BIO 105 WK 9
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This 6 page Class Notes was uploaded by Casslyn on Thursday March 31, 2016. The Class Notes belongs to BIOL 105 at University of St. Thomas taught by Dr. Chester Wilson in Spring 2016. Since its upload, it has received 6 views. For similar materials see Human Biology in Biology at University of St. Thomas.
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Date Created: 03/31/16
TH APRIL 5 2016 CLASS NOTES CELL-MEDIATED RESPONSE, ANTIBODIES 1. THERE WILL BE A QUIZ ON THURSDAY 2. IS A MAST CELL A MORE GENERALIZED OR SPECIFIC RESPONSE OF THE BODY? A. RESPOND TO BASICALLY ANYTHING AND CIRCULATE THROUGHOUT THE BODY 3. REMINDER: WE SPOKE ABOUT A GROUP OF CELLS CALLED B CELLS, NAMED FOR THE PLACE THEY MATURE IN CHICKENS, BUT PRODUCED IN LYMPH NODES OF US. THERE’S A HUGE VARIETY AND THEYRE DISTINGUISHED BY PROTEINS ON OUTSIDE. THERE’S A LARGE VARIETY, BUT ONLY A COUPLE COPIES OF EACH. IF ENCOUNTERS ANTIGEN, BINDS TO IT AND REPRODUCES ITSELF. EFFECTOR CELLS ARE THE ACTUAL DEFENSIVE CELLS. MEMORY CELLS MADE: HANG IN LYMPH NODES KEPT IN RESERVE. ATTRACTS ATTENTION FROM HELPER T CELLS THAT PRODUCES INTERLEUKIN (AMONG THE WHITE BLOOD CELLS) WHICH STIMULATE ANTIGEN-PRESENTING B CELLS TO DIVIDE. 4. QUESTION: AN INTERLEUKIN IS BASICALLY A HORMONE. IS THIS A PROTEIN OR A STEROID? A. INTERLEUKIN IS A PROTEIN! ONLY ONES WITH ANTIGEN CAN RESPOND. B. PROTEIN: ACTIVATES/DEACTIVATES PREEXISTING C. STEROID: SLOW, GENE MANIPULATION, LONG-LASTING 5. ALLERGIES (RESUME FROM LAST TIME) A. B CELL + MAST CELL. OF B CELLS, MANY KINDS, ANTIBODIES PRODUCED = IG (IMMUNOGLOBULIN) B. WHEN EXPERIENCING A HISTAMINE, STARTS TO PRODUCE HUGE NUMBERS OF RECEPTORS AND THEN SENSITIVE TO OWN PRESENSE SO IT MAKES MORE OF ITSELF AND MORE OF ITS RECEPTORS = POSITIVE FEEDBACK. HISTAMINE PRESENT = MAKE MORE HISTAMINE = MAKE MORE HISTAMINE. RESPONSE TO FOREIGN OF ALLERGY. STOP POS FEEDBACK = STOP THE STIMULUS. YOU EITHER STOP STIM OR USE AN ANTIHISTIMINE (IMPORTANT TO ALLERGIES) INDUCES DROWSINESS, DON’T COMBINE WITH ALCOHOL ETC C. ALLERGIES ARE A MAJOR SOURCE OF SYSTEMATIC THINGS. i. TRANSPLANT REJECTION 1. WHEN BOD CAN’T TELL IF IT’S A TRANSPLANT TISSUE OR TUMOR, REJECTS BC IMMUNE SYSTEM DESTROYS SUSPICION ii. TUMOR DETECTIN (IS A GOOD THING, DEFENSE AGAINST CANCERS) 1. EACH OF US ACCUMULATES TONS OF MUTATIONS IN A LIFETIME. WE ALL HAVE A TON OF TUMORS STARTING UP WITHIN OUR BODY, BUT T CELLS COME ALONG AND KILL THEM. iii. AUTOIMMUNE CONDITIONS 1. WHEN BOD CAN’T TELL IF IT’S A TRANSPLANT TISSUE OR TUMOR, REJECTS BC IMMUNE SYSTEM DESTROYS SUSPICION 2. ASTHMA, LEUPIS (CARTELIDGE TREATED AS FOREIGN BODY) 6. T-CELLS A. PHAGOCYTES CLEAN UP AFTER B. MACROPHAGE: SET OF PHAGOCYTE. GENERALIZED. NOT PART OF IMMUNE RESPONSE. C. ROLLS AROUND EATING FOREIGNERS. STICKS DIGESTIVE ONTO MEMBRANE, BECOMES AN ANTIGEN PRESENTING SKILL. D. NAÏVE MACROPHAGE ANTIGEN PRESENTING CELL E. SOMETHING RESPONSE (DIGESTED AND PUT ON SURFACE) HELPER T CELLS: MACROPHAGE EATS EVERYTHING. A CELL THAT HAS ENCOUNTERED SOMETHING FOREIGN, GET RID OF CELL. F. CYTOTOXIC CELLS LOOK FOR CELLS SAYING SIGN THAT THEY’VE BEEN INFECTED. PRODUCE PROTEINS CALLED PERFERINS TO ASSEMBLE INTO A PORE. (SAME MECHANISM AS COMPLEMENT PROTEINS) G. MACROPHAGES EAT STUFF, BUT GET DESTROYED FOR EATING BAD THINGS. H. 1. EATS, DIGESTS, PUTS PIECES OF SELF ON ANTIGEN SURFACE. 2. VIRUS LEAVES PARTS ON ANTIGEN. 7. EVOLUTIONARY PROCESSES A. Genetic change within a species B. Mutation (variation) Migration (mixes variations between populations) and Recombination (mixes variations from different individuals) 2 C. ALL THREE HAPPEN IN VIRUSES. HIV IS TRANSMITTED IN BODILY FLUIDS. HIV IS POPULATION BY BODY. GETS HIV FROM TWO DIF PEOPLE COULD PRODUCE VARIATION BY MIGRATION. D. REDUCES GENETIC VARIATION: NATURAL SELECTION AND GENETIC DRIFT E. Whole point of genetic drift is that it’s random. A small part goes over and founds a new population, a small sample only has some of original population, so it’ll be different genetic of random is involved in genetic drift F. Genetic drift is random (natural selection is nonrandom) 3 BIO IN CLASS APRIL 7 2016 The two types of HIV are HIV 1 (found in chimpanzees) and HIV2 (found in monkeys). They both have multiple origins, with at least four found so far. This makes the creation of a vaccination or a treatment extremely difficult. Infection by blood or sexual contact. One man got infected many times through blood transfusions. Each population of HIV evolves relative to an individual and their particular environment. The virus sheds the capsule upon infection of the host cell. There are multiple proposed places for a treatment or inhibitor. In HIV fusion, three cells react differently. In a glial cell, the HIV virus sits dormant much longer because nerve cells tend not to die or reproduce. In cytotoxic t cells, their function is to blow up helper t cells which results in immunodeficiency. The majority of people with HIV reside in sub-Saharan Africa when compared to the rest of the world until recently. CD4 500 t cells/ ml blood= the clinical point at which AIDS is declared. This means that the virus has killed off about 3/4s of the immune system. Thrush and herpes are both viral conditions. Tuberculosis, cancer of the immune system, and others emerge because HIV targets the immune system that’s responsible for controlling and preventing that. At 250 t cells/ml blood, cancer emerges. Interfering with the viral proteins could lessen the harm to the patient. HIV genes have been long-researched as to the proteins they affect/create. HIV 2 has a longer chromosome than HIV1. But, gag (capsid issues), the pol (reverse transcription), and env (codes proteins in the envelope) HIV intervention is targeted at the fusion, provirus, or mutation mechanisms CLASSES OF ANTIRETROVIRAL DRUGS The combinations tend to work the best in preventing the exponential growth of HIV. HIV in humans can successfully reproduce in about three minutes. Fusion inhibition o CD4 is a protein on a human cell surface that binds the protein and filament. Some people don’t have it, and they function fine. However, a cap on CD4 is not optimal because of it’s importance for communication between immune cells. o HIV mutates super fast. If an inhibitor is added to the fusion gene, the virus will just change. However, only saves about 3 weeks of time. Reverse Transcriptase inhibitors o Today’s most common drugs type. o HIV lasts because it mutates. We have many antiviruses to cycle the mutations and make it ineffective, but eventually HIV wins out because we don’t have an antivirus for every strain. o There are two different types called nucleotide or non-nucleotide inhibitors. The non- nucleotide inhibitor blocks active transport and binds to revers transcriptase so it can’t make covalent bonds. Because RNA is a single strand, RNA to DNA (hybrid DNA/RNA moleculechew up RNAmake second DNA strand) is done really fast without a scan for mutations. o Nucleotide inhibitors are fake nucleotides. To the reverse transcriptase, they look functional (so puts in, and just falls apart w/o checking and it never notices so nothing is created) but the side affects screw up ordinary cells too (especially skin, intestines, and the reparative cells) o With this drug, patients’ digestive system is poorly functioning which leads to weight loss, adverse skin issues. This drug also only increases HIV reproduction time from three minutes to approximately ten minutes. o Non-mutant reverse transcriptase just zips along while the mutant reverse transcript is slow and will eventually make successful DNA and win by natural selection Integrase Inhibitors o Prevents viral DNA placement within the hosts’ DNA o Integrase recognizes the sequences in DNA to cut at specific points (so the H bonds match) o Make synthetic pieces to bind to integrase so that it never cuts the DNA of the human cell, making it mutant. However, the mutation rate makes this absolutely impossible. Protease inhibitors o Make something to bind so the proteins from the virus cell cannot come into the active site. o Yet, once again, any slight change deems it ineffective. Maturation inhibitors o Basically inhibit the maturation, yet ineffective. Combining many and immunotherapy o Interleukins are the chemical signals to help T cells determine which to kill. o Giving someone both drugs and interleukins increases the normal, healthy amount of T Cells while administering drugs alone just stabilizes production. o HAART stands for highly active antiretroviral therapy (which means a cocktail drug) to stay a step ahead of the virus. The side affects include depression, low health, unhealthy skin, unhealthy digestion. When patients became depressed they accepted their death, stopped the drugs, and thought they’d just let the HIV kill them. However, they got better only to face a symptom comeback six months later. o STI, or structured treatment interruption is informally referred to as drug holiday. This basically makes it cycle in and out of drugs to prevent the evolution of the virus’ resistant strain. Without drugs, wild type increases and mutant decreases. When drugs reapplied, wild type decreases and resistant type increases. 2 3
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