Virology question

I'd think so, but any number of things could happen to prove me wrong. Keep in mind the cell has a limited lifespan...

If you don't find a virologist here, you can ofc find one at a university...

The short answer to your question is: it stays attached and becomes completely "wrapped" in the cell membrane. Even after budding (releasing of new viruses the cell has created), the cell stays alive (aka the influenza does not "kill" the cell).

If you need the mechanisms though I'd be happy to type them out for you.

DrZoidberg said:

Any virologists in the house? Here's a pretty specific one.

After a influenza virus (the envelope) has fused with the cell and deposited its capcid, does the virus let go from the cell? Or does it stay attached to the cell for ever?

Yes, I know, it's a pretty specific question. I hope there's anybody here who can answer. My wip is a story about a guy's life seen from the perspective of bodily functions.

Click to expand...

You mean the capsid? So, here's how it works: the envelope (which is the outer coat of the virus) has some specific proteins that attach to the cell. Once the attachment takes place, the virus fuses with the cell and once inside, it inserts its RNA in the nucleus of the cell, and that's where the RNA uses the cell DNA to start the transcription. Other parts of the virion are chopped up and "digested" by the mitochondria, and these bits and pieces will be transported to the surface of the cell by the Golgi apparatus. This is very important, because once they are on the surface of the cell, they are like red flags that label the cell as "infected". In the meantime, the viral RNA gets spliced and new virions are produced. They start budding out of the cell, sometimes a few at a time, sometimes through a "burst" (a whole bunch comes out and the cell dies). The cell will either die because of the burst, or a T-cell or NK-cell will "see" the "red flags", recognize the cell as infected, and kill it.

Does this answer your question?

ETA: actually, some viruses do stay "dormant" in cells, meaning they get inside and stay inactive for a long time. One example would be the herpes zoster virus, but as far as I know, it doesn't happen with the flu virus.

I am most familiar with the genetics of retroviruses, so I confess it's been a while since I studied the immunology details. There's a fabulous immunology book on line:
http://pathmicro.med.sc.edu/book/welcome.htm

If your book is going to go into all these details I suggest that you read the corresponding chapters in the above book. One quote in particular: "Antigen processing and presentation are processes that occur within a cell that result in fragmentation (proteolysis) of proteins, association of the fragments with MHC molecules, and expression of the peptide-MHC molecules at the cell surface where they can be recognized by the T cell receptor on a T cell."
This figure illustrates the process:
http://pathmicro.med.sc.edu/bowers/MHCInew.jpg

I realize I made a wrong statement, the viral proteins are "chopped" up by the proteasome, and reduced into enzymes that are then transported to the surface of the cell by the Golgi apparatus. These are the "red flags" I was talking about. They are chemical signals that tell the T-cell that the cell it's come in contact with has an antigen inside. The T-cell will NOT see the actual virus, because that's been fused inside the cell and taken apart, the genetic material goes into the nucleus, etc.

Interleukins are a type cytokines, but as far as I know they are specific to white cells. I forget if cytokines are produced by the infected cell itself or by the T-cell that attacks the infected cell. I need to go grab my immunology book and I'll get back to you.

The majority of interleukins are synthesized by WBCs (CD4 lymphocytes), monocytes, macrophages, and endothelial cells. They drive the differentiation of T cells, B cells, and hematopoietic (stem) cells.

Signal transduction pathways for influenza are pretty complicated (as they are for many immune responses), and everything kinda mushes together/reacts off one another to create "immune response." In influenza, the defense cell mechanisms are mostly mediated by different intracellular signaling cascades that regulate a variety of events in the infected cell (including expression of cellular antiviral genes and your cytokines).

A good example of how these can get "out of whack" is in certain Pandemic strains. In these, hyperinduction of cytokine genes (referred to as the "cytokine storm") correlates directly with a hyperactivation of certain signaling pathways, such as the p38 MAP kinase pathway.

If you're doing more research into the specific pathways, for Influenza you can look closely at induction of the type I interferon response as well as viral exploitation of the PI3K, NFB and MAPK signaling pathways.

I apologize for taking yet another post, but I wanted to make sure I didn't say anything that wasn't incorrect. I just talked to my boss who's a BIG influenza guy. First of all, a clarification: all cells produce fragmented proteins that are then transported to the cell surface. It's part of their metabolism. Now, if a cell is infected, some of these bits of proteins will be from the virus. These are NOT cytokines. What happens is that T-cells are lurking around and they have the ability to recognize self from non-self; so if they detect something extraneous on the cell surface, that will trigger a cascade effect that will eventually lead the T-cell to kill the infected cell.
Typically though it takes a few days before the body mounts an adequate immune response to the virus. In the case of influenza, you have a first couple of days when cells die because of the infection (the virus takes over the cell resources until it kills it). During this phase, dendritic cells collect foreign protein fragments and migrate to the closest lymphnodes. This is where the activation of T-cells will start. After a few days, when the thymus has been able to produce enough T-cell specific responses, that's when the 'killing' from the T-cells (and all the weapons that our immune system has in store) happens.
This is an awesome book on immunology: How the Immune System Works, by Lauren M. Sompayrac. It's in a very accessible language.
Let me know if you have more questions.

Oh, it's way more complicated than that.... See, the beauty of the immune system is in this delicate and yet vital thing: it has to recognize self from non-self. The deadliest diseases happen when something goes wrong in this process. All you need is a tweak in the pathway, and bad things start to happen. That's why Mother Nature made the process so complicated. You don't want the thymus to start mounting a full blown attack on something that is part of the body. That would mean self-destruction.

There is no such thing like "seeing" when it comes to cells. It's a complicated cascade effect of chemical signals. It's triggered by these proteins fragments, mediated by cytokines, and like cscarlet pointed out, carried on by sophisticated pathways.