Killing viruses

[Yuck]

I thoroughly enjoyed the article on viruses:
“How come we can’t come up with a way to cure viruses?”
found at
http://www.straightdope.com/columns/000204.html

However, in it Cecil said

“The most effective approach is still vaccination, which creates antibodies that intercept the virus before it invades a cell.”

Earlier in the article, he said

“To destroy the virus you have to destroy the host cells and maybe the host, which sorta defeats the purpose.”

I believe this last statement stands on its own and is precisely correct. Viruses (even when encapsulated outside of a living cell) are, as you said, too small to be seen by the human organism and, in fact, our bodies cannot “see” them as living and therefore do not perceive a threat.

As a virus attacks a cell (actually it just “bumps” into it since viruses also don’t have any brain or moving parts), it changes, as Cecil said, the cell’s genetic material. It is at this time the body notes an invader - the formerly “self” cell which is no longer “self” - which it immediately tries to recognize and destroy with newly formed antibodies. If the cell “breaks open” before the body destroys it with antibodies, all those new virus “hang around” waiting to bump into more. During this time as “free” virus, our immune systems do not bother them, since they cannot be “seen.”

If the body successfully destroys all of the cells that had virus in them without killing itself (note how fevers work to protect the species!), the viral infection is gone and the body wins, until another virus “happens” to bump into another cell. Of course, this time the body recognizes the foreign cell faster and often defeats the infection without observable symptoms. However,at least one cell must always die in defeating a viral infection.

All of this to point out that what a vaccination does is “introduce” the body’s immune system to the falsely (or similarly in some cases) infected cell so that it recognizes the real infection faster and creates the specific antibodies faster. But, cells must be invaded before our immune systems can recognize them, then defeat them. Antibodies cannot intercept viruses before they invade cells.

By the way, look at recurrent herpes infections. Somehow, some of the free virus travel to a nerve cell where they do not attack and kill the nerve (also, I have heard it said that our immune systems will not attack nerve cells). Later it comes out of dormancy in the nerve cell to attack the cells it “likes.” Since those cells are skin cells, one
almost always gets at least a little blister as the immune system destroys those invaded cells with antibodies.

It is also a problem in AIDS as the cells that create the antibodies are exactly the cells the AIDS virus invades given the opportunity, meaning that when a cell is invaded and the immune system recognizes it, the body creates a higher concentration of cells in the exact area where there’s an abundance of free virus waiting to bump, thus raising the probability of cell invasion and worsening the infection. Very unpleasant business.

[Alphagene]

…our bodies cannot “see” them as living and therefore do not perceive a threat.

Actually, the immune system sees anything unusual as a threat. Even a piece of a non-self protein can cause the immune system to kick in. Many vaccines are essentially nothing but a piece of a specific protein. If the body can detect protein antigens, it can certainly detect free virus.

As a virus attacks a cell … it changes, as Cecil said, the cell’s genetic material.

Cecil said that “some viruses insert their DNA into the host’s DNA” (emphasis mine) Most viruses don’t do this. They simply add their genetic material to the cell. They’re not really altering the cell’s genetic material. It would be more accurate to say that most viruses add their own DNA to the cell.

It is at this time the body notes an invader.

The body can recognize the invader before it infects the cell. While the most effective vaccines have live infectious virus, many vaccines are composed of inactivated virus that can not infect cells. IIRC, the Salk polio vaccine is such a vaccine. Antibody production is much more efficient and longer lasting if you have an actively replicating virus, but a virus need not be taken up by a cell for antibody production.

the formerly “self” cell which is no longer “self” - which it immediately tries to recognize and destroy with newly formed antibodies.

Antibodies do not destroy cells. They mostly bind to the virus particles are prevent them from binding to other cells. The destruction of infected cells is performed by a class of cells called phagocytes.

If the cell “breaks open” before the body destroys it with antibodies, all those new virus “hang around” waiting to bump into more

Not all viruses require the cell to break open to escape. In fact, most enveloped viruses go to great lengths to keep the cell alive and intact.

During this time as “free” virus, our immune systems do not bother them, since they cannot be “seen.”

This is wrong. Like I said above, blocking antibodies can bind to the free virus and prevent them from attaching to new cells.

If the body successfully destroys all of the cells that had virus in them without killing itself (note how fevers work to protect the species!), the viral infection is gone and the body wins

If there is free virus in the system I wouldn’t say the body wins. In fact free virus particles in the bloodstream (known as viremia) is a very serious condition.

All of this to point out that what a vaccination does is “introduce” the body’s immune system to the falsely (or similarly in some cases) infected cell so that it recognizes the real infection faster and creates the specific antibodies faster.

I’m not sure what a “falsely infected cell” is. An infected cell is an infected cell, whether or not the virus is engineered. But like I said before, some viral vaccines don’t even have active virus particles.

But, cells must be invaded before our immune systems can recognize them, then defeat them.

I’ve already said this but just to repeat. The immune system will react to just about any foreign particle that enters the bloodstream. Invasion is not required.

Antibodies cannot intercept viruses before they invade cells.

Actually, this exactly what antibodies do. Antibodies are crucial in preventing secondary infections.

Somehow, some of the free virus travel to a nerve cell where they do not attack and kill the nerve (also, I have heard it said that our immune systems will not attack nerve cells).

This is true. Nerve cells (and corneal cells, IIRC) are “immunopriveleged”.

Later it comes out of dormancy in the nerve cell to attack the cells it “likes.”

Anthropomorphizing viruses leads to misleading conclusions. What causes reactivation of herpesviruses and its subsequent retrograde motion is still unknown. Viruses don’t really have preferences for different infectable cells.

Since those cells are skin cells, one almost always gets at least a little blister as the immune system destroys those invaded cells with antibodies.

Again, antibodies don’t destroy cells.

[Andy]

… in fact, our bodies cannot “see” them as living and therefore do not perceive a threat.

Futhermore, as Alphagene has pointed out, not only can the immune system recognise non-living foreign bodies, but to consider a virus as living in any biological sense is wrong.

[Yuck]

Alphagene and Android209 make some interesting and unsupported assertions. Dealing first with Android209…

If viruses are not living in a biological sense, in what way are they living? I will grant there was once a debate over whether they were plant or animal, but I didn’t realize that anyone was still debating that they were alive in a biological sense.

On to Alphagene who sounds so much more authoritative.

I assert that everything inside the nucleus of a cell is part of its genetic material. Since viruses specifically attack the nuclei of cells (as opposed to the protoplasm), I claim such an attack alters the genetic material of the infected cell. Once a virus has entered the nucleus of a cell, that cell is no longer recognized by the body as “self.” It is precisely then that the cell becomes an antigen enabling the immune system to create an antibody for it. If the virus does not enter the nucleus, the virus cannot reproduce and the cell does not appear “infected.”

And, if your sources tell you that viruses are “omnivores,” you need new sources. Viruses are very specific about what cells they are able to attack. That’s why mutations are so worrisome; it broadens the targets.

But, as I said, viruses don’t think or move. They don’t “decide” and they can’t “swim” upstream. They merely wait. I apologize for using the word “like.”

Please answer these questions based on your hypotheses…

Why do the “opportunistic diseases” of AIDS not create problems until the immune system’s T-cell defense becomes impaired? According to CDC theory, we (apparently virtually all of us) carry the viruses that cause the opportunistic diseases without any harm. Under your hypothesis, our bodies should recognize those viruses as foreign proteins and destroy all of them, ridding our system of those awful viruses forever.

Using the Herpes example, after the first infection, why can’t the body destroy the free virus as it migrates from the nerve cell to the epithelial cells? Where are those antibodies when you need them?

Using AIDS again, why can’t they (the diagnosticians) find the virus in an infected person’s bloodstream immediately?

P.s. Viremia is different from septicemia.

[Alphagene]

Alphagene and Android209 make some interesting and unsupported assertions

I have four years of experience in molecular virology. I am a former member of the Laboratory of Biochemical Genetics at the National Institutes of Health. I studied under the tutelage one of the most respected influenza virologists in the world, a man who serves on the Editorial Staff of Journal of Virology and patent holder for the reverse engineering protocol for RNA viruses. I can send you references if you want. What are your qualifications?

Once a virus has entered the nucleus of a cell, that cell is no longer recognized by the body as “self.”

Wrong. The body can only recognize a cell by its surface proteins. Unless and until the virus starts synthesizing viral proteins and these proteins get expressed on the cell surface, the immune system does not detect anything is wrong. There is a considerable period of time between viral entry into a cell and the time it expresses proteins.

It is precisely then that the cell becomes an antigen enabling the immune system to create an antibody for it.

Wrong again. The entire cell can not be an antigen. An antigen is a “protein or carbohydrate substance (as a toxin or enzyme) capable of stimulating an immune response”. Antigens represent small portions of individual proteins, not entire cells. The antigens are contained on the viral proteins that are expressed well after the virus enters the cell. You just proved my first point for me.

If the virus does not enter the nucleus, the virus cannot reproduce and the cell does not appear “infected.”

Wrong yet again. Many viruses complete entire infection cycles without ever entering the nucleus. Small pox virus, for example spends its entire time in the cell’s cytoplasm, IIRC. Despite never entering the nucleus, the virus has a severely detrimental effect on the cell. Thus the cell will appear “infected”

And, if your sources tell you that viruses are “omnivores,” you need new sources. Viruses are very specific about what cells they are able to attack.

I’d love to know where I implied that viruses aren’t specific about the cells they infect. I did say “Viruses don’t really have preferences for different infectable cells.” I said infectable cells precisely to indicate cells that are permissive to herpesvirus infection.

That’s why mutations are so worrisome; it broadens the targets

I’d like to see a documented example of a specific virus that changed its host range due to a mutation. Viruses infect specific cells because they have specific surface proteins designed to attach to specific cell urface proteins. Mutating these surface proteins will not increase the range. Mutations are worrisome because they create different antigens. The HIV genome mutates very rapidly. As a result, the viral surface proteins that the immune system recognize are constantly changing. For this reason, it is hard for the immune system to create a lasting immune response. By the time the immune system has responded to one antigen, the antigen has changed due to mutation.

Please answer these questions based on your hypotheses…

You flatter me. I didn’t come up with these hypotheses. “My hypotheses” are the current dogma in the fields of both virology and immunology. There may be other hypotheses, granted, but I challenge you to find an immunologist or virologist who thinks “antibodies cannot intercept viruses before they invade cells.”

Why do the “opportunistic diseases” of AIDS not create problems until the immune system’s T-cell defense becomes impaired? According to CDC theory, we (apparently virtually all of us) carry the viruses that cause the opportunistic diseases without any harm.

This is true. In our system are viruses, bacteria and fungi that can potentially kill an AIDS patient. Let’s use Candida albicans as an example of an opportunistic infection. It is a yeast that we are exposed to constantly will no ill effects, yet immunodepressed patients such as those with AIDS can die from a Candida infection.

Under your hypothesis, our bodies should recognize those viruses as foreign proteins and destroy all of them, ridding our system of those awful viruses forever.

Our body does recognize Candida as foreign, whether or not we are immunosuppressed. Under normal circumstances, the immune system will attack and kill the yeast before it has a chance to cause a significant infection. In the case of AIDS patients, their immune system is deficient (remember, the ID in AIDS stands for Immuno-Deficient). The deficient immune system can’t launch an attack on Candida with the strength that a healthy immune system can. As a result, pathogens that a healthy immune system can normally “clean up” with become a problem for patients with a deficient immune system. To summarize, it’s not the recognition of the pathogen that is the problem, it’s the subsequent clean-up that the immune system must do.

Using the Herpes example, after the first infection, why can’t the body destroy the free virus as it migrates from the nerve cell to the epithelial cells? Where are those antibodies when you need them?

It does destroy the virus over time. When the virus reaches the epithelium, immune cells are recruited to the area and fight the virus. This recruitment of immune cells leads to the formation of a cold sore. In addition, the antibodies contain the spread of virus. The average cold sore would be much much larger if it weren’t for blocking antbodies. It is your body’s immune response that prevents a cold sore from spreading all over your face. But they do not act instantaneously. The immune system must signal the B-Cells to produce these antibodies, which takes time.

Using AIDS again, why can’t they (the diagnosticians) find the virus in an infected person’s bloodstream immediately?

Most diagnosticians don’t look for the virus, they look for antibody to the virus. An HIV test attempts to determine if your body has produced antibodies to HIV. You wouldn’t have these antibodies unless you’ve been exposed to HIV. You are advised to get tested three months and six month after a putative exposure to the virus because production of a primary immune response takes time. By six months, your body would have created enough antibody aginst HIV to be detectable if HIV is present in your system.
There are ways to detect if the virus itself is present though PCRing out the nucleic acid, but that is an expensive and laborious process, and even then a certain amount of virus needs to be present before the test can detect it.

P.s. Viremia is different from septicemia.

Viremia is a form of septicemia. Just like bacteremia is a for a septicemia.

[JillGat]

HIV viral marker tests, such as p24 antigen and viral RNA, are done routinely on people with HIV nowadays. But they aren’t used as diagnostic tests for HIV. The antibody test is still used for that. Viral load tests are used to monitor the effectiveness of medications on people with the disease.

[Alphagene]

Watch it, Jill. You’re starting to muscle in on my hypothesis…

[Yuck]

Alphagene feels that ignorance can be eradicated by changing the subject. But I am not sure Cecil supports such an approach. Actually, I’m a bit surprised that Alphagene is the moderator here since claiming expert authority and stamping one’s foot are hardly appropriate ways of eradicating ignorance. Of course, maybe Alphagene thought “stamping out ignorance” was Cecil’s goal.

Alphagene has a lot of OJT, but must not have much in the way of formal education (certainly, this information would also have been gratuitously given). Killing rabbits and mice in a lab doesn’t make one an expert authority on viruses and antibodies. I am “old school;” I believe that fact stands on its own. Religion and political ideology depend on authority. They produce dogma. Science involves itself in explaining phenomena. Religion and politics shout “wrong” across the millennia.

I hope that Alphagene will stop shouting “wrong” and start providing evidence, since that is what I ask for. The evidence will speak for itself. Alphagene, answer my questions in the context in which they were asked. I am talking about viruses; not dirt, bacteria, yeasts or other foreign matter. Just viruses.

Alphagene’s professed CV does not show experience with small pox virus. And, since Alphagene is using OJT with the flu as the basis of expert authority, the comments on small pox have no value. Of course, Alphagene probably knows that small pox is a herpes virus and thus is basing the broad, unsupported statement about small pox on extensive experience with cold sores.

Further, even if Alphagene’s extensive experience permits unsupported “expert” statements, they remain unsupported, even if they happen to be right. When I said “according to CDC theory,” I was supporting the statement that followed. Of course, maybe I misused their information, but that is a separate issue.

Alphagene’s comments on antigens are interesting. Another great method of disinformation is to attack the words in which information is provided. I guess that Alphagene would say that only my lip has a cold sore, claiming that I, the whole organism, do not have a cold sore.

I think it is sophistry to claim that the infected cell is not an antigen, that only its surface membrane is. Further, is Alphagene saying that viruses somehow “squeeze” a cell in order to “express” something to the surface membrane of the cell? Is the inside of a cell like a breast or a zit under Alphagene’s hypothesis? Or, is Alphagene saying that the immune system can only detect the cell as an antigen for the brief moment that the new generation of virus is “budding” from the cell membrane?

In any event, I believe that it is appropriate to confine oneself to viruses in a discussion of viruses. Alphagene has decided to avoid viruses and talk about bacteria and yeasts. While I agree these are very interesting, they have nothing to do with this discussion.

My qualification is merely that I am interested and able to stay on subject. Viruses.

The CDC has said that AIDS originated in Africa within a population of green monkeys. According to the CDC, the virus mutated and became capable of infecting humans. For me, this is documentation enough. Even the creationists would give me this sort of “micro-evolution.”

Regarding the answer on Herpes. Alphagene says the immune system does not attack the free herpes virus as it migrates from the nerve cell to the epithelial cells, but then it attacks the free virus when the virus is in the vicinity of the epithelial cells. I claim the immune system attacks the infected epithelial cells. It is the destruction of epithelial cells that causes the blisters that are characteristic of herpes simplex. “Recruiting” (by the way, isn’t this “anthropomorphizing”) immune cells does not cause blisters, killing infected epithelial cells does. The immune system does not prevent the spread of blisters, it kills infected cells, causing the blisters.

By the way, herpes never gets defeated - the immune system never kills all of the virus no matter how much time passes. As people began saying in the early 80s (I guess before Alphagene’s time) “Herpes is for ever.”

So, please answer my question under your hypothesis. Why doesn’t the immune system attack the herpes virus during the migration from the nerve cell to the epithelial cells?

But, I am also broad-minded. If you can confine your answer to viruses only, please readdress my other questions (about AIDS). If you need a specific opportunistic viral disease, use cytomegalovirus.
p.s. Alphagene should check sources for viremia, bacteremia and septicemia. While septicemia may be a form of bacteremia or of viremia, it’s not the other way around. Both viremia and bacteremia are conditions that may not be serious. Septicemia is serious.

[Alphagene]

Alphagene’s professed CV does not show experience with small pox virus. And, since Alphagene is using OJT with the flu as the basis of expert authority, the comments on small pox have no value.

And have you worked with smallpox? Flu? Herpes? Any virus? Do you have any basic science training? Any medical training? Any experience with a life science course at the graduate level? How abour undergrad? High school? I have yet to hear why your theories are so much better than mine, especially since there is no one in the medical or scientific field who would identify any of your “facts” as accurate.

I give up, Yuck. You don’t want to understand, you just want to be right.

I could answer your questions and address your own misinterpretations of my explanations. But it still wouldn’t be good enough for you.

My advice? Pick up a book. Read Field’s Virology or Medical Microbiology. They contain the sum data of a century of labor performed by tens of thoudands of scientists regarding the fields of microbiology and immunology. It is from these texts that I am getting my information. If these textbooks, which are used to train the biomedical scientists and medical students all over the world aren’t valid enough for you, Yuck, then I invite you to get bent.

But, apparently citing the duplicatable research of respected scientists isn’t good enough for you. It was good enough for the people who developed the polio vaccine but it’s not good enough for Yuck the arm-chair scientist and his wondrous theories.

If I didn’t think you were totally insane, I’d be insulted by the fact that you don’t think my years of academic and laboratory virology training don’t qualifiy me in the field of viruses.

You seem to be a big fan of evidence, Yuck. My evidence is found in textbooks that chronicle the science of virology. You have yet to mention one person, one paper, one laboratory that supports your idea of viruses.

Perhaps later I will come back and explain again what you find confusing, for the edification of readers of this thread who are genuinely interested in viruses. But for tonight, I’m too burnt out.

In the mean time, I invite the readers of this thread to decide for themselves which of us is more qualified to provide accurate information regarding viruses.

[sailor]

Bout ten days ago I started getting these itchy red spots than are driving me up the wall and I suspect may be shingles (herpes zoster). At the same time I suddenly developed and interest in learning more about viruses. What a coincidence!

As a lay person I have to say Alphagene makes much more sense to me.

Yuck, even if you are right (which I am not in a position to judge), your attitude when you have just arrived is not going to make you many friends. Your posts come across as looking for confrontation (I am not saying you are, just that it seems that way). Maybe you can tone it down a notch or two and the discussion will be more productive.

Oh, sorry, I have to go back to scratching myself… but I’m interested in learning about this topic.

[Alphagene]

OK, I got some sleep and I’m ready to address the questions. The virus questions, that is. Yuck’s confusion as to my education and job history is due to an ego problem I can’t begin to address here.

I think it is sophistry to claim that the infected cell is not an antigen, that only its surface membrane is.

An antigen can not a cell and it can not be a surface membrane. This isn’t “sophistry” or a crazy theory. This is the definition of the word. To call any kind of cell an “antigen” is, by definition, incorrect. The immune system recognizes antigens via small proteins on its surface known as receptors. Receptors are incapable of recognizing entire cells because they are so small. They can only regonize other proteins.

Further, is Alphagene saying that viruses somehow “squeeze” a cell in order to “express” something to the surface membrane of the cell?

What fever dream did you get the word “squeeze” from? Viruses synthesize proteins during their time in the cell. This is how they replicate. This synthesis of proteins from a gene is known as “gene expression”. Many of these proteins are shuttled to the surface of the cell. Once again, this is textbook cell biology.

Is the inside of a cell like a breast or a zit under Alphagene’s hypothesis?

Now who’s the sophist?

Or, is Alphagene saying that the immune system can only detect the cell as an antigen for the brief moment that the new generation of virus is “budding” from the cell membrane?

Please tell me where you got your virology education. Viruses don’t bud “for a brief moment”. Many viruses continue to replicate and bud for the life of the cell. Plus before the virus can bud off, the viral surface proteins must be present on the cell surface. These proteins contain the antigens that the immune cells recognize.

In any event, I believe that it is appropriate to confine oneself to viruses in a discussion of viruses. Alphagene has decided to avoid viruses and talk about bacteria and yeasts. While I agree these are very interesting, they have nothing to do with this discussion.

I’m sorry it’s confusing to you. My discussion of Candida was very relevant to my point about AIDS.

The CDC has said that AIDS originated in Africa within a population of green monkeys. According to the CDC, the virus mutated and became capable of infecting humans.

Oh I see what you’re thinking of. But the process that allowed SIV to become HIV wan’t just an instantaneous single mutation, it was a series of many mutations that occurs over a very long period of time. Thousands to millions of years. SIV and HIV are related, but they are two different viruses. The mutations that medical doctors worry about when in a patient with HIV are the mutations that make it difficult to treat at the rapid point mutations that alter the antigenicity of the virus. This makes an HIV vaccine very difficult to construct.

The HIV in the body of a patient is not going to evolve into a completely new virus. Mutations that change antigenicity can and do occur quickly, mutations that chance the identity of the virus take hundreds to thousands of years of evolution.

That may seem arbitrary but think of it this way. You can change the color (“antigeniticity”) of your car from red to blue overnight, But it would take months of overhaul and many brand new parts to change car you have from a sportscar to an SUV. One change is superficial, the other is complex.

Alphagene says the immune system does not attack the free herpes virus as it migrates from the nerve cell to the epithelial cells, but then it attacks the free virus when the virus is in the vicinity of the epithelial cells.

No I did not. The virus migrates through nerve cells by infecting them. Therefore they are not “free”. Free virus refers to virus particles in the absence of a cell.

I claim the immune system attacks the infected epithelial cells. It is the destruction of epithelial cells that causes the blisters that are characteristic of herpes simplex.

Hooray! We agree on something!

“Recruiting” (by the way, isn’t this “anthropomorphizing”) immune cells does not cause blisters, killing infected epithelial cells does.

First off, “recruiting” is the accepted immunological term for the migration of immune cells to a site of infection. This is a term used in the scientific community. Your words that viruses “like” cells, or that viruses can’t be “omnivorous” are not immunological jargon. But seeing as how you obviously have had no detailed education in immunology, I can’t really fault you for not knowing that.

Second, it is the recuitment of immune cells that kills the epithelial cells causing the blister. We are almost in agreement here, but you have a hard time accepting that it is not antibodies that destroy cells.

My question to you is, how would antibodies destroy cells? In detail, explain it to me.

The immune system does not prevent the spread of blisters, it kills infected cells, causing the blisters.

By killing the infected cells, and by blocking the free virus with antibody, the immune system prevents the spread of blisters.

By the way, herpes never gets defeated - the immune system never kills all of the virus no matter how much time passes. As people began saying in the early 80s (I guess before Alphagene’s time) “Herpes is for ever.”

Correct. Herpes remains in the body for ever. BUT it is not free virus. The virus remains inside cells in the spinal column. The virus is not actively dividing in these cells, but its genome is present. The virus is in what scientists call a latent state. Because it goes latent in a nerve cell, which is you remember is “immunoprivledged”, the immune system can not detect it.

But, I am also broad-minded. If you can confine your answer to viruses only, please readdress my other questions (about AIDS). If you need a specific opportunistic viral disease, use cytomegalovirus.

How borad-minded can you be if you only want me to discuss viruses on your terms? OK, since Candida was confusing to you. Go back to my AIDS explation and replace “Candida” with “CMV”. It’s the same answer. The immunodeficent body recognizes CMV, but lacks the immune strength to fight it off. Feel better now?

I must be pretty obtuse if I’m confusing an “expert” in virology like Yuck.

And please tell me where you got your explanation of viruses. I didn’t know the planet Bizzaro had a university.

[sailor]

Alphagene, from what I am understanding a herpes virus is safe in the nerves but it cannot replicate. Why is this? What makes nerve cells different in that sense? Why can the virus only replicate in the cells of the skin?

[Alphagene]

OK, let me expand upon what I said earlier.

Herpesvirus goes latent a specific clump of nerve cells located in the spinal chord known as the dorsal root gangia. When it is latent, it is not replicating. At some point, HSV replication will resume. During this replication, virus will bud off the membrane of one nerve cell and enter the next adjacent nerve cell. This cell-to-cell transmission occurs from the dorsal root ganglia in the spinal chord all the way to the skin epithelium.

Scientists still aren’t sure why nerve cells aren’t attacked by the immune system, AFAIK. It may be related to surface proteins called MHC-I receptors that certain immune cells use to determine if a cell is infected or not. All that we do know is that due to this property of nerve cells, the immune system does not kill infected nerve cells. For this reason, herpes can migrate through nerve cells unaffected by the immune system until it infects a cell that can be destroyed by the immune system, like a skin cell.

So the virus replicates in both nerve cells and skin cells but the immune system attacks infected skin cells while leaving the infected nerve cells intact.

[Duck_Duck_Goose]

Well, as long as we’re talking about immunizations here (“Ask the Expert”?), I have a couple of questions I’ve always wondered about.

First, my daughter, who will be entering the 5th grade next fall, had to have a state-mandated series of hepatitis vaccinations, along with all the other 4th graders in the state. My question is, how come these hepatitis vaccinations had to be spread out over 6 months of the school year (she had to have 3 shots altogether)? Other vaccinations, you just get one shot and then a booster every few years. Is it something different about hepatitis? Or is the state of Illinois just doing the PC thing as per instructions from the CDC?

Second question, what is the deal with the chicken pox vaccinations, anyway? First we hear, “New Medical Breakthrough!” and the next thing you know, it’s “Oops, never mind!” Did they skimp on the guinea pigs, or what? Fortunately, all my kids have already had it, besides which they’re too old to require the vaccinations. But I have friends who have preschool-age kids, and they’re currently agonizing over whether to go for the shot, or wait and see.

But what is the problem with getting a vaccination serum ready for chicken pox, anyway? I thought all it took was isolating a sample of the virus, finding the right growth medium (duck eggs or whatever), and a matter of time, and presto! a batch of serum. At least, that’s how they do it on Star Trek–they encounter a new disease, Dr. McCoy fires up the bunsen burners, and it’s one Venusian singing fever vaccination, coming right up…

[sailor]

Oh that is interesting, the herpes virus does replicate in the nerve cells but this does not cause those cells any harm?

So, I should understand that the harm to the skin cells comes from the body’s counter-attack rather than from the virus attack itself? So if we could stop the body’s reaction (immunosuppressants?)the skin cells would be OK and just keep producing more virus?

If this is the case wouldn’t a herpes outbreak be like an allergy in the sense that it is an unneeded defense which causes a problem much larger than it is trying to solve?

Also, I believe the AIDS virus also has some hiding place but it is somewhere else, not the nerves. can you confirm this?

[Loren_Pechtel]

**
state. My question is, how come these hepatitis vaccinations had to be spread out over 6 months of the school year (she had to have 3 shots altogether)? Other vaccinations, you just get one shot and then a booster every few years. Is it something different about hepatitis? Or is the state of Illinois just doing the PC thing as per instructions from the CDC?
**

 I've had that hepatitis series as an adult--the three shots are standard. It's that you don't get adequate immune response with only one shot.

 If you think three is bad, look at rabies. IIRC 5 shots. The "vaccine" simply reduces the number of shots needed in case of exposure.

**
But what is the problem with getting a vaccination serum ready for chicken pox, anyway? I thought all it took was isolating a sample of the virus, finding the right growth medium (duck eggs or whatever), and a matter of time, and presto! a batch of serum. At least, that’s how they do it on Star Trek–they encounter a new disease, Dr. McCoy fires up the bunsen burners, and it’s one Venusian singing fever vaccination, coming right up…
**

 That's Star Trek, not real life. Culture a sample of the virus on a suitable medium and you don't get a vaccine, you get a live copy of the virus--just as lethal as what you start with!

 You might be able to make a quick-and-dirty vaccine by culturing, then throughally killing the cultured material. Safety and effectiveness unknown, though.

[Duck_Duck_Goose]

**You might be able to make a quick-and-dirty vaccine by culturing, then throughally killing the cultured material. Safety and effectiveness unknown, though.
**

Well, gee, that’s how they do it on Star Trek all the time. And it’s always 100% effective. But it does mean that you have to watch William Shatner overact shamelessly on a sickbay couch for 35 seconds, so that’s the trade-off I guess.

[Duck_Duck_Goose]

Okay, so here’s another question.

I just had a conversation with someone who has terrible chronic cold sores in his mouth, and his doctor has prescribed a course of treatment that involves acyclovir.

1. I thought there wasn’t anything they could do for cold sores, they’re just something you have to live with.

2. I thought acyclovir was just for organ transplant patients, to suppress their immune systems and keep them from rejecting the transplant. Am I thinking of the wrong drug?

3. If it’s the right drug, then how does suppressing your immune system help get rid of cold sores? I would think that you’d want something that would boost your immune response, instead.

[sailor]

not that I know the answer but it could be that the inflammation is due more to the immune response than to the damage the virus does? Check out http://www.healthcentral.com/mhc/top/001716.cfm

[sailor]

Here it says:

According to Mertz, both famciclovir and acyclovir have similar molecular mechanisms of action. “Like acyclovir, Famvir inhibits a viral enzyme that allows the virus to make copies of itself,” he explains.