The "key" influenza uses to unlock the cell.

the "key" to the cell of influenza

literally "blood agglutination"

(blood clumping)

this is because hemagglutinin can bind to multiple cell's receptors causing clumping

what strategy for cellular entry does influenza use?

(it's strategy 1)

it's called receptor mediated endocytosis

(the whole virus is absorbed into the cell)

how does a virus get its genome out of the endosome?

psitive strand viral RNA

(in single stranded RNA viruses)

RNA is ready to translate into proteins inmediatemente

Negative strand RNA

single stranded RNA viruses

The complement copy of the RNA

First make the real RNA, then make the proteins.

what is different about viruses and polymerase?

polymerase is the stuff that replicates the RNA.

For possitive strand RNA, they have the encoding for the polymerase, so once protein production takes place the polymerase will follow.

In negative strand RNA, the virus has to make that second RNA  strand, so it actually has to carry polymerase with it.

viruses  rip apart the cell's mRNA and use the snippts to get the production of viral mRNA under way.

They contain a "cap" that gets ribosomes working on cellular (or, now, viral) proteins. Once viruses hijack these, the cell can't produce any more protein for itself and it dies (cytolitic viruses)

the blob that creates a new strand of DNA or RNA  based off another DNA or RNA template.

Protein Kinase

 This is the stuff that cells start pumping out after they get an interferon warning. PKR then floats around, and if it finds double stranded RNA (that's replicating viral RNA) then it binds to it, goes on high alert, and starts throwing phosphate molecules onto it.

Basically it becomes a waring system for double stranded (replicating viral) RNA.

PKR targets a cellular protein called eIF2. eIF2 is needed to start the manufacturing of proteins, and when it is shut down, no more proteins can be produced. The result? Niether the cell nor the hopeful virus can reproduce, and both are killed.

killer T cells

destroying infected cells and the virus within.

Ducks

and other waterfowl.

pigs

Pigs can get both human and bird flues, and then they mix up inside the pig, creating new and drastically different strains.

drastic changes to a virus's genome.

like in pigs.

the interferon immune response.

influenza activates a crap load of interferon, causing the fever, aches and fatigue.

the possitive copies of viral genomes

(like in rhinoviruses)

influenza buds.

rhinoviruses.....

influenza hijacks caps.

rhinoviruses.......

instead carry their own, coded form of a cap.

but in addition they also encode for a protein that disrupts the production of cellular caps. The result is the same as that with flue. The cell can't produce and mRNA, and the cell eventually starves.

the lower tract. It has to back paddle against the current that brings mucous up from the lungs toward the throat to be swallowed.

it interferes with the system that looses the interferon from the cell.

Because the virus does't set off much interferon, it has not developed any clever strategies for avoiding interferon.

Because the innate immune system handles rhinovirus infections, the struggle is long over before the adaptive immune system can kick in and produce antibodies. The result? The immune system won't recognize the virus when it hits again and the common cold can reinfect the same host.

Because it can reinfect people over and over again, and because of slight antigenic drifts.

However there are no antigenic shifts because humans are its only resevoires.

for the Greek word rhinos, or nose.

 during the innate immune response, the immune system targets the capilarry filled surface areas of the upper respiratory tract. They rupture, causing swelling and halting viral spread. This inflammation causes the runny nose and can constrict the mucous filled airways.

1. They don't activate much interferon, so there's less of an explosive reaction from the immune system.

2. Rhinoviruses like cooler temps, so they don't go for the deep tissues in the lungs, just the higher up, respiratatory tract.

the respiratory tract

the whole body.

to leave its coat at the door.

the virus fuses with the cell membrane and injects its genome into the cytoplasm.

making short segments of RNA, which encode for seperate proteins each.

when it comes time to assembling new genomes for the baby viruses, some of the extra, new viral proteins drift over to the mother genome, and mask the RNA bits that signal for stopping and starting the short RNA segments. The result? A new, full, single strand of RNA complement of mama's RNA. Now just go over it again and you have the original, negative strand of RNA.

measles: bud or burst?

bud

CD46

"silent" measles

it doesn't reproduce hardly at all.

because it can't wait for the butler to flee to the lymph nodes, where it readily infects the activated and hungry macrophages.

Once the macrophages are infected, the virus is then carried throughout the entire blood stream, where it can infect more CD46 cells, especially epithelial cells. The virus then has it made throughout the entire body.

it's because the measles protein coat is so specific that almost any mutation will render the virus helpless.

Consequently, there is only one strain of measles.

viruses that have different binding sites for neutralizing antibodies

Because it needs an unbroken chain of infection.

Because measles is so specific, it can't mutate, therefore there's only one strain. Once a person contracts that one strain, the adaptive immune system documents it, and life long immunity is gained. That means the virus must consistently find new hosts to infect. These new hosts must be in the near vicinity (coughing distance), and large, congested populations did not exist until about 6,000 years ago, so the virus could not have had a population to infect. So it's new.

To never leave the inside of the cell.

The fusion protein which allows the virus to check its coat at the doof is also capable of fusing with multiple cell membranes. The result? Large blobs of fused cells, containing many nuclei and many hijackable organelles. This lets the virus replicate more in one go, before having to exit the cell and risk the run of meeting with antibodies.

They're not sure.

It's suspected to be like rhinoviruses, stopping the release,but they're really not sure.

what is an advantage of measles attacking dendritic cells?

Infecting dendric cells causes measles to attack macrophages and the lymph nodes as well. The fewer macrophages, the weaker the immune response. The destroyed dendritic and macrophages are also the leaders, they direct the immune response. Consequently, some times the wrong antibody is produced, or not enough killer T cells are activated.

Oh, and there is research to support that measles also can trigger T cells to commit suicide.

Flu peeps usually rub their eyes with contaminated hands.

Measles just likes to attack the mucous membranes.

sometimes, measles will infect the brain. Then the immune response causes swelling, which then destroys myelin sheath, resulting in destruction of the nervous system and possible brain damage and death.