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6.3 Defence Against Infectious Disease

6.3 Defence Against Infectious Disease. 6.3.4 Outline how phagocytic leucocytes ingest pathogens in the blood and in body tissues. 1 type of WBCs—macrophages Lg, change shape to engulf invaders (phagocytosis) & squeeze in/out of capillaries Recognizes self/non-self Proteins on cell surface

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6.3 Defence Against Infectious Disease

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  1. 6.3Defence Against Infectious Disease

  2. 6.3.4 Outline how phagocytic leucocytes ingest pathogens in the blood and in body tissues. 1 type of WBCs—macrophages Lg, change shape to engulf invaders (phagocytosis) & squeeze in/out of capillaries Recognizes self/non-self Proteins on cell surface Self  left alone Non-self  phagocytosis, lysosomes of macrophage digest it “NON-SPECIFIC” DEFENSE b/c invader’s identity’s not known, just that it’s non-self

  3. 6.3.5 Distinguish between antigens and antibodies. ABs-specific proteins we produce, in response to a specific pathogen Flu AB, measles AB, etc. Y-shaped, Ag-binding sites at each tip AB attaches to Ag’s sfc Cellular invaders (bacteria) Foreign Proteins @ outer sfc = ANTIGENS (Ags) Usually have several diff Ag on sfc, so make several diff Abs against it Viral invaders too

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

  5. 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) HIV (virus)  AIDS (symptoms) Infects Helper T cells Latency period (infected cells remain alive) of several years before AIDS Helper T cells communicate which cells need to clone & produce AB They die  no more communication, AB not produced Can no longer fight off pathogens (even mild ones), often die of 2-ary infections

  6. 6.3.8 Discuss the cause, transmission and social implications of AIDS. Cause: HIV (6.3.7) difficult 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 research Transmission: person-person body fluids: sex, drugs, blood transfusions (not always tested in past!!) Test: ELISA (HIV-AB test) Social Implications: Once thought only homosexuals & drug abusers (not so!—rapidly spreading, all at risk) HIV+ discrimination: employment, insurance, education access, social acceptance, etc. Not all countries have education/medical treatment to deal w/disease Inadequate 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.

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