1
BIOL132A EXAM STUDY GUIDE WITH
COMPLETE SOLUTIONS
Why is innate immunity important?
o It is our body’s first defense and barrier to pathogen/infection. Adaptive
immunity doesn’t kick in right away, so we need innate immunity to keep us
safe.
How does innate immunity know a microbe is present?
o PAMPs through PRR… through the complement pathway… chemokines
/ cytokines.
What innate immunity mechanisms contribute to pathogen clearance, how do they work?
o Skin, secretions = antimicrobial agents (lysozyme, lacteroferrin, lactoperoxidase)
o Antimicrobial peptides (cationic- disrupts bacterial plasma membranes)
o Microbiota secrete bacteriocins (L-antibiotics)
o Complement pathway (adaptive/lectin) lysis via MAC
o Neutralization/opsonization
o NK cells
o Type I IFN blocks viral replication
Which innate mechanisms clear bacteria; which are important for viruses?
o Bacteria
▪ Bacteriocins
▪ Complement
▪ Neutralization
▪ Secretions
o Viruses
▪ NK cells
▪ Type I IFN
How does innate immunity contribute to adaptive immunity?
o It primes the adaptive immunity. Innate produces IFN which blocks
viral replication but also increases number of MHC class I.
o Macrophages need helper T cells to kill some pathogens that are intracellular.
ADAPTIVE
Which types of adaptive immunity clear extracellular vs intracellular microbes?
mechanism details?
o Extracellular
, 2
▪ Produce antibodies NK cells (ADCC)
▪ B cells produce antibodies
o Intracellular
▪ Classical complement pathway (IgM) phagocytosis
▪ Humoral/Cell mediated immunity
T cell kill cell / help macrophage kill cell
What are similarities, differences between VDJ recombination and class
switch recombination?
o VDJ recombination makes changes in the variable region; while CSR
makes changes in the constant region.
o VDJ has loss of genes inbetween; while CSR uses the loop splicing technique.
o CSR requires AID gene (activation induced cytidine deaminase which
convers dC to dU in DNA)
o In CSR the rearranged variable region moves by DNA recombination next to
the constant region gene.
Why is class switch recombination important from the perspective of host response
to pathogen?
o This allows the host to create different classes of antibodies that are
responsible for different immune responses.
▪ IgM – complement
▪ IgG – oposonization/neutralization (passes to placenta)
▪ IgA – mucosal surfaces
EPIDEMIOLOGY
Why are vectors and/or reservoirs important in disease transmission, and why are
they issues for microbial eradication?
o Reservoirs are the havens for disease and some diseases become more virulent
(biologic transmission) inside of a vector. It’s a problem for microbial
eradication because it’s hard to track a disease inside of a vector (arthropod for
example), and it’s hard to destroy a reservoir.
Are certain types of microbe transmission more ‘significant’ than others re: easy
transmission?
o Airborne is probably easiest.
o Direct contact less virulent than vector borne. The better a pathogen can live
outside a host, the more virulent it is.
Which transmission modes are more important for enteric diseases, respiratory diseases?
o Respiratory diseases would probably be airborne.
o Enteric diseases would probably be vehicle (oral/fecal)
PATHOGENESIS
How do toxigenic bacteria contribute to pathogenesis?
o They secrete toxins which are virulence factors.
o They can be exotoxins or endotoxins.
How do pathogenicity islands contribute to spread of antibiotic resistance or toxin
acquisition?
o Through HGT, large chunks of DNA can be inserted and this can either code
for antibiotic resistance or contain the operon for a toxin gene.
How does quorum sensing/two-component regulatory systems contribute to
pathogenesis?
, 3
o Quorum sensing is the cell-cell communication that involves the autoinducers
which regulate gene expression, and can activate virulence genes.
o The two-component regulatory system works as a signal transduction
pathway that results in the activation of transcription factors which will
ultimately and potentially lead to the synthesis of virulence genes.
IMMUNE EVASION
How do bacteria, viruses evade innate/adaptive immunity?
o Bacteria can undergo mutations, phase variation, and genetic variation/DNA
recombination. They can put proteins on their surfaces to evade or inhibit
phagocytosis. They can secrete chemicals that allow them to withstand the
environment within a phagolysosome, or they can escape from the phagosome
before fusion with the lysosome. They can alter LIPID A so that TLR4 doesn’t
recognize it, they can evade Nod1/Nod2 by acting on peptidoglycan synthesis.
They can produce outer membrane protease that resists antimicrobial peptides
(defensins). They can interfere with TLR signaling. Produce non-antigenic
capsules, produce IgA proteases, produce proteins that interfere with antibody-
mediated opsonization. They canThey can secrete products that are
mimic/decoy antigens.
o Viruses can undergo mutations and have genetic variation via recombination.
They can directly destroy the immune system (HIV). They can secrete proteins
that mimic function of host membrane receptors (decoys/mimics – interfere with
host cell receptors – ex: proteins that bind IFN, complement). Secrete products
that interfere with, inhibit, inactivate host pathways. Infect tissues with few MHC
molecules. Production of agents that immunosuppress T cells, macrophages.
Hige (syncytia). Inhibit TLR signaling. ncRNAs and miRNAs (HCMV ncRNA
block apoptosis, and miRNA blocks expression of MICB stress antigens-
prevents NK recognition leading to lysis).
Why is antigenic variation so important?
o It allows a pathogen to get in, replicate, spread, get out. It makes it much
harder for the host’s immune system to eradicate the bug.
What is phase variation, why is it important, what are the mechanisms (examples) [a
gimme: know this]
o Phase variation is a change in expression (on/off); heritable, reversible switch
that often alters expression state of a surface structure (capsule, pili, flagellin).
▪ Inversion: Flagellin protein (H1/H2)
▪ Slipped strand mispairing: opa gene (repeat extension on new strand,
repeat contraction on template strand); LOS variety (N.
meningitidis).
▪ pilE gene- P+/Ps. Nick at P+=hydrophobic + pilus, nick at Ps =
non- hydrophobic + no pilus assembly.
VACCINATION
Why is vaccination of the population important?
o It can create herd immunity
What things need to be considered in making an effective vaccine?
o Safety. Risk/benefit. Cost. Effectiveness. Duration. Ease of delivery. Stability.
Is a killed vaccine better, more effective?
o There isn’t one good way. It has its benefits. If it’s killed, it won’t ever
replicate, but there is a weaker immune response, need multiple doses, it’s
expensive.
Is there a relationship between an effective vaccine and microbial antigenic variation?
, 4
o If bacteria or a virus have antigenic variation capabilities, then it might be hard
to create an effective vaccine. For example, influenza needs a new vaccine
every year.
- What I think we should know:
o Staph. Epidermidis
o Staph. Aureus
o Infective dose:
▪ 10-100 Shigella needed for dysentery
▪ >104 Salmonella are needed for diarrhea
o Growth rate
▪ Fast- E.coli + S. aureus (20,30 min)
▪ Slower- M. Tb (18 hrs)
▪ Slower- Treponema pallidum (33 hrs)
▪ VIRUSES ( fast polio (6hrs) vs slow herpes (36 hrs) )
Lecture 7: innate immunity
Human pathogens:
Extra cellular bacteria, parasites: fungi = Strept. pneumoniae = pneumonia; Trypanosoma brucei
= sleeping sickness; Pneumocystis carinii = pneumonia
Intracellular bacteria, parasites: Mycobacterium tuberculosis = Tb; Leishmania donovani –
Leishmaniasis; Plasmodium falciparum = malaria
Intracellular viruses: Influenza = flu; Varicella = chicken pox
Extracellular parasitic worms: Schistosomes = Schistosomiasis
Levels of body defense:
1st (innate): Skin = outer surface of dead cells that shed; slightly acidic, salty; barrier to infection;
mucosal surfaces = viscous layer of glycoprotein secreted by goblet cells; urogenital, GI tracts
(conjunctiva); epithelial lining barrier; moist sticky surfaces; small intestine sheds/replaces
mucosal lining; Movement = ciliary (respiratory tract lined with ciliated epithelial cells, sweeps
particles toward throat [coughed up, plus mucus]; Peristalsis (small intestine contraction [plus
mucus])
2nd (innate): nonspecific response = block entry of pathogens, block the spread of infection; NK
cells and phagocytic WBC (macrophages, neutrophils; dendritic cells); inflammation; fever; anti-
microbial substances; molecules (type I interferons [IFN , ]; cytokines [TNF , IFN , IL-12];
chemokines [IL-8]; complement)
3rd (adaptive): specific responses = antibody-mediated response, cell-mediated response
Innate immunity: 1st line of defense = clear or contain; components (cells, molecules) = pre-
existing (may be in inactive state), do not need to be induced, already present (do not need
to differentiate, immediate availability, activates adaptive immunity)
Secretions:
mucus (mucosal surfaces); digestive enzymes in stomach, small intestine (HCl, pH 2-3)
urine (low pH); vaginal secretions (low pH; Lactobacilli produce lactic acid)
Anti-microbial agents = Lysozyme (saliva, tears, sweat; mucosal secretions; hydrolyzes , 1-4
linkage of NAM-NAG); Lactoferrin (released by macrophages, neutrophils into mucosal
BIOL132A EXAM STUDY GUIDE WITH
COMPLETE SOLUTIONS
Why is innate immunity important?
o It is our body’s first defense and barrier to pathogen/infection. Adaptive
immunity doesn’t kick in right away, so we need innate immunity to keep us
safe.
How does innate immunity know a microbe is present?
o PAMPs through PRR… through the complement pathway… chemokines
/ cytokines.
What innate immunity mechanisms contribute to pathogen clearance, how do they work?
o Skin, secretions = antimicrobial agents (lysozyme, lacteroferrin, lactoperoxidase)
o Antimicrobial peptides (cationic- disrupts bacterial plasma membranes)
o Microbiota secrete bacteriocins (L-antibiotics)
o Complement pathway (adaptive/lectin) lysis via MAC
o Neutralization/opsonization
o NK cells
o Type I IFN blocks viral replication
Which innate mechanisms clear bacteria; which are important for viruses?
o Bacteria
▪ Bacteriocins
▪ Complement
▪ Neutralization
▪ Secretions
o Viruses
▪ NK cells
▪ Type I IFN
How does innate immunity contribute to adaptive immunity?
o It primes the adaptive immunity. Innate produces IFN which blocks
viral replication but also increases number of MHC class I.
o Macrophages need helper T cells to kill some pathogens that are intracellular.
ADAPTIVE
Which types of adaptive immunity clear extracellular vs intracellular microbes?
mechanism details?
o Extracellular
, 2
▪ Produce antibodies NK cells (ADCC)
▪ B cells produce antibodies
o Intracellular
▪ Classical complement pathway (IgM) phagocytosis
▪ Humoral/Cell mediated immunity
T cell kill cell / help macrophage kill cell
What are similarities, differences between VDJ recombination and class
switch recombination?
o VDJ recombination makes changes in the variable region; while CSR
makes changes in the constant region.
o VDJ has loss of genes inbetween; while CSR uses the loop splicing technique.
o CSR requires AID gene (activation induced cytidine deaminase which
convers dC to dU in DNA)
o In CSR the rearranged variable region moves by DNA recombination next to
the constant region gene.
Why is class switch recombination important from the perspective of host response
to pathogen?
o This allows the host to create different classes of antibodies that are
responsible for different immune responses.
▪ IgM – complement
▪ IgG – oposonization/neutralization (passes to placenta)
▪ IgA – mucosal surfaces
EPIDEMIOLOGY
Why are vectors and/or reservoirs important in disease transmission, and why are
they issues for microbial eradication?
o Reservoirs are the havens for disease and some diseases become more virulent
(biologic transmission) inside of a vector. It’s a problem for microbial
eradication because it’s hard to track a disease inside of a vector (arthropod for
example), and it’s hard to destroy a reservoir.
Are certain types of microbe transmission more ‘significant’ than others re: easy
transmission?
o Airborne is probably easiest.
o Direct contact less virulent than vector borne. The better a pathogen can live
outside a host, the more virulent it is.
Which transmission modes are more important for enteric diseases, respiratory diseases?
o Respiratory diseases would probably be airborne.
o Enteric diseases would probably be vehicle (oral/fecal)
PATHOGENESIS
How do toxigenic bacteria contribute to pathogenesis?
o They secrete toxins which are virulence factors.
o They can be exotoxins or endotoxins.
How do pathogenicity islands contribute to spread of antibiotic resistance or toxin
acquisition?
o Through HGT, large chunks of DNA can be inserted and this can either code
for antibiotic resistance or contain the operon for a toxin gene.
How does quorum sensing/two-component regulatory systems contribute to
pathogenesis?
, 3
o Quorum sensing is the cell-cell communication that involves the autoinducers
which regulate gene expression, and can activate virulence genes.
o The two-component regulatory system works as a signal transduction
pathway that results in the activation of transcription factors which will
ultimately and potentially lead to the synthesis of virulence genes.
IMMUNE EVASION
How do bacteria, viruses evade innate/adaptive immunity?
o Bacteria can undergo mutations, phase variation, and genetic variation/DNA
recombination. They can put proteins on their surfaces to evade or inhibit
phagocytosis. They can secrete chemicals that allow them to withstand the
environment within a phagolysosome, or they can escape from the phagosome
before fusion with the lysosome. They can alter LIPID A so that TLR4 doesn’t
recognize it, they can evade Nod1/Nod2 by acting on peptidoglycan synthesis.
They can produce outer membrane protease that resists antimicrobial peptides
(defensins). They can interfere with TLR signaling. Produce non-antigenic
capsules, produce IgA proteases, produce proteins that interfere with antibody-
mediated opsonization. They canThey can secrete products that are
mimic/decoy antigens.
o Viruses can undergo mutations and have genetic variation via recombination.
They can directly destroy the immune system (HIV). They can secrete proteins
that mimic function of host membrane receptors (decoys/mimics – interfere with
host cell receptors – ex: proteins that bind IFN, complement). Secrete products
that interfere with, inhibit, inactivate host pathways. Infect tissues with few MHC
molecules. Production of agents that immunosuppress T cells, macrophages.
Hige (syncytia). Inhibit TLR signaling. ncRNAs and miRNAs (HCMV ncRNA
block apoptosis, and miRNA blocks expression of MICB stress antigens-
prevents NK recognition leading to lysis).
Why is antigenic variation so important?
o It allows a pathogen to get in, replicate, spread, get out. It makes it much
harder for the host’s immune system to eradicate the bug.
What is phase variation, why is it important, what are the mechanisms (examples) [a
gimme: know this]
o Phase variation is a change in expression (on/off); heritable, reversible switch
that often alters expression state of a surface structure (capsule, pili, flagellin).
▪ Inversion: Flagellin protein (H1/H2)
▪ Slipped strand mispairing: opa gene (repeat extension on new strand,
repeat contraction on template strand); LOS variety (N.
meningitidis).
▪ pilE gene- P+/Ps. Nick at P+=hydrophobic + pilus, nick at Ps =
non- hydrophobic + no pilus assembly.
VACCINATION
Why is vaccination of the population important?
o It can create herd immunity
What things need to be considered in making an effective vaccine?
o Safety. Risk/benefit. Cost. Effectiveness. Duration. Ease of delivery. Stability.
Is a killed vaccine better, more effective?
o There isn’t one good way. It has its benefits. If it’s killed, it won’t ever
replicate, but there is a weaker immune response, need multiple doses, it’s
expensive.
Is there a relationship between an effective vaccine and microbial antigenic variation?
, 4
o If bacteria or a virus have antigenic variation capabilities, then it might be hard
to create an effective vaccine. For example, influenza needs a new vaccine
every year.
- What I think we should know:
o Staph. Epidermidis
o Staph. Aureus
o Infective dose:
▪ 10-100 Shigella needed for dysentery
▪ >104 Salmonella are needed for diarrhea
o Growth rate
▪ Fast- E.coli + S. aureus (20,30 min)
▪ Slower- M. Tb (18 hrs)
▪ Slower- Treponema pallidum (33 hrs)
▪ VIRUSES ( fast polio (6hrs) vs slow herpes (36 hrs) )
Lecture 7: innate immunity
Human pathogens:
Extra cellular bacteria, parasites: fungi = Strept. pneumoniae = pneumonia; Trypanosoma brucei
= sleeping sickness; Pneumocystis carinii = pneumonia
Intracellular bacteria, parasites: Mycobacterium tuberculosis = Tb; Leishmania donovani –
Leishmaniasis; Plasmodium falciparum = malaria
Intracellular viruses: Influenza = flu; Varicella = chicken pox
Extracellular parasitic worms: Schistosomes = Schistosomiasis
Levels of body defense:
1st (innate): Skin = outer surface of dead cells that shed; slightly acidic, salty; barrier to infection;
mucosal surfaces = viscous layer of glycoprotein secreted by goblet cells; urogenital, GI tracts
(conjunctiva); epithelial lining barrier; moist sticky surfaces; small intestine sheds/replaces
mucosal lining; Movement = ciliary (respiratory tract lined with ciliated epithelial cells, sweeps
particles toward throat [coughed up, plus mucus]; Peristalsis (small intestine contraction [plus
mucus])
2nd (innate): nonspecific response = block entry of pathogens, block the spread of infection; NK
cells and phagocytic WBC (macrophages, neutrophils; dendritic cells); inflammation; fever; anti-
microbial substances; molecules (type I interferons [IFN , ]; cytokines [TNF , IFN , IL-12];
chemokines [IL-8]; complement)
3rd (adaptive): specific responses = antibody-mediated response, cell-mediated response
Innate immunity: 1st line of defense = clear or contain; components (cells, molecules) = pre-
existing (may be in inactive state), do not need to be induced, already present (do not need
to differentiate, immediate availability, activates adaptive immunity)
Secretions:
mucus (mucosal surfaces); digestive enzymes in stomach, small intestine (HCl, pH 2-3)
urine (low pH); vaginal secretions (low pH; Lactobacilli produce lactic acid)
Anti-microbial agents = Lysozyme (saliva, tears, sweat; mucosal secretions; hydrolyzes , 1-4
linkage of NAM-NAG); Lactoferrin (released by macrophages, neutrophils into mucosal
