1. 6.3 Defence Against Infectious Disease

4. 6.3.4 Outline how phagocytic leucocytes ingest pathogens in the blood and in body tissues. 1 type of WBCs—macrophages1 type of WBCs—macrophages Lg, change shape to engulf invaders (phagocytosis) & squeeze in/out of capillariesLg, change shape to engulf invaders (phagocytosis) & squeeze in/out of capillaries Recognizes self/non-selfRecognizes self/non-self Proteins on cell surfaceProteins on cell surface Self  left aloneSelf  left alone Non-self  phagocytosis, lysosomes of macrophage digest itNon-self  phagocytosis, lysosomes of macrophage digest it “NON-SPECIFIC” DEFENSE b/c invader’s identity’s not known, just that it’s non-self“NON-SPECIFIC” DEFENSE b/c invader’s identity’s not known, just that it’s non-self

6. 6.3.5 Distinguish between antigens and antibodies. ABs-specific proteins we produce, in response to a specific pathogenABs-specific proteins we produce, in response to a specific pathogen Flu AB, measles AB, etc.Flu AB, measles AB, etc. Y-shaped, Ag-binding sites at each tipY-shaped, Ag-binding sites at each tip AB attaches to Ag’s sfcAB attaches to Ag’s sfc Cellular invaders (bacteria)Cellular invaders (bacteria) Foreign Proteins @ outer sfc = ANTIGENS (Ags)Foreign Proteins @ outer sfc = ANTIGENS (Ags) Usually have several diff Ag on sfc, so make several diff Abs against itUsually have several diff Ag on sfc, so make several diff Abs against it Viral invaders tooViral invaders too

9. 6.3.6 Explain antibody production. B Cells (type of WBC)B Cells (type of WBC) We all have lots diff B cells, each makes a diff ABWe all have lots diff B cells, each makes a diff AB 1.Specific AG identified (cold virus) 2.Specific B lymphocyte id’d that can produce AB to bind to AG (to proteins on virus coat) 3.B cell & many identical B cells clone selves (mitosis)  LOTS in a short period of time 4.“army” of B cells produce ABs 5.ABs released to bloodstream, find AG 6.ABs help eliminate the pathogen (various ways) 7.Some of cloned B cells remain in bloodstream, give immunity from 2 nd infection by same pathogen: MEMORY CELLS

12. 6.3.7 Outline the effects of HIV on imm sys. Viruses work by finding a cell type in body that matches its proteins (complementary)—why only some body cells affected by flu virus (nasal cells  nasal symptoms)Viruses work by finding a cell type in body that matches its proteins (complementary)—why only some body cells affected by flu virus (nasal cells  nasal symptoms) HIV (virus)  AIDS (symptoms)HIV (virus)  AIDS (symptoms) Infects Helper T cellsInfects Helper T cells Latency period (infected cells remain alive) of several years before AIDSLatency period (infected cells remain alive) of several years before AIDS Helper T cells communicate which cells need to clone & produce ABHelper T cells communicate which cells need to clone & produce AB They die  no more communication, AB not producedThey die  no more communication, AB not produced Can no longer fight off pathogens (even mild ones), often die of 2-ary infectionsCan no longer fight off pathogens (even mild ones), often die of 2-ary infections

16. 6.3.8 Discuss the cause, transmission and social implications of AIDS. Cause: HIV (6.3.7)Cause: HIV (6.3.7) difficult to make vaccine b/c it hides latent for yrs & b/c it mutates quicklydifficult to make vaccine b/c it hides latent for yrs & b/c it mutates quickly Medication-ethical reasons not researched much in past (drug abuse, sexual activity leading to HIV); recently, lots of $$ for researchMedication-ethical reasons not researched much in past (drug abuse, sexual activity leading to HIV); recently, lots of $$ for research Transmission:Transmission: person-person body fluids: sex, drugs, blood transfusions (not always tested in past!!)person-person body fluids: sex, drugs, blood transfusions (not always tested in past!!) Test: ELISA (HIV-AB test)Test: ELISA (HIV-AB test) Social Implications:Social Implications: Once thought only homosexuals & drug abusers (not so!—rapidly spreading, all at risk)Once thought only homosexuals & drug abusers (not so!—rapidly spreading, all at risk) HIV+ discrimination: employment, insurance, education access, social acceptance, etc.HIV+ discrimination: employment, insurance, education access, social acceptance, etc. Not all countries have education/medical treatment to deal w/diseaseNot all countries have education/medical treatment to deal w/disease Inadequate medical care  increase in infection ratesInadequate medical care  increase in infection rates Education is key, decrease risk of exposure: GLOBAL problem, needs a GLOBAL solution...not just within the boundaries of our own country.Education is key, decrease risk of exposure: GLOBAL problem, needs a GLOBAL solution...not just within the boundaries of our own country.