply With Quote | Top

howl (Guest) (288 posts) Nov-19-02, 06:12 PM (CST) 8. "Yes, it helps." Thank you for taking the time to post, BH. And thanks MsMom for forwarding that question. Maybe now I can go back to the literature and get a little more out of it . . .   Remove | Alert Edit | Reply | Reply With Quote | Top

I_amso (468 posts) Nov-25-02, 01:42 AM (CST) 11. "RE: Which nerve fibers does herpes infect? " Oh! Well that is different than what my (limited) understanding of it was. I thought it could go from cell to cell directly. So basically, it is still spreading IN the ganglia--but just going though doors and windows instead of through walls, right?   Remove | Alert Edit | Reply | Reply With Quote | Top

starratt (135 posts) Nov-25-02, 11:55 PM (CST) 12. "RE: Which nerve fibers does herpes infect? " For some strange reason I'm in a mood to be corrected, so here goes my argument. Not entirley well thought out as I'm exhausted from editing stuff. When you envision a periphreal nerve fibre it is important to understand that how it communicates with either skin or muscle is through "junctions". For example the pain receptor in the skin says "ouch", that message jumps from the receptor across a junction (via a chemical neurotransmitter) to the nerve fibre, and travels up the nerve fibre to the cell body, from the cell body to the spinal cord where it will make another "jump" to an interneuron, and then "jump" again to a motor neuron to tell you to move that part of your body away from the painful stimulus. Neurons don't communicate nerve messages directly from cell body to cell body, but through their processes (i.e. dendrites and terminals). It would seem to me it stands to reason that the most effective way a virus can move from neuron to neuron is by taking advantage of the communication systems at these junctions. I believe some research has surfaced that indicates that herpes imitates some of the proteins that are involved in these transfers so that it can bind with the ends of the neurons and penetrate that way. However, last time I checked much of the virus's activity in this area is a mystery. Once it gets into the neuron it goes and hangs out at the ganglia (a cluster of cell bodies located close to the spinal cord). But going on the theory above, it is difficult (I won't say impossible tho) for the virus to move from neuron to neuron here. Where it will have an opportunity to move most easily to a different neuron is where there is communication between neurons. Since it also likes skin cells, a very effective spot for it to move about is in the skin cells. I would think it does its most impressive nerve jumps during primary infection before your immune system has a chance to catch up to it. Once you have antibodies built up they will clean up a lot of the virus that tries to jump at junctions as it will be in the "open" at this point (i.e. not hiding in a cell someplace where the immune system won't see it). It has a few extra tricks for getting around in the skin without getting detected as quickly (it can literally fuse skin cells together and open channels between them so that it doesn't have to leave the skin cells right away). However, once it exits the skin cells in an effort to spread, yet again established antibodies will attack it and eliminate it. From what reading I've done, some of the virus's game is a race between itself and the immune system. Can it trick the cell it wants to enter into believing it is something necessary to communicate a message (i.e. a messenger amino acid or something) so that the cell will bind with it so that it can get in? Or will the immune system detect it and eliminate it before it can spread? I'm sure I meant to go someplace brilliant with this, but I've lost my thread here. But I did want to toss in something here more erudite than "surf boards". Be well, Lorraine   Remove | Alert Edit | Reply | Reply With Quote | Top

windy (2401 posts) Nov-26-02, 08:56 AM (CST) 13. "RE: Which nerve fibers does herpes infect? " From some reading and phone conversations with people at UW clinic, I'm under the impression that there's still some debate about whether the virus replicates in skin cells or not during recurrences. I think Sacks says that it does, and the UW folks can't decide based on the evidence, but I don't know what the evidence is. Have you seen anything about this? Maybe I'm thinking of latency in skin cells. Now I can't remember for sure.   Remove | Alert Edit | Reply | Reply With Quote | Top

starratt (135 posts) Nov-26-02, 10:03 PM (CST) 14. "RE: Which nerve fibers does herpes infect? " Okay, I'm going by what sacks had to say about replication and he definately claims it replicates in the skin. You've probably done more reading then me, but I haven't seen anything to contradict this. In fact my memory is getting fuzzy, but I'm not certain it does a lot of its replication in the ganglia compared to the amount of replication it does in the skin cells. (When I get time again I may do some more concerted research to see what there is to know.) I haven't heard about it going dormant anywhere but in nerve ganglia. Of course, lying dormant in skin cells would be a limited time offer since all skin cells die off and sluff away within 24-45 days of originally being formed (gad, if we could be so lucky for it to go dormant in the skin rather than in the nerves). Whereas sensory neurons have life spans of 100+ years and are a much safer place to establish dormancy. Here's a question for you. Does it actually destroy nerve cell bodies like it does skin cells when it replicates there? I've been pondering this and the answer to me appears to be no as that would defeat the purpose of lying dormant in the nerve to start with. Granted we have lots of nerves, but over time theoretically destroying various nerve cells should have a catastrophic affect on the sensory nerve system. Or am I off on a tangent? Be well Lorraine   Remove | Alert Edit | Reply | Reply With Quote | Top

windy (2401 posts) Nov-27-02, 07:35 AM (CST) 15. "RE: Which nerve fibers does herpes infect? " OK, it wasn't latency in the skin I was thinking of, but just the question of whether it replicates in skin cells during recurrences. Dig around in the studies by Anna Wald for mention of it. I think what they said was that they couldn't find evidence of replication in the skin, but I'm not sure what they were looking for. It might be in the one called "Virilogic Characteristics" or else "shedding in women - effects of acyclovir" (something like that - AKA Study from Hell). BH, are you still on this thread? In one of the recent Aurx threads, there was a link to a study by Calton, I think, that showed a neuroprotective effect of some viral enzyme (ICP10K?). On the other hand (or the other lip) the site of my primary has some decreased sensitivity to touch compared to the surrounding area. That's after 40 years of recurrences. It may have been like that for a long time, but I only noticed it recently. It's a half-centimeter numb spot, and it's still the most likely place for my cold sores to pop up when they do.   Remove | Alert Edit | Reply | Reply With Quote | Top

msmom (1289 posts) Nov-27-02, 10:48 AM (CST) 16. "windy, was it this one?" I seem to remember wondering why that statement about biopsies of genital mucosa was in there. MM ===== Frequent genital herpes simplex virus 2 shedding in immunocompetent women A Wald, L Corey, R Cone, A Hobson, G Davis, J Zeh. ABSTRACT Reactivation of herpes simplex virus type 2 (HSV-2) occurs intermittently as perceived clinically and by viral culture. We performed a series of studies to evaluate the frequency and anatomic pattern of HSV-2 reactivation using both viral isolation and HSV PCR assay. Daily samples of genital secretions were obtained from 27 HSV-2 seropositive women; a subset of subjects obtained samples while receiving oral acyclovir 400 mg PO twice a day. HSV DNA was detected in genital swab specimens on 28% of 1410 days compared with 8.1% of days by viral isolation. Eleven of 20 women had HSV DNA detected on >20% of days, 4 on >50%, and 2 on >75% of days; in contrast, none of women shed on more than 21% of days by viral isolation. The daily administration of oral acyclovir promptly reduced the frequency of HSV DNA detection by a median of 80%. Within 3-4 days of discontinuing daily acyclovir, HSV DNA again appeared in the genital area. Biopsies showed no evidence of latent HSV DNA in genital mucosa. HSV-2 shedding in the genital mucosa occurs much more frequently than previously appreciated. This frequent reactivation likely plays a role in the continued epidemic spread of genital herpes worldwide.   Remove | Alert Edit | Reply | Reply With Quote | Top

windy (2401 posts) Nov-27-02, 02:07 PM (CST) 17. "RE: windy, was it this one?" That be the one. Of course, that doesn't mean that it doesn't happen; just that they didn't find it that time. OK, I went looking, and I found one. Spinosum cells are skin cells. J Cutan Pathol 1987 Jun;14(3):165-75 Related Articles, Links HSV-2 replication sites, monocyte and lymphocytic cell infection and virion phagocytosis by neutrophils, in vesicular lesions on penile skin. Electronoptical studies of a biopsy. Boddingius J, Dijkman H, Hendriksen E, Schift R, Stolz E. From a heterosexual male with recurrent genital herpes simplex virus (HSV-2) infection, a fresh intraepidermal vesicle on the penile skin was excised by punch biopsy, fixed and processed for electron microscopy. Differing locations and appearances of capsids and virions were studied to elucidate true host or destroyer cells. HSV-2 propagation and virion formation occurred predominantly in multi- or mononucleate spinosum cells situated at the base of the vesicle. However, some of the monocytes, young histiocytes and lymphocytic cells floating in the vesicle fluid were also involved. They harbored a small number of intranuclear capsids, designating the cells as viral (capsid) carriers. Infrequently encountered free virions in the vesicle fluid were invariably seen near neutrophils. All neutrophil granulocytes examined lacked intranuclear capsids. In contrast, distinct evidence of phagocytosis of virions and some capsids by neutrophils was found in the vesicle fluid near apical portions of spinosum cells packed with virions, or in neutrophils located between virion-loaded spinosum cells in the base lining of the vesicle. In the cytoplasm of neutrophils, single and lysosome-enclosed clusters of virions were noted. Myelin figures and vacuolation of lysosomes in free-floating neutrophils were suggestive of virion distintegration. Viral propagation and abundant virion formation, beside neutrophil and lymphocyte attack, eventually lead to spinosum cell destruction. The minimal cytopathic effects (CPE) observed in involved monocytes and lymphocytic cells floating in the vesicle fluid suggest that these cells might function as vehicles for HSV-2 (capsid) transport to the exterior or interior. PMID: 3038975   Remove | Alert Edit | Reply | Reply With Quote | Top

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