Cecil didn’t name any non-HIV medications. I’m sure there must be several but they are specific rather than all purpose.
Viral pneumonia can be treated with tetracycline - I’m thinking of the Eaton Agent pneumonia, AKA walking pneumonia, AKA micoplasia pneumonia, there might be another name but they are one one type of viral pneumonia.
Why does tetracycline work on this kind of pneumonia and not on other viral diseases?
What other kinds of viral diseases have effective medical treatments?
Oh, I’m gonna keep using these #%@&* codes 'til I get 'em right.
I’m surprised Cecil didn’t mention the latest breakthrough, a medicine designed to inhibit two major classes of viruses (rhinovirus and enterovirus I believe) from hooking up with our cells.
It’s undergoing testing right now, and should be out by the end of year. From the reports, it seems to have no side-effects, probably due to it’s specific design and targetting.
Also, what’s this about viruses being the smallest parasites? What about prions?
Sure prions aren’t considered to be alive, more like self-replicating proteins, but then, viruses usually aren’t considered to be alive either.
And for those who protest that we haven’t shown that prions do it all on their own, I’d recommend reading the dramatic article in the latest issue of “Science” magazine.
Tetracycline specifically prevents bacterial protein synthesis. It is ineffective against viral diseases. Mycoplasma pneumonia is caused by Mycoplasma bacterium. It is not a viral disease. Mycoplasma is an unusal bacterium. It is smaller than other bacteria and many antiviral drugs are ineffective.
By far the most successful antiviral medications to date have been the anti-herpes drugs. Acyclovir was the first and most of the anti-herpes drugs on the market are related to it including penciclovir and gancyclovir. While they can’t eliminate herpes from the body they are very effective at reducing the symptoms.
Prions are still a controversial topic. Whether or not they alone are the infectious agent is still under debate. Many researchers belive that the prion protein is merely the receptor for some unknown virus.
I used to rock and roll all night and party every day. Then it was every other day. Now I’m lucky if I can find a half an hour a week in which to get funky.
Walking pneumonia and “Eaton agent” pneumonia are both alternate names for mycoplasma pnuemonia. All three are the same thing and they are all bacterial.
Before the mycoplasma bacteria were discovered by Eaton in 1944, walking pneumonia was thought to be viral in origin.
There are viral pneumonias, it’s just that mycoplasma pneumonia isn’t one of them.
Hope that’s not too confusing, Jois.
Marge: Your father is… resting. Bart: “Resting” hung over? “Resting” got fired? Help me out here.
Viral DNA is inserted into your cells, but that doesn’t mean your original DNA doesn’t keep on working. The only problem is that it does the viral code too.
Inserting more copies of your original DNA in another virus probably wouldn’t help much.
However, crippled retroviruses are I think the instrument of choice for gene engineering of adults today, no?
As far as I know, it allows all the infected cells (that survive) to produce the much needed protein, or whatever.
I’d also like to see you take a stab at pweetman’s question. What seems logical to us on-lookers is often, I know, a far cry from what is possible. It’s still very interesting.
pweet, it’s not moronic at all. Viruses can be very confusing.
Not all viruses implant DNA into cells. Many viruses don’t even have DNA but carry their genetic information in RNA. Most viruses just use the DNA and RNA to replicate themselves.
Anyway, the main problem with attempting to reverse or repair the insertion of viral DNA by making a virus containing human DNA is that these viruses tend to insert DNA into the genome more or less at random. We do have the technology to manipulate the genome of many viruses to a certain extent, inlcuding insertion of human DNA. We don’t have the ability at present to get the virus to insert the DNA wherever we want it.
We can engineer viruses to contain human DNA. Ideally, we could also use the virus to replace mutant genes in humans. This is the basis of viral gene therapy.
Kyber is correct regarding retroviruses being used for gene therapy. They encode protein that can integrate viral DNA into the human genome. However it can’t do it at a specific location. IIRC, adenoviruses are also capable of integrating viral DNA into the host genome.
Marge: Your father is… resting. Bart: “Resting” hung over? “Resting” got fired? Help me out here.
I would add to this discussion a couple of things:
Among the oldest antiviral drugs is Amantadine, and a related drug Rimantadine. One of these, I forget which, is the only treatment for RSV, Respiratory Syncytial Virus, which causes pneumonia in newborns, especially preemies & has about a 50-75% mortality rate without treatment IIRC (long time since Pediatric rotations). Amantadine, until this year, was the drug used to treat type A flu.
2 new drugs (Relenza is one of them), effective against influenza have been released in the past year. These are effective against both type A & type B flu.
Acyclovir, mentioned above by Alphagene, is also used to treat adults & immunocompromised kids with varicella, aka Chicken Pox.
While everyone would love to see drugs to treat viruses like Ebola & Lassa, the problem is that these illnesses occur too sporadically & develop too quickly to effectively get any experimental treatment to affected people. Most of the time, the initial cases are dead before the cause is suspected. There may be stockpiles of drugs to try out in the event of a widespread outbreak, however.
Sue from El Paso
Siamese Attack Puppet - Texas
Experience is what you get when you didn’t get what you wanted.
Another theory I have heard is that many/most/all humans carry in the genome DNA from a latent virus. The prion, once ingested, enters a cell, enters into the cell nucleus, and then interacts with a nuclear receptor, or directly with a promoter sequence of DNA just before the viral DNA, and causes the viral DNA to be transcribed. This then triggers viral replication, and further production of the prion protein. If another individual carrying the latent viral DNA is exposed to the prion, the cycle can begin again.
I won’t guarantee this is a moron-level explanation, pweetman, but if you’re smart enough to think of questions like this, I just hope I’m smart enough to add something coherent to the discussion already in progress.
I’ll start with talking about implanting DNA. Actually, most viruses don’t “implant” their genome anywhere. Most (RNA or DNA types) either come with the enzymes they need to make more copies of their genome, or (DNA types only) get into the cell nucleus & use the cell’s enzymes to make more copies of their genome. They do not need to be attached to the cell’s DNA to do this.
A few viruses do have their genome physically incorporated into host cell DNA. These include herpes viruses (Herpes, Epstein-Barr, Cytomegalovirus, & Varicella/Chicken Pox). Since these are DNA viruses, their genome can be directly added to cellular DNA. Much later, when you get a fever, the Herpes 1 virus reactivates, and you get a fever gblister, or something happens & your Varicella virus gets re-activated & you get shingles.
The other class of virus to do something like this is retroviruses. These carry their genetic information as RNA. An enzyme carried with the virus, reverse transcriptase, is needed before the RNA template can be used to build complementary DNA (cDNA). The cDNA can then be incorporated into the host cell DNA. Whenever the cells replicates, the viral DNA is copied & both daughter cells are infected.
As Alpha mentioned above, either of these techniques can be used to add genetic information to cells. This is known as gene therapy, and is being tested in several conditions caused by a broken gene, so that an affected person lacks the normal protein. Cystic fibrosis is one such disease. Hemophilia is another.
One of the biggest problems is that the virus usually inserts DNA randomly into the host cell DNA. Insertion generally requires that a certain sequence in the viral DNA match a sequence of host DNA, but since these sequences need to be only a few base pairs in length, there may be hundreds of potential insertion points in our 46 chromosomes.
For an inserted gene to work properly, it must either include all of the regulatory sequence (promoter region, etc.) before it (sometimes as long as the gene itself), or be inserted in exactly the right place, so it gets inserted just after its regulatory sequence.
Many centers doing gene therapy are not enrolling new patients, due to the unexplained death of an 18 year-old patient after receiving the new genes. The new genes seemed to be working properly, but something went seriously wrong, and the doctors working with the patient are at a loss just now as to what it was.
Let’s lie and say diabetes is caused by a single pair of genes–one was working just fine but the other was inhereted as recessive for diabetes.
After time passed the working gene became defective (mutated?) and the part of the gene that said, “Turn off or turn on insulin” NOW just is stuck in the off position.
So now the person has diabetes because the gene no longer turns on to make insulin.
Someone will have to know where the gene is located on the DNA chain. So we’ll say it’s located at Spot 15 (remember this is just another lie).
Then somebody has to know the enzyme that opens the DNA chain at Spot 15. The name of the enzyme is OPEN.
Then you’d have to have the REPAIR and connect the REPAIR to OPEN.
Then you’d have have a way into the DNA of the diabetic (Here I’m reduced to a sling shot because I can see how to get a cell into a brand new embryo but into a full grown adult?) This could be the virus or other
vehicles mentioned above call it THE BUS.
So then you’d load the REPAIR & OPEN onto THE BUS and into the diabetic and that’s it?
And I left out removing the defective part!
Can you bring your explaination down to this level without just making it alphabet soup?
As I mentioned, a recent research study described in “Science” magazine involved creating an artificial prion which infected yeast. It seems there isn’t an unkown viral agent after all, and this is in fact a sort of replication.
This is all very interesting. I pulled out a first year biology textbook that I bought once for cheap. It has pictures of two cycles called the Lytic and Lysogenic cycles. I think this maybe only for the DNA type of virus.
It seems from these pictures that the Lysis of the cell (virions destroy the cell upon exit?) is the nastiest part of the process. I guess other than producing mutant cells.
Is there a way to inhibit the production of these virions or prevent them from escaping the cell?
Not all viruses have a lytic cycle like that book probably describes. Many viruses do replicate to the point where the cell bursts and all the viral particles are released. But many do not. Herpes virus paricles, for example, can replicate and exit the cell without bursting the cell open. In some ways, allowing the cell to survive increases the amount of virus the cell can produce. Many viruses encode proteins that ensure that the host cell does not die.
Regardless, there are ways to prevent the virus from exiting the cell but they are all in the experimental phase. IIRC, it block the assembly of new virus particles in the cell. Without assembly, the virus (i forget which one it was specifically) can not exit the cell.
However all of these antiviral solutions are much less effective than creating a vaccine for a virus. Once vaccinated, the virus gets cleared by the immune system before it can infect a cell to begin with. The problem is some viruses like HIV are designed to mutate to evade the immune system, making vaccine development extremely difficult.
Marge: Your father is… resting. Bart: “Resting” hung over? “Resting” got fired? Help me out here.