Final Exam for micro

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kwoolley
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120325
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Final Exam for micro
Updated:
2011-12-05 18:55:22
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micro
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micro final exam
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  1. GP proteins are comprised of...
    proteins and carbohydrates
  2. Explain what occurs to the genome of a retrovirus after the virus has entered a host cell and uncoated.
    after entering a host cell and uncoating, the RNA genome of a retrovirus is used to make a DNA version of a genome. this viral DNA then becomes integrated into the DNA of the host cell.
  3. Transcriptase does...
    reverse transcriptase is the enzyme responsible for reading RNA in order to produce DNA
  4. gp41 does...
    plays a role in helping HIV fuse with the membrane of host cell (to allow for entry)
  5. gp120
    Attaches HIV virus to receptor of host cell
  6. matrix
    maintains the structure of the virus
  7. integrase
    helps DNA copy of HIV genome become integrated into DNA of a host cell
  8. protease does...
    cleaves a newly made viral proteins so that they may fold properly
  9. Vpr
    prevents host cell from dividing
  10. Tat protein does...
    a regulation transcription of viral and host cell genes
  11. Nef
    Prevents host cell from synthesising MHC I molecules
  12. what HIV is most prevalent in North AMerica, europe and asia is...
    HIV 1
  13. The HIV most prevalent in west africa and india is
    HIV 2
  14. The type of HIV thats mmost easily transmitted from person to person is...
    HIV 1
  15. whats the main receptor that HIV binds too?
    CD4 (Helper T cell, macrophages and certain brain cells ecpress it)
  16. what are 2 other tyoe of coreceptor that HIV can bind too
    CX CR 4 and CCR5
  17. Fusion inhibitors
    inhibit fusion of HIV to the host cell
  18. reverse transcriptase inhibitors
    slows down or gets rid of reverse transcriptase
  19. integrase inhibitor
    so that HIV DNA doesn't get into the host cells DNA
  20. protease inhibitor
    stop HIV from forming fully fuctioning proteins.
  21. Attenuated HIV
    (Weakened HIV) HIV already has a high mution rate so it's chance of mutating back into the activated form isw likely. and when tested on money's the money's exhibited AID's like symptoms, in other words NO BEUNO! lol
  22. inactivated HIV
    Doesvn;t cause enough of a infection so that a insuficant immune response happens (since the only weak spot on the gp120 are covered by carbohydrates so that antibodies can't bind onto them) so that doesn't help.
  23. HIB subunit
    just like inactivated HIV it doesn't cause enough of a response in the immune system to really have any good result on it.
  24. HIV DNA vaccine
    There is a promise of HIV DNA since peices of the DNA that's the same as all the HIV's can be taken and put in the cell and stimulate the immune system enough to at least, it is found, slow down the HIV
  25. Paul Ehrlich
    he discovered the first selectively toxic antimicrobial (salversan) which treated syphilis, but it was a arsenic but better then being like Napoleon
  26. Alexander Fleming
    he discovered the first antibiotiv penicillin, he discovered it on accident, a mold didn't let his staphylococcus grow. but he didn't know how to isolate this mold or stabilize it so nothing happened with it.
  27. Howard Florey and ERnst chain
    they discovered Flwmings paper nad purified and stabilized the mold and mass produced penicillin molecule.
  28. antibiotic
    substance that attacks bacterial structures. the first antibiotivd were isolated from various types of microbes. but many of today's antibiotics are synthetic
  29. Antibiotics that inhibit cell wall synthesis
    • This is selective because eukaryotes don't have cell walls
    • It binds to the transpeptidase and breaks it the bonds so there is no bonds holding the wall together making the cell wall weak.(leading to abnormal osmotic pressure from the weak wall or the cell preforms autolysis (kills itself))
  30. transpeptidase
    enzyme that helps form linkade between NAMS, the penicillin bonds to it and break this is there is no transverse bond so the wall becomes incrediably weak.
  31. inhibition if protein sythesis
    • prevents ribosomes from buidling protiens, the only problems is that eukarotes have ribosomes that are only slightly different from prokarotic ribosomes so they are NOT ENTIRELY SELECTIVE
    • the mitochondria in eukaroytic cells have their own ribosomes that are like prokaryotic DNA so this antibiotic hurts our mitochondria
  32. Nucleic acid synthesis
    prevent bacterial nucleic acid synthese from happening, their DNA is going to have different polymease than eukaryotics so they will go after the bacterial one.
  33. Analog
    a molcule with a similar structure to another molecule
  34. Growth factor analogs
    • bacteria have different growth factors then us
    • PABA is a nutrient that bacteria need to convert that PABA into folic acid (which we get from our diet) which ends up as nucleic acids. This antibiotic (sulfanilamide) is similar to PABA and blocks the receptor that breaks down PABA
  35. prevalence of antibiotic-resistant bacteria can be explained by natural selection
    as more antibiotics come into the envirment the reisistant bactera are better able to replicate (even in the antibiotic soaked enviroment) so these type of bacteria are going to be found and picked up more readily.
  36. why is it good to finish your antibiotics
    for the tougher bacteria to get through they need more time and more antibiotics to actually kill them, if you stop to soon then it's those tough ass bacteria that are going to be left and that's not what you want.
  37. nucleoside Analogs
    • antiviral drug they insert a analog that looks like a nucleotide when the virus is replicating but its not and no other nucelotide can bind after the analog so its called a chain terminator.
    • acyclovir is a example of this
  38. interferons
    a virus in a cell triggers interferons, specifically double standed RNA (since eukaryots don't have that) look at the 4 ways that cells respond to interferon for more info
  39. four ways in whcih cells may respond to inteerferon
    • 1. a neighboring cell recieves intferon and creases RNAase
    • 2. recieves interferons activates transcrition factor and MHC I molcules so when the cell is infected with the virus they show it to the cytotoxic T cell and it goes from there.
    • 3. a interferon can activate a natural killer cell
    • 4. inhibit cell division so that the virus can't divide like it wants too
  40. penicillin harms bacteria by...
    disrupting cell wall synthesis
  41. erythromycin harms bacteria by
    disrupting protein synthessi
  42. ampicillin harms bacteria by
    disrupting cell wall synthesis
  43. ciprofloxacin harms bacteria by...
    • disrupting nucleic acid synthesis
    • (interesting not this gained a lot of presses a few years back as being the drug of choice againes those affected with teh anthrax mailings
  44. streptomycin harms bacteria by...
    disrupting protein synthesis
  45. name 4 ways that bacteria can be resistant to certain antibiotics
    • 1) some bacteria are resistant to antibiotica because the antibiotics cannot enter the bacterium (some antibiotics are ti big to pass through the out membrane of Gram negatives)
    • 2) some bacteria are resistant to antibiotics because they have experianced a mutatuin that resulted in alteration of bacterial structure that's normally targeted by an antibiotic
    • 3) some bacteria are resistant to antibitics because they have a mechanism for actiely pumpimh out the antibiotic after it enters the bacterium.
    • 4) some bacteria are resistant to antibiotics because they hace the ability to produce and secrete enzymes that deactivate the antibiotic
  46. hypersensitivity
    exaggerated immune response to something that won't huty you
  47. Type 1 hypersensitivity
    This is a common allergy. This one a allergan goes to a B cell antibodies are made and IgE antibodies are made which binds to mast cells. When the antigen comes and cross binds (the antigen binds to 2 of the IgE antibodies found on the mast cell) this releases histamines. (if it produces IgG it binds to the mast cell and no over reaction will happen.)
  48. anaphylactic shock
    sudden decrease in BP due to allergen in the blood
  49. How do anti-histamines work
    they block the receptor in the blood vessels so that no histamine can get in and tear the blood vessels apart
  50. type 2 hypersensitivty
    • If the the mother is negative and the baby is positive blood antigen and they exchange blood in the delivery, the mom while sense it is a foreign thing and make antibodies. if the baby has another positive baby the immune system will attack.
    • To prevent this the mom is given antibodies so that the mom's B cells don't have to make it so no memory cells are made.
  51. Type 3 hypersenstivites
    it's triggered when a high amount of antigen in a short period of time that involved a complement protein. a whole bunch of antigens bound by a whole lot of antibodies (called a complex) the complement binds to the antigen starting the cascade and a basophile can bind to the complement and it releases histamine. The complex gets stuck in the blood vessels and the complemt is still being released and the neutrophil comes along and releases bad enzymes. (we see this with sermun sickness when we can give them other animals serum)
  52. Type 4
    (TB test responds to this) It's a direct involvement of T cells triggered by antigen that activates T cells. so first exposure to the antigen causes the production of memory cells, the 2nd exposure releases cytokines that recruit macrophages (which leads to a lump in a positive test)

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