TOPIC 2

METHODS OF STUDYING CELLS

-LIGHT MICROSCOPES

-USE PAIR OF CONVEX GLASS LENSES THAT CAN RESOLVE IMAGES 0.2um APART

-REASON= IT IS WAVELENGTH OF LIGHT & THEREFORE RESTRICTS RESOLUTION THAT MICROSCOPE RESOLVES TO (COMPARED TO ELECTRONIC MICROSCOPE THAT CAN DISTINGUSH BETWEEN ITEMS 0.1nm APART)

-RESOLUTION= MINIMUM DISTANCE APART THAT 2 OBJECTS CAN BE DISTINGUISHED AS SEPERATE OBJECTS IN A PHOTO

-MAGNIFICATION= IMAGE / ACTUAL

-LIMITATION MEANS ELECTRONIC MICROSCOPES CAN BE USED TO LOOK AT OBJECTS THAT ARE CLOSER THAN 0.2um APART

METHODS OF STUDYING CELLS

-ELECTRONIC MICROSCOPES

-USE BEAM OF ELECTRONS THAT ARE FOCUSED BY ELECTROMAGNETS INSIDE VACUUM ENVIRONMENT

-VACUUM ENVIRONMENT NEEDED SO PARTICLES IN AIR DON'T DEFLECT ELECTRONS OUT OF BEAM ALIGNMENT

-2 TYPES

-TRANSMISSION ELECTRON MICROSCOPE (TEM)- BEAM OF ELECTRONS PASSES THROUGH THIN SECTION OF SPECIMEN, AREAS THAT ABSORB ELECTRONS APPEAR DARKER ON ELECTRON MICROGRAPH PRODUCED

-SCANNING ELECTRON MICROSCOPE (SEM)- BEAM OF ELECTRONS PASSES ACROSS SURFACE AND SCATTER, PATTERN OF SCATTERING BUILDS UP 3D IMAGE DEPENDING ON CONTOURS OF SPECIMEN

METHODS OF STUDYING CELLS

-LIMITATIONS OF SEM & TEM

• WHOLE SYSTEM MUST BE IN VACUUM SO LIVING SPECIMEN CAN'T BE OBSERVED
• COMPLEX STAINING PROCESS REQUIRED, MAY INTRODUCE ARTEFACTS INTO IMAGE
• SPECIMENS HAVE TO BE VERY THIN (PARTICULARLY FOR TEM) SO ELECTRONS CAN PASS THROUGH
• SEM HAS LOWER RESOLVING POWER THAN TEM (BUT BOTH HAVE GREATER RESOLVING POWER THAN LIGHT MICROSCOPE)

-CELL FRACTIONATION & ULTRACENTRIFUCATION

-CELL FRACTIONATION= PROCESS IN WHICH DIFFERRENT PARTS & ORGANELLES OF CELL SEPERATED SO THEY CAN BE STUDIED IN DETAIL (MOST COMMON METHOD= DIFFERENTIAL CENTRIFUGATION)

METHODS OF STUDYING CELLS

-HOMOGENATION

• BLENDER- RUPTURING CELL MEMBRANES TO RELEASE ORGANELLES
• HOMOGONATE PRODUCED & FILTERED
• PLACED IN CENTRIFUGE & SPUN AT SLOW SPEED
• HEAVIEST ORGANELLE FORCED TO BOTTOM (PELLET)- LEFT OVER FLUID CALLED SUPERNATANT
• SPUN AGAIN

-ORDER: NUCLEI, CHLOROPLASTS, MITOCHONDRIA, VESICLES, MEMBRANES (FRAGMENTS), ER, RIBOSOMES

-CONDITIONS FOR HOMOGENATION

-COLD- STOP REACTIONS (REDUCE KINETIC ENERGY) &LOWER RATE OF ENZYMES

-ISOTONIC- EQUAL WP, EQUAL WC & LIMITS OSMOSIS OF H20 INTO ORGANELLES WHICH WOULD CAUSE DAMAGE (BURSTING-H20 IN, SHRINKING-H20 OUT)

-BUFFERED- CONSTANT pH ( NOT TOO ACIDIC, NOT TOO ALKALINE)

CELL STRUCTURE

CELL STRUCTURE

-HOW DO CELLS WORK

• 1. GENES EXPRESSED AS mRNA (IN NUCLEUS)- GENES STAY IN NUCLEUS
• 2. mRNA BONDS TO RIBOSOMES- LEAVES NUCLEUS THROUGH PORES
• 3. PROTEIN SYNTHESISED ON RIBOSOMES ON mRNA (SANDWICH)
• 4. TRANSPORT, STORAGE & MODIFICATION OF PRODUCT P (RER, SER, GOLGI APPARATUS)
• 5. VESICLE BUDS OFF FROM GOLGI APPARATUS (PROTEINS ENTER GOLGI- PRODUCE VESICLES)
• 6. VESICLE FUSES TO CELL WALL & RELEASES OUT HORMONES

-1 GENE= 1 PROTEIN= 1 ENZYME= CATALYSTS= 1 PRODUCT

-PROTEIN- IN= ENZYME- ASE

-1 GENE: 1 mRNA (mRNA ATTATCHES TO RIBOSOME, HELPS FORM PROTEIN)

-CELLS OF MULTICELLULAR ORGANISMS ORGANISED INTO TISSUES, TISSUES INTO ORGANS & ORGANS INTO SYSTEMS

CELL STRUCTURE

-NUCLEUS= DOUBLE MEMBRANE CALLED ENVELOPE CONTAINING 3000 PORES THAT ENABLE MOLECULES TO ENTER & LEAVE (ALSO CONTAINS CHROMATIN, NUCLEOLUS, SITE OF RIBOSOME PRODUCTION)

-ROUGH ENDOPLASMIC RETICULUM= SERIES OF FLATTENED SACS ENCLOSED BY MEMBRANES WITH RIBOSOMES ON SURFACE, FOLDS & PROCESSES PROTEINS MADE ON RIBOSOMES

-SMOOTH ENDOPLASMIC RETICULUM= MEMBRANE BOUND SACS, PRODUCES & PROCESSES LIPIDS

-GOLGI APPARATUS= SERIES OF FLUID FILLED, FLATTENED & CURVED SACS WITH VESICLES SURROUNDING EDGES, PROCESSES & PACKAGES PROTEINS & LIPIDS & PRODUCES LYSOMES

-MITOCHONDRIA= OVAL SHAPED, BOUND BY ENVELOPE (INNER MEMBRANE (CRISTAE) WITH MATRIX ON INSIDE CONTAINING ENZYMES FOR RESPIRATION)

-CENTRIOLES= HOLLOW CYLINDERS CONTAINING RING OF MICROTUBULES ARRANGED AT RIGHT ANGLES TO EACH OTHER, INVOLVED IN PRODUCING SPINDLE FIBRES FOR CELL DIVISION

-RIBOSOMES= COMPOSED OF 2 SUB UNITS & ARE SITE OF PROTEIN PRODUCTION

CELL STUCTURE

-NUCLEUS

CELL STUCTURE

-ENDOPLASMIC RETCULUM

CELL STRUCTURE

-GOLGI APPARATUS

CELL STRUCTURE

-MITOCHONDRIA

CELL STRUCTURE

-CHLOROPLASTS

CELL STRUCTURE

-CELL WALL

• CELLULOSE
• PERMEABLE
• PECTIN HOLDS WALLS TOGETHER
• MIDDLE LAMELLAE LAYER
• PLASMODESMATA= SMALL HOLE
• STRANDS OF CYTOPLASM CONNECTNBCELLS TOGETHER
• EXCHANGE
• COORDINATION & RESPONSE

CELL STRUCTURE

-PROKARYOTIC CELLS- BACTERIA

-CELL WALL= RIGID OUTER COVERING MADE OF PEPTIDOGLYCAN

-CAPSULE= PROCTECTIVE SLIMY LAYER WHICH HELPS CELL TO RETAIN MOISTURE & ADHERE TO SURFACES

-PLASMID= CIRCULAR PIECE OF DNA

-FLAGELLUM= TAIL LIKE STRUCTURE THAT ROTATES TO MOVE CELL

-PILI= HAIR LIKE STRUCTURE WHICH ATTRACTS OTHER BACTERIAL CELLS

-RIBOSOMES= SITE OF PROTEIN PRODUCTION

-MESOSOMES= INFOLDINGS OF INNER MEMBRANE WHICH CONTAIN ENZYMES REQUIRED FOR RESPIRATION

CELL STRUCTURE

-PROKARYOTIC CELLS- BACTERIA

CELL STRUCTURE

-VIRUSES

CELL STRUCTURE

-VIRUSES

CELL DIVISION (MITOSIS)

-ROLE OF MITOSIS & CELL CYCLE= PRODUCE IDENTICAL DAUGHTER CELLS FOR GROWTH & ASEEXUAL REPRODUCTION (ALL CELLS ARE GENETICALLY IDENTICAL, MITOSIS DOESN'T GIVE RISE TO GENETIC VARIATION)

-3 STAGES OF CELL CYCLE

• MITOSIS: 4 STAGES= PROPHASE, METAPHASE, ANAPHASE & TELOPHASE
• INTERPHASE: CELL GROWS & PREPARES TO DIVIDE-CHROMOSOMES & SOME ORGANELLES REPLICATED & CHROMOSOMES BEGIN TO CONDENSE
• CYTOKINESIS: PARENT & REPLICATED ORGANELLES MOVE TO OPPOSITE SIDES OF CELL & CYTOPLASM DIVIDES, PRODUCING 2 DAUGHTER CELLS

-MITOSIS IMPORTANCE

• GROWTH- IDENTICAL CELLS PRODUCED SO ORGANISMS CAN GROW
• REPAIR- INDENTICAL CELLS PRODUCED SO ORGANISMS CAN REPLACE DEAD TISSUES
• REPRODUCTION- SOME SINGLE-CELLED ORGANISMS (E.G., YEAST) REPRODUCE BY / INTO 2 (IDC)

CELL DIVISION (MITOSIS)

-MITOSIS PROCESS

CELL DIVISION (MITOSIS)

-PROCESS SPLIT

CELL DIVISION (MITOSIS)

-BINARY FISSION (PROKARYOTIC CELLS DIVIDE)

• CIRCULAR DNA IN CELLS REPLICATES & BOTH COPIES ATTACH TO CELL MEMBRANE
• CELL MEMBRANE BEGINS TO GROW BETWEEN  DNA MOLECULES & BEGINS TO PINCH INWARDS, DIVIDING CYTOPLASM INTO 2
• NEW CELLS FORMS BETWEEN 2 DNA MOLECULES DIVIDING ORIGINAL CELL (IDENTICAL DAUGHTER CELLS EACH HAVE SINGLE COPY OF CIRCULAR DNA & VARIABLE NUMBER OF PLASMIDS)

-VIRUSES NON-LIVING= DON'T UNDERGO CELL DIVISION (INJECTION OF THEIR NUCLEIC ACIDS INTO ANOTHER CELL-INFECTED HOST CELL REPLICATES VIRUS PARTICLES)

CELL DIVISION (MITOSIS)

-BINARY FISSION PROCESS

BIOLOGICAL MEMBRANES

-STRUCTURE OF CELL MEMBRANE

• SURROUNDED BY PARTIALLY PERMEABLE MEMBRANE COMPOSED OF PHOSPHOLIPIDS WITH PROTEIN MOLECULES BETWEEN THEM
• MAIN FUNCTION= CONTROLLING MOVEMENT OF SUBSTANCES IN & OUT OF CELL
• ALSO= CONTAINS RECEPTORS FOR OTHER MOLECULES (E.G., HORMONES) & ENABLES ADJACENT CELLS TO STICK TOGETHER
• FLUIDITY OF MEMBRANE & MOSAIC ARRANGEMENT OF POTEIN= FLUID MOSAIC MODEL
• COMPRISED OF PHOSPHOLIPIDS IN WHICH HYDROPHILIC HEADS POINT OUTWARDS & HYDROPHOBIC TAILS POINT INWARDS (ALLOWS LIPID SOLUBLE MOLECULES TO PASS THROUGH MEMBRANE, BUT NOT WATER SOLUABLE MOLECULES & MEANS MEMBRANE IS FLEXIBLE & SELF-SEALING)

BIOLOGICAL MEMBRANES

-STRUCTURE OF CELL MEMBRANE

BIOLOGICAL MEMBRANES

-MEMBRANE COMPONENTS

• PROTEINS: ON SURFACE (EXTRINSIC) OR INTEGRATED THROUGHOUT MEMBRANE (INTRINSIC)- INCLUDE CARRIER PROTEINS WHICH ALLOW SUBSTANCES TO CROSS MEMBRANE& CHANNEL PROTEINS- PROTEINS PRESENT TO AID MOVEMENT ACROSS ACROSS MEMBRANE, PROVIDE MECHANICAL SUPPORT & ACT IN CONJUCTION WITH GLYCOLIPIDS AS RECEPTORS
• CHOLESTROL: PRESENT TO MAKE MEMBRANE MORE RIGID, REDUCE LATERAL MOVEMENT OF PHOSPHOLIPIDS & PREVENTS LEAKAGE OF WATER & DISSOLVED IONS FROM CELLS AS IT'S HYDROPHOBIC
• GYCOLIPIDS: MADE UP OF CARBOHYDRATE BOUND TO LIPIDS (EXTEND FROM SURFACE OF CELL)- ACT AS CELL SURFACE RECEPTORS FOR CERTAIN MOLECULES & ALLOW CELLS TO ADHERE TO 1 ANOTHER TO FORM TISSUES
• GLYCOPROTEINS: CARBOHYDRATES ATTATCH TO EXTRINSIC PROTEINS- ACT AS CELL SURFACE RECEPTORS & NEUROTRANSMITTERS- ALLOW CELL TO RECOGNISE 1 ANOTHER & FORM TISSUES

BIOLOGICAL MEMBRANES

-TYPES OF MOVEMENT

• DIFFUSION= PASSIVE MOVEMENT OF SMALL, NON-POLAR, LIPID SOLUBLE MOLECULES (E.G., CO2 & O2) FROM AREA OF HIGH CONCENTRATION TO AREA OF LOW CONCENTRATION (MOLECULES MOVE DIRECTLY THROUGH PHOSHOLIPID LAYER)
• FACILITATED DIFFUSION= REQUIRES CHANNEL PROTEIN IN CELL MEMBRANE TO TRANSPORT POLAR MOLECULES, CHARGED & WATER SOLUBLE MOLECULES ACROSS MEMBRANE
• OSMOSIS= DIFFUSION OF WATER MOLECULES FROM AREA OF HIGH WP TO AREA OF LOW WP THORUGH PARTIALLY PERMEABLE MEMBRANE
• ACTIVE TRANSPORT= TRANSPORT ALL TYPES OF MOLECULES THROUGH CARRIER PROTEINS FROM AREA OF LOW CONCENTRATION TO AREA OF HIGH CONCCENTRATION (REQURIRES ATP ENERGY)
• CO-TRANSPORT= USES IONS TO MOVE SUBSTANCES INTO & OUT OF CELLS (OCCURS PARTICULARLY IN EPITHELIAL CELLS OF ILEUM)- SODIUM & POTASSIUM IONS PUMPED OUT OF EPITHELIAL CELL BY (AT) INTO BLOOD LEAVING LOWER CONCENTRATION IN CELL (CAUSES IONS TO MOVE IN FROM LUMEN BY (FD) WHICH ALSO BRINGS IN GLUCOSE & AMINO ACIDS INTO CELL)- THESE THEN DIFFUSE FROM HIGH CONCENTRATION IN EPITHELIAL CELL TO LOW CONCENTRATION IN BLOOD)

BIOLOGICAL MEMBRANES

-TYPES OF MOVEMENT

• EXOCYTOSIS & ENDOCYTOSIS= TRANSPORT LARGE PARTICLES- PARTICLES ENCLOSED IN VESICLES MADE FROM CELL SURFACE MEMBRANE & TRANSPORTED INTO CELL (ENDOCYTOSIS) & THEN VESICLES CONTAINING LARGE MOLECULES FUSED WITH CELL SURFACE MEMBRANE & RELEASED FROM CELL (EXOCYTOSIS)

-RATE OF GAS EXHANGE BY DIFFUSION BECOMES MORE RAPID AS

• SURFACE AREA INCREASES
• DIFFUSION DISTANCE DECREASES
• DIFFUSION GRADIENT STEEPENS
• TEMPERATURE INCREASES

BIOLOGICAL MEMBRANES

-DIFFUSION & FACILITATED DIFFUSION

BIOLOGICAL MEMBRANES

-OSMOSIS

BIOLOGICAL MEMBRANES

-ACTIVE TRANSPORT

BIOLOGICAL MEMBRANES

-CO-TRANSPORT

BACTERIA AND VIRUSES

-BACTERIA & VIRUSES= MAIN DISEASE CAUSING PATHOGENS IN HUMANS

-DIFFERENCES

• BACTERIA= PROKARYOTIC CELLS- GENETIC INFO STORED IN FORM OF CIRUCLAR STRAND OF DNA WHEREAS VIRUSES= CONSIST OF JUST NUCLEIC ACID ENCLOSED IN PROTEIN COAT & GENETIC MATERIAL CAN TAKE FORM OF DNA OR RNA
• BACTERIA DON'T REQUIRE HOST TO SURVIVE WHEREAS VIRUSES ARE ENTIRELY DEPENDENT ON HOST & CAN'T SURVIVE WITHOUT THEM
• VIRUSES SIGNIFICANTLY SMALLER THAN BACTERIA
• BACTERIA HAVE CELL MEMBRANE, CELL WALL & CYTOPLASM AS WELL AS OTHER ORGANELLES (RIBOSOMES, PLASMIS, FLAGELLUM & PILI) WHEREAS VIRUSES POSESS NO SUCH STRUCTURES

BACTERIA AND VIRUSES

-BACTERIAL DISEASE EXAMPLE= TUBERCULOSIS (TB)

• CAUSED BY BACTERIA CALLED MYCOBACTERIUM TUBERCULOSIS WHICH INFECTS PHAGOCYTES IN LUNGS
• FIRST INFECTION IS SYMPTOMLESS AS INFECTED PHAGOCYTES ARE SEALED IN TUBERCLES AS RESULT OF IMFLAMMARTORY RESPONSE IN LUNGS
• BACTERIA LIE DORMANT INSIDE TUBERCLES (NOT DESTROYED BY IMMUNE SYSTEM DUE TO THICK WAXY TUBERCLES COAT)
• WHEN IMMUNE SYSTEM WEAKENED, BACTERIA BECOME ACTIVE AGAIN & SLOWLY DESTROY LUNG TISSUE- LEADS TO BREATHING PROBLEMS, COUGHING, WEIGHT LOSS & FEVER (CAN LEAD TO DEATH)

-VIRAL INFECTION EXAMPLE= HUMAN IMMUNODEFICIENCY VIRUS (HIV)

• CAUSES AIDS (EVEMTUAL SYMPTOMS= WEIGHT LOSS, DIARRHOEA, DEMENTIA, CANCERS & OPPORTUNISTIC INFECTIONS (E.G., TB))
• FIRST SYMPTOMS= FEVERS, TIREDNESS & HEADACHES
• AFTER SEVERAL WEEKS, HIV ANTIBODIES  APPEAR IN BLOOD- MAKES PERSON HIV POSITIVE
• SYMPTOMS DISSAPEAR UNTIL IMMUNE SYTEM BECOMES WEAKENED AGAIN (LEADING TO AIDS)

IMMUNE RESPONSE

-PHYSICAL BARRIERS TO INFECTION

• SKIN- TOUGH PHYSICAL BACTERIA CONSISTING OF KERATIN
• STOMACH ACID (HYDROCHLORIC ACID)- KILLS BACTERIA
• GUT & SKIN FLORA- NATURAL BACTERIAL FLORA COMPETES WITH PATHOGENS FOR FOOD & SPACE

-IMMUNE SYSTEM RESPONDS TO ANTIGENS FOUND ON SURFACE OF CELLS (PROTEINS THAT HAVE COMPLEX STRCUTURE, UNIQUE FOR EACH CELL- IDENTIFIESCELL AS SELF OR NON-SELF)

IMMUNE RESPONSE

-NON-SPECIFIC  IMMUNE RESPONSE

• INFLAMMATION- HISTAMINES RELEASED BY DAMAGED WHITE TISSUES CAUSE VASODILATION WHICH INCREASES FLOW OF BLOOD TO INFECTED AREA & INCREASES PERMEABILITY OF BLOOD VESSELS (RESULT= ANTIBODIES, WHITE BLOOD CELLS & PLASMA LEAK OUT INTO INFECTED TISSUE & DESTROY PATHOGEN)
• LYSOZYME ACTION- ENZYMES FOUND IN SECRETION (E.G., TEARS & MUCUS) WHICH KILL BACTERIAL CELLS BY DAMAGING THEIR CELL WALL
• INTERFERON- PREVENT VIRUSES SPREADING TO UNINFECTED CELLS BY STOPPING PROTEIN SYNTHESIS IN VIRUSES
• PHAGOCYTOSIS- PROCESS IN WHICH WHITE BLOOD CELLS ENGULF PATHOGENS, DESTROYING THEM (DO THIS BY FUSING TO PATHOGEN & ENCLOSE THEM IN PHAGOCYTIC VACUOLE WITH LYSOME)- THEN PATHOGEN ENGULFED & DESTROYED, ITS CHEMICAL MARKERS (ANTIGENS) PRESENTED ON SURFACE OF PHAGOCYTE- PHAGOCYTE THEN BECOMES ANTIGEN PRESENTING CELL WHICH ACTIVATES IMMUNE RESPONSE IF ANTIGEN RECOGNISED AS FOREIGN

IMMUNE RESPONSE

-SPECIFIC IMMUNE RESPONSE

-ANTIGEN SPECIFIC & PRODUCES RESPONSES SPECIFIC TO 1 TYPE OF PATHOGEN

-RELIES ON LYMPHOCYTES PRODUCED IN BONE MARROW

• B CELLS MATURE IN BONE MARROW & ARE INVOLVED IN HUMORAL RESPONSE
• T CELLS MOVE FROM BONE MARROW TO THYMUS GLAND WHERE THEY MATURE & ARE INVOLVED IN CELL MEDITATED RESPONSE

-MEMORY CELLS= CELLS WHICH REPLICATE THEMSELVES WHEN EXPOSED TO INVADING PATHOGEN & REMAIN IN LYMPH NODES FOR DECADES SEARCHING FOR SAME ANTIGEN (RESULT= MUCH FASTER IMMUNE RESPONSE SHOULD INDIVIDUAL BE INFECTED BY SAME PATHOGEN AGAIN)

-B EFFECTOR OR PLASMA CELLS= ANTIBODY PRODUCING CELLS

-T HELPER CELLS= STIMULATE B CELLS & T KILLER CELLS TO DIVIDE

-T KILLER CELLS= DESTROY PATHOGEN INFECTED CELLS

CELL MEDIATED RESPONSE

HUMORAL RESPONSE

HUMORAL RESPONSE

-ANTIBODIES

• PLASMA CELLS PRODUCE ANTIBODIES
• MADE OF 4 POLYPEPTIDES CHAIN FORMING Y SHAPED STRUCTURE
• COMPLEMENTARY TO SINGLE ANTIGEN
• WORK BY FORMING ANTIGEN- ANTIBODY COMPLEX WHICH SERVES AS MARKERS FOR PHAGOCYTES TO DESTROY ATTTACHED CELLS
• DUE TO ANTIBODIES HAVING 2 BINDING SITES, THEY CAN CLUMP CELLS TOGETHER, MAKING THEM EASIER FOR PHAGOCYTES TO FIND (AGGLUTINATION)

IMMUNE SYTSTEM

-PRIMARY IMMUNE RESPONSE

• WHEN ANTIGEN ENTERS BODY FOR 1ST TIME IT ACTIVATES IMMUNE SYSTEM
• SLOW BECAUSE THERE AREN'T MANY B CELLS THAT CAN MAKE ANTIBODY NEEDED TO BIND TO IT
• EVENTUALLY, BODY PRODUCES ENOUGH OF RIGHT ANTIBODY TO OVERCOME INFECTION (INFECTED PERSON SHOWS SYMPTOMS OF DISEASE)
• AFTER BEING EXPOSED TO ANTIGEN, T- & B-CELLS PRODUCE MEMORY CELLS (REMAIN IN BODY FOR LONG TIME)- MEMORY T-CELLS REMEMBER SPECIFIC ANTIGEN & RECOGNISE IT 2ND TIME ROUND & MEMORY B-CELLS RECORD SPECIFIC ANTIBODIES NEEDED TO BIND TO ANTIGEN
• PERSON IS NOW IMMUNE (IMMUNE SYSTEM HAS ABILITY TO RESPOND QUICKLY TO 2ND INFECTION)

-SECONDARY IMMUNE RESPONSE

• IF SAME PATHOGEN ENTERS BODY AGAIN, IMMUNE SYSTEM WILL PRODUCE QUICKER, STRONGER IMMUNE RESPONSE
• CLONAL SELECTION HAPPENS FASTER- MEMORY B-CELLS ACTIVATED & DIVIDE INTO PLASMA CELLS THAT PROODUCE RIGHT ANTIGEN & MEMORY T-CELLS ACTIVATED & DIVIDE INTO CORRECT TYPE OF T-CELLS TO KILL CELL CARRYING ANTIGEN
• GETS RID OF PATHOGEN BEFORE SYMPTOMS SHOW (IMMUNE TO PATHOGEN)

IMMUNITY

-PASSIVE OR ACTIVE

-ACTIVE IMMUNITY RESULTS FROM PRODUCTION OF ANTIBODIES BY IMMUNE SYSTEM IN RESPONSE TO PRESENCE OF ANTIGEN 

-PASSIVE IMMUNITY RESULTS FROM INTRODUCTION OF ANTIBODIES FROM ANOTHER PERSON OR ANIMAL

-SUBTYPES: NATURAL OR ARTIFICIAL

• NATURAL ACTIVE IMMUNITY ARIES FROM BEING EXPOSED TO ANTIGEN OR GETTING THE DISEASE
• ACTIVE ARTIFICIAL IMMUNITY ACQUIRED THROUGH VACCINATIONS WHICH STIMULATE IMMUNE SYTEM & LEAD TO PRODUCTION OF ANTIBODIES
• NATURAL PASSIVE IMMUNITY IS RSULT OF CROSSING OF MOTHER'S ANTIBODIES THROUGH PLACENTA & THEIR PRESENCE OF BREASR MILK
• PASSIVE ARTIFICIAL IMMUNITY IS WHERE ANTIBODIES INJECTED INTO BODY

IMMUNITY

-VACCINES= WAY OF INTRODUCING PATHOGEN INTO BODY IN ORDER TO PRODUCE IMMUNE RESPONSE

-PATHOGEN MAY BE DEAD OR INACTIVATED, BUT PATHOGENS ON SURFACE STILL PRODUCE IMMUNE RESPONSE (EXAMPLE OF ACTIVE IMMUNITY)

-RESULTS IN CREATION OF MEMORY B CELLS WHICH WILL TRIGGER RAPID SECONDARY IMMUNE RESPONSE SHOULD PATHOGEN EVER BE DETECTED AGAIN

-SUCCESS OF VACCINATION PROGRAM, DEPENDENT ON FACTORS

• COST OF VACCINE
• SEVERITY OF SIDE EFFECTS
• EASE OF PRODUCTION, TRANSPORTATION & ADMINISTRATION
• NUMBER OF PEOPLE NEEDED FOR HERD IMMUNITY (IF ENOUGH PEOPLE ARE VACCINATED, PATHOGEN WON'T BE ABLE TO BE TRANSMITTED FROM DIFFERETN HOSTS)

-VACCINES NOT ALWAYS USEFUL IN PREVENTING OUTBREAK (ANTIGEN ON SURFACE OF PATHOGEN CAN CHANGE, REMOVING IMMUNITY (E.G., INFLUENZA- RAPIDLY CHANGING)- HERD IMMUNITY SHORT-LIVED

IMMUNITY

-ETHICAL CONSIDERATIONS

• PRODUCTION & TESTING OF VACCINES MAY BE DONE ON ANIMALS
• RISKS OF VACCINE NEEDS TO BE BALANCED WITH BENEFITS
• VACCINE MUST BE TESTED ON HUMANS 1ST TO DETERMINE TOXICITY
• VACCINATIONS EXPENSIVE

-MONOCLONAL ANTIBODIES= PRODUCE MANY CLONES OF SINGLE ANTIBODY TYPE

-MANY TYPES OF ANTIGENS= EACH B-CELL  PRODUCES DIFFERENT COMPLEMENTARY ANTIBODY

-DIFFERENT USES

• DIRECT THERAPY- (MA) SPECIFIC TO ANTIGENS FOUND ON SURFACE OF CANCEROUS CELLS CAN BE USED TO TARGET & DESTROY CELLS AS PART OF IMMUNE RESPONSE (E.G., HERCEPTIN & BREAST CANCER)
• INDIRECT THERAPY- DRUGS CAN BE ATTACHED TO (MA) (E.G., CYTOTOXIC DRUG)- ANTIBODY THEN USED TO DIRECT DRUG TOWARDS CELL DISPLAYING PARTICULAR ANTIGEN RATHER THAN TOWARDS OTHER CELLS
• DIAGNOSIS- PARTICULAR ANTIGENS TARGETED BY ANTIBODIES TO MEASURE LEVELS OF ANTIGEN IN BODY
• PREGNANCY TESTING- (MA) IN HOME PREGNANCY KITS SPECIFIC TO HORMONE HUMAN CHORIONIC GONADOTROPHIN

IMMUNITY

-HIV= PATHOGEN THAT CAN LEAD TO AIDS

-STRUCTURE

• LIPID ENVELOPE WITH EMBEDDED ATTACHMENT PROTEINS
• INSIDE PROTEIN CAPSID, GENETIC MATERIAL (RNA) & REVERSE TRANSCRIPTASE ENZYMES PRESENT- CATALYSES PRODUCTION OF DNA FROM RNA

-IN ORDER TO REPLICATE HIV BINDS TO PROTEIN CD4 (MOST FREQUENTLY FOUND ON T-HELPER CELLS)

-CAPSID FUSES WITH CELL MEMBRANE & RNA & REVERSE TRANSCRIPTASE ENTER CELL

-REVERSE TRANSCRIPTASE CONVERTS RNA TO DNA, WHICH THEN MOVES INTO NUCLEUS OF CELL (CELL NOWS HAS INSTRUCTION TO BEGIN PRODUCING VIRAL HIV COMPONENTS)

-ANTIBODIES INEFFECTIVE AGAISNT HIV & VIRUSES- MANY ANTIBODIES WORK BY PREVENTING BACTERIA FROM MAKING CELL WALLS (WITHOUT THIS BACTERAIL CELLS CAN'T CONTROL ENTRY & EXIT OF WATER & THEREFORE BIRST)- SINCE VIRUSES DON'T HAVE CELL WALL & ARE REPRODUCED WITHIN HOST CELL THEY ARE UNAFFECTED BY ANTIBODIES (INSTEAD HIV TREATED BY ANTIRETROVIAL DRUGS WHICH KEEP HIV LEVELS IN BLOODSTREAM VERY LOW, REDUING IMPACTS ON HOST'S IMMUNE SYSTEM)

IMMUNITY

-HIV STRUCTURE

IMMUNITY

-TO IDENTIFY HIV, USE ENZYME LINKED IMMUNOSORBENT ASSAY (ELISA)

-DETECTS PRESENCE & QUANTITY OF ANTIGEN FOUND ON HIV