Biology 6 Test 3 Study Guide
Chapter 13 – Viruses et al.
A. General characteristics
a. Definition
i. Acellular particle
ii. Uses host cell for reproduction
1. Replication and gene expression comes from host cell
2. Specificity
a. Viruses may be very specific for different hosts or have a broad
range of hosts.
b. Viruses may have cell specificity (e.g. HIV infects only certain
immune cells in humans)
b. Structure
i. Components (Fig. 13.2)
1. Nucleic acid – can be single or double stranded RNA or DNA
2. Capsid – protein coat. Made from capsomere subunits
3. Optional components
a. Some have envelopes – uses host membrane with virus proteins
(spikes) embedded. These spikes are used for attachment or can
be enzymes. (Fig. 13.3)
b. Complex components – bacteriophages have other structures for
injection of DNA (Fig. 13.5)
ii. Size – varied, but in nanometers. (Fig. 13.1)
iii. Shape – varied. Some helical, round, polyhedral, long.
c. Origin – probably coevolved with cellular organisms.
d. Classification – based on type of nucleic acid, components, hosts, and shape (Tab 13.2)
i. Nucleic acids: double/single stranded RNA, DNA
ii. Single stranded RNA
1. Sense (+): can be directly translated
2. Antisense (-): need to make the complement for translation
B. Cultivation
a. Non-animal viruses – phages grow on bacterial lawns (Fig. 13.6)
b. Animal viruses
i. Use whole animals – mice are widely used.
ii. Eggs – a fertilized (embryonated) egg can be injected (Fig. 13.7)
iii. Cell culture – easiest and most efficient. Use variety of cell lines. (Fig. 13.8).
Many cell types show a visible difference called a cytopathic effect (Fig. 13.9)
C. Life Cycles
a. General stages of virus life cycles
i. Attachment (adsorption) – virus attaches to host cell by specific binding
ii. Penetration – genome enters the cell
iii. Synthesis – replication and gene expression of viral components for next
generation
iv. Maturation – processing and assembly of viral components
v. Release – exit of newborn viruses from cell
b. Bacteriophages
i. Lytic – phage makes particles and kills host (Fig. 13.11)
1. Attachment – uses tail fibers to attach to cell.
2. Penetration – DNA is injected into cell
3. Synthesis – replication, transcription, and translation
4. Maturation – components assembled
5. Release – lyses the cell.
ii. Lysogenic – some bacteriophages can alternate between lytic and lysogenic
(latent) cycles (Fig. 13.12)
1. Integration – DNA is integrated into host DNA and can be carried on
indefinitely as a prophage.
2. Excision – under bacterial stress, virus may re-enter lytic cycle by first
excising the DNA and continuing with the synthesis stage.
c. Animal viruses
i. DNA viruses – stages similar to general life cycle. Uncoating is breakdown of
capsid after penetration. DNA needs to enter nucleus (Fig. 13.15)
ii. RNA viruses (Fig. 13.17)
1. ssRNA viruses – RNA has to be transcribed into complementary strand
for replication. Only the sense (+) strand can be translated into viral
proteins.
2. Retroviruses – ssRNA is reverse-transcribed into DNA, than made
doublestranded. dsDNA integrates into chromosome and directs
transcription as a prophage. Exits by budding (13.19)
D. Viruses and Cancer
a. Cancer is uncontrolled cell division and invasive growth. (13.8)
b. Integrative viruses can land next to a gene and cause it to over or underexpress.
i. Overexpressed genes that cause cancer are called oncogenes. The normal protooncogene is usually involved in activating cell division
ii. Underexpressed ones are tumor suppressors. These are normally inhibitors of
cell division.
c. Types of cancer causing viruses
i. DNA – e.g. HPV (human papilloma virus) gives cervical cancer
ii. Retroviruses – e.g. HTLV (human T cell leukemia virus) causes leukemia.
E. Virus-like Particles
a. Viroids – “naked RNA”
i. Found in plants and causes deformation, lesions, stunted growth. (Fig. 13.23)
ii. Circular ssRNA, 200-400 bp long.
iii. Replicates in nucleus using host machinery.
iv. Viroids bind plant mRNA preventing translation. May also bind up plant
proteins.
b. Prions – “proteins gone wild”
i. Causes “mad cow disease” and Creutzfeldt-Jakob (CJD). Neurological
degeneration (dementia, loss of motor control, wasting). Post mortem plaques
and lesions in brain found.
ii. Protein alone is infectious agent. PrPC is a normal cell-surface protein involved in
neuronal function. It can normally be destroyed when not needed by proteases.
iii. PrPSc is a rare conformational form of PrPC that is resistant to proteases. It also
converts normal PrPC into PrPSc. (Fig. 13.22)
iv. Buildup of PrPSc causes cell death and plaques forming in the brain.
Chapter 13 Problems: Review 1, 4, 5. MC 1, 4, 6-8. CT 2, 3. CA 1
Chapter 12 – Eukaryotes
A. Parasitology
a. Types of hosts
i. Intermediate host – harbors asexual (juvenile) stage
ii. Definitive host – harbors sexual (adult) stage
b. Some ways parasites can evade the immune system
i. Encystment – formation of an outer shell that is resistant to environment. Much
like a spore
ii. High mutation rate of surface antigens
iii. Antigen decoys – molecules released to elicit immune response. These are not
present on the parasite and are meant to distract immune system.
iv. Hide inside of cells
B. Protists
a. Algae – “plant-like”
i. General characteristics
1. Photosynthesis
2. Asexual and sexual
3. Must be in water
ii. E.g. Dinoflagellates
1. Have flagella and very hard cell wall plates. (Fig. 12.15)
2. Comprise plankton but can be dangerous in high numbers (red tide)
3. Many produce neurotoxins that concentrate in fish and shellfish.
b. Protozoa – “animal-like”
i. General characteristics
1. Chemoheterotrophs
2. Mostly asexual, some sexual
ii. Archaezoans
1. Have flagella
2. Most lack mitochondria and are digestive tract symbionts.
3. E.g. Giardia can infect the intestines and cause “backpacker’s diarrhea”
(Fig. 12.18b,c)
iii. Amoebas
1. Have amorphic shape and move by pseudopods.
2. E.g. Entamoeba causes amoebic dysentery. (Fig. 12.19)
iv. Apicomplexans
1. Immobile
2. Enzymes at apex of cell are used to digest host membranes for entry.
3. E.g. Plasmodium (causes malaria) life cycle (Fig. 12.20)
a. Mosquito injects sporozoites into human. Move to liver.
b. Sporozoites produce merozoites that reproduce in red blood
cells.
c. Merozoites produce gametocytes that get picked up by mosquito.
d. Male and female gametocytes fuse to form sporozoites in
mosquito.
v. Ciliates – have cilia. E.g. Paramecium (not a parasite) (Fig. 12.21)
c. Slime Molds – “fungal-like” and amoeboid
i. General characteristics
1. Chemoheterotrophic, absorbs food.
2. Asexual and sexual
3. Movements similar to amoeba
ii. Cellular slime mold (Fig. 12.22)
1. Amoeboids congregate upon release of cAMP signal.
2. Slug (pseudoplasmodium) is formed and fruiting body is produced.
3. Spores released (asexual)
iii. Plasmodial slime molds (Fig. 12.23)
1. Zygote will form a multinucleate mass called a plasmodium.
2. Cytoplasmic streaming allows for movement.
3. Sexual spores are released producing gametes.
C. Fungi
a. General features
i. Nutrition: aerobic chemoheterotrophs. Absorb food.
ii. Body is called mycelium composed of threadlike hyphae. Reproductive portion is
fruiting body. Yeasts are unicellular. (Fig. 12.2)
iii. Reproduce asexually and sexually.
1. Spore formation can be asexual or sexual.
2. Fertilization can occur in two steps: plasmogamy is when the cells fuse
without fusion of nuclei. Karyogamy is when nuclei fuse.
iv. Many cause opportunistic infections
b. Zygomycete (bread mold) life cycle (Fig. 12.7)
i. E.g. Rhizopus.
ii. Asexual: haploid hyphae produce sporangium that release haploid spores.
iii. Sexual: haploids of opposite mating type can fuse to form zygospore (diploid).
Zygospore undergoes meiosis and produces sexual spores.
c. Ascomycete (sac fungus) life cycle (Fig. 12.9))
i. E.g. Candida (causes “yeast infections”)
ii. Asexual: haploid hyphae produce conidia that release haploid spores.
iii. Sexual: mating produces an ascus that releases sexual ascospores.
d. Basidiomycete (club fungus) life cycle (Fig. 12.10)
i. E.g. Agaricus (button mushroom)
ii. Asexual: no spores produced, just vegetative growth.
iii. Sexual: mating produces fruiting body (mushroom) that contains basidiospores.
D. Animals
a. Flatworms (Platyhelminths)
i. Flukes (Trematodes) – life cycle (Fig. 12.26)
1. Mates in human (definitive). Eggs released.
2. Larvae attach to snails (intermediate).
3. Juveniles encyst in crayfish muscle (intermediate).
4. Adults mature in human
ii. Tapeworms (Cestodes) (Fig. 12.27, 12.28)
1. Structures: scolex is head. Proglottids are rest of segments (sexual and
produce eggs)
2. Life cycle:
a. Eggs released from intestine of definitive host
b. Intermediate host eats eggs, eggs hatch and encyst.
c. Definitive host eats cysts, the uncyst and scolex attaches to
intestine and forms proglottids.
b. Roundworms (Nematodes)
i. E.g. Ascaris life cycle (dimorphic – separate males and females)
1. Eggs eaten
2. Larvae hatch in small intestine and burrow into the bloodstream and
carried to lungs.
3. Juveniles develop in lung, get coughed up and swallowed.
4. Adults mature and mate in the small intestine.
ii. E.g. Trichonella life cycle
1. Encysted larvae eaten (raw pork)
2. Adults develop in small intestine, reproduce.
3. Eggs hatch and larvae enter bloodstream/lymph and spread throughout
body. Larvae encyst in muscles.
c. Arthropods – common vectors (Fig. 12.33)
i. Arachnids
1. Two body regions – cephalothorax and abdomen
2. Eight legs
3. E.g. spiders, ticks. Ticks can spread Rickettsia
ii. Insects
1. Three body regions – head, thorax, and abdomen
2. Six legs
3. E.g. Mosquitoes spread Plasmodium, Tsetse fly spreads Trypanosoma
iii. Crustaceans
1. Aquatic with shells
2. E.g. Crayfish, crabs, lobsters may carry encysted flukes.
Chapter 12 Problems: Review 4, 7, 8, 10. MC 5-10. CT 1, 3. CA 3
Chapter 7 and 20 – Antimicrobial Agents
A. Testing Antimicrobial Agents for Effectiveness
a. Testing Specific Agents
i. Disk Diffusion Method (Fig. 7.6)
1. Plate a lawn of bacteria
2. Soak paper disks with agent and look for zones of inhibition on plate
3. Can estimate minimum inhibitory concentration (MIC) of agent (Fig.
20.18).
ii. Dilution Method (Fig. 20.19)
1. Make dilutions of agent and find lowest concentration that kills culture.
2. More quantitative than disk method because of known concentrations in
each well. Can calculate MIC.
B. Nonspecific Agents
a. Physical Agents
i. Temperature and Drying
1. Heat
a. Dry heat can reach hotter temperatures and is necessary when
moisture cannot be used (sterilizing equipment that could rust)
b. Moist heat is more effective because it is more penetrating. The
autoclave is a moist heat sterilizer. Uses high pressure to help
increase temperature (Fig. 7.2)
c. Pasteurization – heat at a lower temperature to prevent proteins
from denaturing, but kills most microbes (e.g. milk)
2. Cold
a. Freezing, refrigeration
b. Freeze-drying – freeze quickly in dry ice/nitrogen under a
vacuum to remove water.
ii. Filtration – trap organisms on a filter (Fig. 7.4)
iii. Osmotic Pressure – high solute (e.g. salt) will plasmolyze most organisms.
iv. Radiation
1. Ionizing radiation – damages molecules by charging them and making
them highly reactive
2. UV light causes DNA mutations
3. Microwaves generate heat by vibrating molecules
v. Sonication – sounds vibrations disrupt organelles/membranes
b. Chemicals
i. Phenols – disrupt membranes and denature proteins. E.g. phenol, cresol
ii. Halogens and metals – act as oxidizing agents (addition of oxygen and sulfurcontaining groups) or replace existing chemical groups. E.g. iodine, nickel
iii. Detergents and alcohols – act as surfactants to dissolve membranes. E.g. soap,
ethanol.
iv. Acids/Bases – will break hydrogen bonds, covalent bonds, and ionize many
molecules. E.g. bleach, acetic acid.
v. Peroxygens – free radical oxidizing agents. E.g. hydrogen peroxide
vi. Alkylating agents – add methyl groups to molecules. E.g. ethylene oxide
C. Specific Agents
a. Mechanisms of action (Fig. 20.2)
i. Inhibition of cell wall synthesis
1. Enzymes that crosslink peptidoglycans are inhibited.
2. E.g. penicillin. Discovered by Alexander Fleming by accident in 1928
ii. Membrane disruption
1. Bind membrane of specific type of organism
2. E.g. polymyxins distort outermembrane of Gram negative bacteria
iii. Inhibition of protein synthesis
1. Bind to bacterial ribosomes. Bacterial ribosomes are smaller and have a
different shape than eukaryotes.
iv. Inhibition of nucleic acid synthesis
1. Transcription can be disrupted by targeting RNA polymerase
v. Antimetabolites
1. Mimic building blocks of macromolecules
2. E.g. Sulfa drugs resemble PABA, a precursor to folic acid. Acts as an
enzyme inhibitor. Discovered by Domagk and Fourneau in 1936
b. Side effects
i. Toxicity – sometimes, there may be an effect on our own molecules. E.g.
polymyxins can disrupt our own membranes. Kidney failure and respiratory
arrest are possible.
ii. Allergy – immune reaction to drug or breakdown products. E.g. penicillin
iii. Disruption of normal flora – our “good” bacteria can be killed off and this may
allow opportunistic infections. Products are available to replace normal flora.
c. Resistance
i. Acquired by mutation, transformation, transduction, conjugation
ii. Mechanisms
1. New enzymes. Penicillin can be broken down by -lactamase.
2. Membrane permeability is blocked. Import mechanisms are change that
makes the drug no longer transported across membrane.
3. Target is altered. E.g. ribosomes changed shape so that penicillin no
longer binds
4. Ejection of drug. New mechanism that exports the drug rapidly before it
can harm the cell.
iii. Selective pressures that cause resistance
1. Unnecessary prescriptions – about 50% of all antibiotic prescriptions are
unnecessary.
2. Cross-resistance – acquired resistance to one drug can also give
resistance to other related drugs.
3. Premature termination of treatment results in greater chance of having
surviving resistant organisms
Chapter 7 Problems: Review 1, 2, 7. MC 1, 2, 4, 7, 9. CT 1a. CA 1.
Chapter 20 Problems: Review 2, 4, 6, 8. MC 5, 7-10. CT 1, 4a, 4b, 6a. CT 3.
Chapter 14 – Pathology
A. Overview of terms
a. Pathology – study of disease
b. Etiology – cause of disease
c. Pathogenicity – how a pathogen overcomes host defenses to produce disease
d. Pathogenesis – development and progression of disease
e. Epidemiology – occurrence and spread of disease
B. Microbial - Host relationships
a. Normal Flora
i. Resident flora – permanent microbes in the body.
1. Most are commensals, some mutualistic.
2. Located on skin, mucous membranes of urinary and respiratory systems,
intestines (Fig. 14.1)
ii. Transient flora – temporary microbes
b. Symbiosis – relationship between two organisms (Fig. 14.2)
i. Mutualism – both benefit. E.g. E. coli break down food and release vitamin K.
Also may outcompete pathogens: microbial antagonism.
ii. Commensalism – one benefits, other unharmed. E.g. organisms that live on our
skin.
iii. Parasitism – one benefits, other is harmed. Diseases caused by these. Some are
opportunistic – causes disease in different environment. E.g. E. coli outside of
intestine can be harmful, or breakage in skin lets in Staph, or weakened immune
system lets in Pneumocytis.
C. Etiology - Koch’s Postulates
a. Postulates (Fig. 14.3)
i. Same pathogen must be present in every case of disease.
ii. Pathogen must be able to be isolated and cultured in pure media.
iii. Cultured pathogen must be able to cause disease again.
iv. Same pathogen must be able to be isolated from the organism given disease.
b. Exceptions
i. Pathogen may not be able to be cultured in pure media (e.g. viruses, Rickettsia).
ii. Diseases with multiple causes (e.g. nephritis, UTI)
iii. Pathogen causes multiple diseases/symptoms (e.g. Mycobacterium tuberculosis)
D. Pathogenesis
a. Types of infections
i. Duration and severity
1. Subclinical – no symptoms (e.g. Hepatitis A)
2. Acute – quick and severe (e.g. flu)
3. Chronic – slow but continuous (e.g. tuberculosis)
4. Latent – has an inactive phase (e.g. HIV)
ii. Placement
1. Local – confined to one area
2. Focal – localized to one area but toxins/pathogens can affect other areas
3. Systemic – affects entire body
iii. Sequence
1. Primary infection – the first infection of a healthy person
2. Secondary infection – the second pathogen. Usually opportunistic
b. Disease progression – general stages (Fig. 14.5)
i. Incubation – initial infection but no symptoms yet
ii. Prodromal – early/mild symptoms
iii. Illness – most acute symptoms, immune system overrun. Acme is the peak.
iv. Decline – begin recovery. Symptoms subside, immunity recovers
v. Convalescence – recovered. Body regains strength.
E. Epidemiology
a. Spread of infection
i. Occurrence
1. Incidence - # of people who got the disease during a period of time
2. Prevalence - # of people who have the disease at a given point in time
ii. Degree of spreading
1. Endemic – localized to a certain geographic region and considered
“normal”. Sometimes seasonal (e.g. chickenpox)
2. Epidemic – an outbreak at higher than normal rates (e.g. Diphtheria in
former USSR 1990s)
3. Pandemic – world wide. E.g. 1918 flu or current AIDS
iii. Reservoirs – sources of infection
1. Human – e.g. HIV
2. Animal – usually vectors such as arthropods
3. Non-living – soil and water are main ones
iv. Transmission (Fig. 14.6-8)
1. Contact
a. Direct – requires touching of individuals
b. Indirect - use nonliving intermediate called a fomite
c. Droplet – in a liquid droplet (e.g. sneezing)
2. Vehicle – uses medium (e.g. water, air, food)
3. Vector – uses a living organisms
a. Mechanical – passive transfer
b. Biological – transfer is necessary for lifecycle of pathogen
b. Nosocomial infections – spread through hospitals (Fig. 14.9)
i. Common microbes and infections (Tab. 14.4)
ii. Compromised host – wounds, lowered immunity
iii. Chain of transmission – hospital practices may spread disease
1. Multiple modes of transmission
2. Equipment and procedures contribute to transmission
iv. Prevention: wear gloves, masks. Wash hands. Proper disposal of fluids, needles,
etc.
c. Methods of investigation
i. Descriptive – describes occurrence of disease to trace back to origin. E.g. John
Snow (1850) solved cholera outbreak by mapping individuals and finding
common water source.
ii. Analytical – cause and effect relationship of disease. E.g. Florence Nightingale
found factors contributing to epidemic typhus (poor sanitation and food)
1. Handout on hot tub rash
iii. Experimental – potential causative agents are tested to see if they cause disease.
Not ethical in humans.
F. Public Health Organizations
a. Center for Disease Control and Prevention (CDC) – US organization
i. Charge
1. Provide safety guidelines
2. Recommendations on drugs and vaccines
3. Storing drugs and vaccines in cases of emergency
ii. Morbidity an Mortality Weekly Report (MMWR)
b. World Health Organization (WHO) – International
i. Similar charge as CDC but on a global scale. Have many direct activities as well
ii. Publishes Weekly Epidemiological Record.
Chapter 14 Problems: Review 2-4, 6-8, 10. MC 2, 4, 6, 7. CT 2, 4. CA 1-3.
Chapter 15 – Pathogenicity
A. Host Entry
a. Portals
i. Mucous membranes – on most inner linings (e.g. respiratory, gastrointestinal,
enitourinary, conjunctiva)
ii. Skin – outer lining.
iii. Parenteral – directly deposited on target tissue. Usually due to wounds, surgery,
animal bites.
b. Dosage
i. ID50 – pathogen dose necessary to infect half of population.
ii. LD50 – toxin dose necessary to kill half of population.
c. Adherence
i. Use pili, fimbriae, capsule, cell wall etc. for binding.
ii. May use adhesins to specifically bind receptors in tissue specific adherence. (Fig.
15.1)
iii. Biofilms – mass of pathogens in cooperative adherence. First organisms attached
secrete materials that assist others to help form the biolayer. E.g. dental plaques
on teeth.
B. Tissue Penetration – most pathogens must enter a cell to thrive.
a. Entry
i. Endocytosis – adherence can trigger endocytosis in host cell. Invasins may be
involved that help rearrange cytoskeleton to facilitate entry and intracellular
movements. (Fig. 15.2)
ii. Tissue degradation – enzymes secreted that dissolve barriers.
1. E.g. hyaluronidase – produced by strep breaks down hyaluronic acid, a
sugar that holds cells together. This is the cause of gangrene.
2. E.g. collagenase - produced by Clostridium breaks down protein collagen
which holds together connective tissue.
b. Evasion
i. Structures
1. Capsules – resists phagocytosis by white blood cells.
2. Cell wall – proteins and waxes in cell wall also resist phagocytosis.
ii. Enzymes
1. Induce clots – coagulases produced by staph allow clots to form and
shield the pathogen from host defenses.
2. Break down antibodies – certain proteases break down antibodies.
iii. Antigenic variation – surface proteins are changed to avoid immune detection.
Due to built-in variation and high mutation rate.
C. Tissue Damage
a. Use up resources – nutrients are taken from host. E.g. mechanism of siderophores that
scavenge iron.
b. Direct damage – physical destruction by movements, digestion.
c. Toxins (Fig. 15.4)
i. Exotoxins – secreted proteins
1. A-B toxins (Fig. 15.5)
a. B binds host cell receptor, A inhibits protein synthesis.
b. E.g. diphtheria toxin – nerve, heart, kidney cells.
2. Membrane-disrupting – may lyse cell by forming protein channels in
membrane, or direct interference of phospholipids bilayer.
3. Superantigens – provoke intense immune response.
ii. Endotoxins – lipopolysaccharides (LPS) of cell wall
1. In Gram- bacteria only. Released upon death of bacterium.
2. Effects
a. Stimulate macrophages to release cytokines. This may result in
fever, chills, shock etc. (Fig. 15.6)
b. Activates blood clotting.
Chapter 15 Problems: Review 2, 3, 5, 6, 8. MC 2, 3, 5, 6, 8, 10. CT 1-3. CA 3.
Chapter 16 – Innate Immunity (Non-specific Defenses)
A. Barriers - physical and chemical protection
a. Skin – protective layer + oil glands (Fig. 16.2)
b. Mucous membranes – acids, mucous, saliva, tears (Fig. 16.3, 4)
c. Competition with normal flora.
B. Cellular
a. Cell types (Tab. 16.1)
i. Granulocytes – have granules. Some release chemicals, others are phagocytic
ii. Agranulocytes – no granules. Some release chemicals, others are phagocytic,
lymphocytes are used in specific defense.
b. Phagocytosis
i. Steps: chemotaxis, adherence, ingestion, digestion, excretion (Fig. 16.7).
ii. Some will hold on to antigens to activate specific defenses.
C. Inflammatory Response
a. Caused by direct damage to tissue. Symptoms include swelling, redness, pain.
b. Mechanism (Fig. 16.8)
i. Damaged tissue releases chemicals that lead to vasodilation and leaky vessels.
E.g. histamine released by mast cells in connective tissue.
ii. White blood cells migrate to site of damage by squeezing through leaky walls by
diapedesis (includes margination and emigration). Some cells fight infection,
platelets help clot broken vessels.
iii. Abscess forms with pus from concentration of cells and debris.
iv. Repair – scab forms. Epidermis regenerates. Scar tissue replaces irreplaceable
cells.
c. Chronic inflammation
i. Continuous inflammation response due to persistent damaging agent.
ii. Granulomas can form – a pocket containing the walled-off agent. E.g. tubercles
in tuberculosis.
D. Fever – raised body temperature
a. Mechanism
i. Phagocyte stimulation releases IL-1 which stimulates hypothalamus to raise
thermostat set point. Other cytokines (e.g. TNFs) may also stimulate
hypothalamus. (Fig. 15.6)
ii. Temperature raised by blood vessel constriction, increase metabolism, shivering.
b. Purposes – slow pathogen growth, stimulate macrophages, speed tissue repair.
c. Complications – heart dysfunction, metabolic side effects (dehydration, acidosis,
electrolyte imbalance)
E. Complement System
a. Components – made of proteins that activate and work with one another. Activation
through cascades.
b. Pathways of action (Fig. 16.9)
i. Opsonization – enhancement of phagocytosis by coating bacteria.
ii. Inflammation – stimulates mast cell release of histamine and a chemoattractant
for macrophages. (Fig. 16.11)
iii. Cytolysis – membrane attack complex (MAC) forms and creates pores in
membrane of pathogen. (Fig. 16.10)
c. Pathways for activation – these allow for multiple ways to initiate cascade.
i. Classical – uses antibodies to recognize antigens (Fig. 16.12)
ii. Alternative – uses protein factors to recognize lipocarbohydrates. (Fig. 16.13)
iii. Lectin – uses lectin to recognize carbohydrates. (Fig. 16.14)
F. Interferon
a. Small proteins that induce transcription.
b.
-IFN and -IFN produced by infected cells as a distress signal. (Fig. 16.15)
i. Txn and tln of IFN triggered by infection.
ii. IFN is released and sensed by uninfected cells. Usually by cell signaling
(receptor, signal transduction, response)
iii. Uninfected cell produces antiviral proteins (AVP) which inhibit viral replication.
c. -IFN produced by lymphocytes. Stimulates neutrophils and macrophages.
Chapter 16 Problems: Review 2-4, 8. MC 2, 3, 10. CT 2, 4. CA 3, 5.