Exam 3 Flashcards
(115 cards)
1
Q
- What does it mean that viruses areobligate intracellular parasites.?
A
—They need host cells in order to reproduce, and take over cell functions in order to multiply at the cost of the host (ribosomes, amino acids, ATP, enzymes, etc.)
2
Q
- There is debate whether viruses are alive. Most in the scientific community claim they are not. Give 5 characteristics of life that viruses lack.
A
—They are acellular, can’t carry out metabolic function outside host, can’t reproduce without host, has no cytoplasmic membrane, cytosol or organelles.
3
Q
- Relative to other types of life, how small are viruses? Compare it specifically to a bacteria.
A
—cannot be seen by light microscope, much smaller than bacteria
—smallest have diameter of 10nm, largest 400nm
4
Q
- Differentiate the extracellular state and intracellular state of a virus.
A
—extracellular: called virion, protein coat surrounding nucleic acids, RNA or DNA, some have phospholipid envelope, outermost layer provides protection, recognition
—intracellular: no capsid, virus exists as nucleic acid
5
Q
- Describe the following characteristics of a virus (be detailed!):
viral genome, capsids, envelope
A
a. The viral genome: DNA, RNA, dbl stranded or single (dsDNA, ssDNA, dsRNA, ssRNA)
b. Capsids: protein coat, has function of protection for viral nucleic acid (uses endonucleases to destroy foreign RNA/DNA), composed of capsomeres (protein subunits) which is coded for by viral genome.
c. Envelope: cell membrane surrounding capsid (with envelope=virion, without=naked virion), acquired from host cell during replication or release, made of phospholipid bilayer and proteins (glycoproteins, coded by spikes)
6
Q
- What is meant by the host range of a virus? What determines the hostrange of a virus? What is meant by spillover?
A
glycoproteins for complementary proteins or glycoproteins on the host cell surface.
—spillover: virus jumping hosts and expanding host range(ex: avian flu now infects humans)
7
Q
- Describe the 3 basic shapes of a virus?
A
—helical: capside made of capsomeres that bond in spiral way and form tube around nucleic acid (ebola)
—polyhedral: many sided (poliovirus)
—complex viruses: have capsids of different shapes (bacteriophage: virus that infects bacteria)
8
Q
- What characteristics are used to classify viruses?
A
—type of nucleic acid, presence or no envelope, shape, size
9
Q
- How are viral families and genera named? What is a viral species? How are species named? How are subspecies designated? Give an example.
A
—names end in -viridae
—genus names end in -virus
—viral species are a group of viruses that share same genetic info and niche
—sub-species named by number (HHV-1, HHV-2 etc)
10
Q
- Why can viruses NOT reproduce themselves?
A
—they don’t have replication genes for all enzymes needed and don’t have functional ribosomes for protein synthesis
—Instead, they are completely dependent on hosts’ organelles and enzymes to produce new virions
—Once the host cell is infected by a virus, it is forced to replicate viral genetic material and translate viral proteins (mainly capsomeres and viral enzymes)
11
Q
- What is the difference between the outcome of the lytic cycle and lysogenic cycle of bacteriophage replication?
A
— Lytic cycle: results in death and lysis of host cell
—lysogenic cycle: host remains alive, called latency in animal cells
12
Q
- Describe each of the steps of the lytic cycle of a T-even (e.g., T4) bacteriophage. Remember to be detailed in your description of each stage.
A
—1) attachment: virion attaches to host cell at attachment site
—2) penetration: viral enzymes released from capsid and break open cell wall to inject DNA into host cell
—3) synthesis: viral enzymes degrade the host DNA and produce viral components using host’s ribosomes and enzymes. Eclipse period occurs.
—4) assembly/maturation: complete virions form viral components spontaneously, capsomeres form around viral nucleic acid.
—5) release: phage lysozyme breaks host cell wall and releases virions. Infect other cells.
13
Q
- Describe what happens during andeclipse period. When does the eclipse period occur?
A
—period of time where only biosynthesis of parts is occuring; no complete phages have assembled yet.
14
Q
- Describe what happens during the lysogenic cycle of the bacteriophage λ. Make sure you point out specific differences in the replication cycle (additional steps, different outcome, etc.) Again, be detailed!
A
—lysogenic cycle: modified replication cycle.
—STEPS:
o 1.Attachment: same as lytic
o 2.Entry: same as lytic, but host cell’s DNA is not degraded
o 3.Integration: Viral genome is integrated into host dell genome (prophage)
• Virus is “latent” (inactive)
• Genes for biosynthesis are repressed/not transcribed
o 4..Host cell replication
• As host cell chromosome replicated, prophage DNA replicated too (since “part” of chromosome”
• all daughter cells are infected with virus; remains latent
o 5..Induction: Return to lytic cycle
• Prophage “excises” from chromosome/ genes “turned on”
o 6. Biosynthesis/ 7. Assembly / 8. Release
15
Q
- What is a prophage? How does this relate to lysogeny?
A
—physical part of bacterial chromosome once inserted into DNA
16
Q
- Describe 3 results of lysogeny on the host cell.
A
—lysogenic cells are immune to being infected again by same viral species
—phage conversion: phage carries genes that confer host cell new properties like producing toxins
17
Q
- Although the basic steps are the same, why are there differences between animal viral replication and bacteriophage replication?
A
—same basic pathway as bacteriophages, but:
o Presence of envelope around some viruses
o Eukaryotic nature of animal cells
o Lack of cell wall in animal cells
18
Q
- Briefly describe (do not list!) the stages of the multiplication of animal viruses (we’ll get in to the details of specific stages below).
A
—Stage 1: attachment: animal viruses attach by glycoprotein spikes or other molecules on capsid envelopes
—Stage 2: penetration: direct, fusion and endocytosis
o Direct penetration: viral capsid attaches and sinks into membrane, creating a pore thru which the genome alone enters the cell
• Naked viruses
o Fusion: viral envelope fuses with plasma membrane, and entire capsid and nucleic acid enter
• Some enveloped viruses, including HIV
o Endocytosis: virus attaches to membrane; membrane infolds, and virus enters thru vesicle
—Stage 3: uncoating: capside removed to release viral DNA
—Stage 4: synthesis: enzymes and proteins synth in cytoplasm
• If DNA virus, enters the nucleus to replicate
• If RNA virus, replicates in the cytoplasm
—Stage 5/6: assembly and release: most DNA viruses assemble in nucleus, RNA in cytoplasm. Portion of membrane is used to make envelope. Naked viruses released by exocytosis or lysis (kills host)
19
Q
- What are 3 different ways that animal viruses penetrate a host cell? What type of viruses use each of the ways.
A
o Direct penetration: viral capsid attaches and sinks into membrane, creating a pore thru which the genome alone enters the cell (Naked viruses)
o Fusion: viral envelope fuses with plasma membrane, and entire capsid and nucleic acid enter, Some enveloped viruses, including HIV
o Endocytosis: virus attaches to membrane; membrane infolds, and virus enters thru vesicle (enveloped viruses)
20
Q
- How are enveloped viruses released from a host cell? Naked viruses? Describe each of the processes.
A
— Portion of membrane is used to make envelope. Naked viruses released by exocytosis which is like budding but does not gain envelope, or lysis which is rupturing cell membrane (kills host).
21
Q
- What are proviruses? Describe the 2 ways that latent viruses can exist within a cell.
A
—proviruses are latent viruses, which can remain dormant for years.
—most become incorporated into host chromosome, occurs with DNA viruses or retroviruses
—some not incorporated into chromosome, induction never occurs
22
Q
- What is THE major difference regarding how (or where…) RNA and DNA viruses are assembled? Where are the nucleic acids replicated? How about the proteins? How about complete virions?
A
—RNA viruses assemble in cytoplasm, DNA in nucleus.
—Enzymes and capsid proteins migrate into the nucleus after being synthesized in the cytoplasm.
23
Q
- Briefly describe the replication cycles of the following types of viruses. You do not have to go thru all of the steps, but give the basics of the replication strategy and describe unique features (such as enzymes), and give examples of viruses for each:
A
a. dsDNA virus
—dsDNA virion synthesis is similar to the normal replication and transcription/translation of cellular DNA, where each strand of viral DNA is used as a template for its complement.
—The viral genomes enter the nucleus where replication of DNA and transcription of mRNA occur. mRNA leaves nucleus to get translated by host’s ribosomes, mainly into capsomeres and any essential enzymes
—Proteins migrate back into into the nucleus, where assembly occurs
—ex: Adenoviridae, Poxviridae
b. ssDNA virus
—Cells do not use single-stranded DNA, Replication varies in its details, Parvoviruses
—Single stranded folds back onto itself to form dsDNA, this dsDNA is replicated by cellular DNA polymerase
—Transcription/translation occurs to form proteins and the folded dsDNA unfolds into ssDNA and is packaged into virons and released
c. +ssRNA virus
—Sense strand (+) serves as viral nucleic acid, Sense strand RNA (or positive-strand RNA) acts as mRNA and can be directly translated into proteins to make capsomeres and enzymes (enzyme RNA-dependent RNA polymerase, which produces the antisense RNA strand (negative-strand RNA) from the sense strand)
—The antisense strand is then used to synthesize copies of the sense strand
d. –ssRNA virus
—Sometimes, the genome is the antisense (-) strand—In their capsid, the virus carries a copy of the enzyme RNA-dependent RNA polymerase which is used to transcribe a sense (+) strand.
—The sense (+) strand then serves as mRNA, and is translated into capsid proteins and enzymes which transcribes more antisense (–) strands—Which is nucleic acid packaged into capsid to form new virions
e. Retroviruses (in particular HIV)
—Retroviruses such as HIV are +ssRNA viruses that carry reverse transcriptase to transcribe DNA from their RNA. This reverse process (DNA transcribed from RNA) is reflected in the name retrovirus (ex: HIV carries 2 complementary strands of ssRNA; reverse transcriptase produce DNA from the RNA strands, and they come together to form dsDNA)
—This DNA serves a couple of purposes: used as template for mRNA (for translation into proteins) and more +ssRNA, and becomes a provirus (incorporates into host cell DNA)
f. dsRNA virus
—One strand of the RNA molecule is the sense (+) strand and functions in translation and in the synthesis of the antisense strand which encodes for viral RNA polyermase which is used to produce antisense RNA. other strand is the antisense strand, which functions as a template for the synthesis of the sense strand—uses the RNA polymerase translated from the sense strand to do this
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Q
- What is the difference between the sense and antisense strand of RNA. What are each used for?
A
—One strand of the RNA molecule is the sense (+) strand and functions in translation and in the synthesis of the antisense strand which encodes for viral RNA polyermase which is used to produce antisense RNA. other strand is the antisense strand, which functions as a template for the synthesis of the sense strand—uses the RNA polymerase translated from the sense strand to do this
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25. What is neoplasia, tumor, benign, malignant, and metastasis?
—Neoplasia: uncontrolled cellular reproduction in multicellular animal
—tumor: mass of neoplastic cells
—malignant: tumors that are cancerous
—metastasis: spreading of malignant cells
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26. What are protooncogenes and oncogenes?
—proto-oncogenes: genes that promote cell division, if repressed, no cancer
—oncogenes: a turned-on proto-oncogene
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27. What percentage of cancers do viruses cause? What role do viruses play in cancer (there are 3)? Give examples of cancers caused by viruses.
—20-25%
—some viruses carry copies of oncogenes that are inserted into the host cell
—interferes with tumor repression
—Specific viruses are known to cause ~15% of human cancers (Burkitt’s lymphoma (throat cancer), Hodgkin’s disease, Kaposi’s sarcoma, Cervical cancer (HPV))
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28. Discuss the 3 ways that viruses are cultured in a lab.
—cultured in media that has mature organisms (bacteria, phages, plants, animals), embronated eggs, cell tissue culture (diploid cell culture or continuous cell culture)
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29. What are viroids? How do they cause disease? What type of organisms do they infect?
—like RNA viruses, but lack capsid
— Viroid RNA adheres to complementary plant RNA, plant enzyme degrades the dsRNA which results in a disease state
—Because of our sophisticated immune system, some say that viroids could not infect humans so RNA is readily destroyed
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30. What are prions? Describe, in detail, how they cause encephalopathy? Give some examples of prion disease.
—proteinaceous infectious agents, have cellular PrP protein—Brain cells made by all mammals (Normal structure with -helices called cellular PrP)
—Prion diseases can be inherited, sporadic, or infectious
—Prion PrP changes shape of cellular PrP so it becomes prion PrP (called templating), which results in neuronal death, leaving holes and a spongy appearance in the brain (spongiform encephalopathy)
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1. Describe the 4 types of symbiotic relationships we have with microbes. Give a microbial example of each.
Mutualism is when both organisms benefit, commensalism is when one organism benefits, the other is unaffected, amensalism is when one organism is harmed while the second is neither harmed nor benefited and parasitism is when one organism (the parasite) benefits at the expense of the other (the host).
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2. Define the following terms: pathogen, disease, infectious disease
a. Pathogen—microbe that causes disease
b. Disease—when the body does not function normal from a cause
c. Infectious disease—disease from a pathogen
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3. What is meant by normal microbiota? What are other names for it? What is the difference between resident and transient microbiota?
Normal microbiota is the normal flora that the body has. Transient is when the microbes remain in the body for only a few hours, days, or months before disappearing, whereas resident is when microbes are in the body naturally and stay.
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4. List some factors that determine the distribution and composition of normal flora.
—Development in womb is essentially axenic (Microbe free), but during the birthing process, our first normal flora acquired (Lactobacillus)
—Intestinal bacteria acquired from first meals
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5. What are the 6 areas in which our normal flora are concentrated? Which of those areas host the highest diversity and number of microbes?
Found throughout the body but are localized in certain places: Nose, mouth, skin, lungs, GI tract, urinary/genital tract. Highest diversity in GI tract.
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6. What is microbial antagonism?
When no 2 species can simultaneously and continuously occupy the same niche (area/role)--one will ultimately outcompete the other
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7. Define opportunistic pathogens. Discuss the 3 conditions which can lead to an infection by an opportunistic pathogen.
Bacteria that ordinarily do not cause a healthy host, but may do under certain environments. Conditions: Introduction of normal microbiota into unusual site
in body, Immune suppression, Changes in the normal microbiota
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8. What is meant by “reservoir of infection”? Describe the 3 types of reservoirs, giving examples of each. Which is the most important reservoir?
—Sites where pathogens are maintained as a source of infection. Three types of reservoirs:
—Animal reservoirs (wild and domestic, Lyme disease)
—Human carriers (most important, symptoms show, carriers not affected, AIDS)
—Nonliving reservoirs (soil, water, food, Clostridium botulinum)
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9. What is a zoonose? Give some examples of zoonoses.
Diseases that can be transmitted from animal host to humans, ex: eating animals, vectors, direct contact with animal or waste.
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10. What is a portal of entry? Describe the 3 main portals of entry (be sure to elaborate on mucuos membranes, discussing specific areas). Put a star (or other mark) next to the most commonly traveled portal of entry.
—portal of entry: Sites through which pathogens enter the body
— Major pathways: Mucous membranes (Respiratory Tract*, Gastrointestinal tract, Genitourinary tract)
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11. What is meant by “parenteral route” of entry?
—Not really a portal of entry, but a way to circumvent the skin and mucous membranes, when microorganisms are deposited into the tissues below the skin or mucus membranes, (Punctures, Injections, Bites, Scratches, Surgery, Splitting of skin due to swelling or dryness)
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12. What is meant by the “preferred portal of entry”?
Way a pathogen enters body and infects, will not infect if not correct route.
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13. What is adhesion? Discuss how bacteria and viruses “adhere” to their hosts.
Process by which microorganisms attach themselves to hosts.
—adhesion factors allow some pathogens to attach (suckers)
—ligands: surface molecules on bacteria (attachment sites) that allow them to attach to host cell receptor sites (fimbraie, glycocalyces)
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14. What is the difference between contamination, infection, and disease? Explain why infections do not necessarily result in disease.
—Infection: is the invasion of the host by a pathogen
—Disease: happens when the invading pathogen alters normal body functions
—Contamination: when sterile/clean/normal is disrupted by outside microbe
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15. Differentiate symptoms and signs of disease. What is a syndrome?
—Symptoms: Subjective characteristics of disease felt only by the patient, pain and tiredness
—Signs: Objective manifestations of disease observed or measured by others, such as fever and swelling
—Syndrome: Symptoms and signs that characterize a disease or abnormal condition, ex: malaise, loss of helper T cells, diarrhea, weight loss, toxoplasmosis, and tuberculosis characterize AIDS
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16. What is meant by etiology? What is germ theory?
—Cause of disease
| —germ theory: the theory that certain diseases are caused by the invasion of the body by microorganisms
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17. Describe the 4 steps of Koch’s postulates. What are they used for?
1. The suspected pathogen must be found in all organisms suffering from the disease
2. The pathogen must be isolated from a diseased organism and grown in pure culture
3. The cultured pathogen must cause the disease when introduced into a healthy organism.
4. The microorganism must be re-isolated from the inoculated, diseased host
— used to outline the criteria that need to be met in order to link a specific pathogen to a specific disease
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18. Discuss several exceptions to Koch’s postulates.
— Some microbes cannot be cultured in a lab, diseases can be caused by a combination of pathogens or other factors, different microbes can cause same symptoms (hence same disease), same pathogen can cause multiple diseases depending on location and host, ethical considerations.
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19. Define pathogenicity and virulence.
—pathogenicity: Ability of a microorganism to cause disease
| —Virulence: The degree of pathogencity, the relative ability of a pathogen to invade a host and cause disease
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20. What are virulence factors? List several different types of virulence factors (general types…we’ll get into the details below).
—Virulence Factors contribute to the ability of pathogens to invade a host (Adhesion factors (already discussed), Biofilms (already discussed), Extracellular enzymes, Toxins, Antiphagocytic factors)
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21. Describe the following extracellular enzymes:
a. Hyaluronidase—Breaks down hyaluronic acid which holds cells together
b. Collagenase— Exotoxin that breaks down collagen, which is the chief structural protein in connective tissue
c. Coagulases—Cause blood to clot “hiding” the bacteria, converts fibrinogen to fibrin, which forms blood clots
d. Kinases—Digest blood cots by breaking down fibrin, allowing bacteria to spread
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22. Define the following:
a. Toxin—Chemicals that harm tissues or trigger host immune responses that cause damage
b. Toxemia—toxins in the bloodstream
c. Antitoxin—an antibody designed to bind to a specific toxin, neutralizes toxin, making it harmless
d. Toxoid—exotoxin that has been inactivated by some chemical means
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23. Compare and Contrast Exotoxins from Endotoxins. Be sure to include information such as their general description, the kind of bacteria that produce them, the type of molecule, LD50, whether antitioxins are available, and any other meaningful comparisons.
—exotoxins: Produced within bacteria cell, but secreted outside the cell into the surrounding medium, proteins
—endotoxins: Endotoxin is part of the LPS layer of gram-negative bacteria, Lipid A portion, released during cell lysis
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24. Describe how endotoxins cause fever.
—Cause fever, inflammation, shock, antitoxins not generally produced against endotoxins, endotoxins typically cause fever
—Endotoxins cause macrophages to release interleukin-1 (IL-1)
—IL-1 is carried to hypothalamus gland (in brain) via blood stream
—Hypothalamus releases prostaglandins, which raise the body temperature
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25. What is shock? Describe how endotoxins cause shock.
—life-threatening decrease in blood pressure
—Endotoxins cause bacterial phagocytes to release TNF (tumor necrosis factor)
—TNF damages blood vessels, making them more permeable, which causes them to lose fluid, thus losing blood pressure
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26. What are antiphagocytic factors? Describe an example.
—factors prevent phagocytosis by the host’s phagocytic cells, ex: bacterial capsules which are composed of chemicals not recognized as foreign so body doesn’t mount a defense (example: Streptococcus pneumoniae can only cause disease if it has a capsule. Unencapsulated cells are quickly engulfed and killed by body defenses)
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27. Describe the 5 stages of disease development.
—incubation period: time between infection and the first appearance of any signs/symptoms
—prodromal period: short period of time; characterized by early, mild symptoms of disease (aches, fatigue, etc.)
—period of illness: time period when disease is most severe; overt symptoms/signs of disease (such as fever, muscle pain, sore throat, enlarged lymph nodes, etc.)
—period of decline: signs/symptoms subside as immune response/medications take effect
—period of convalescence: body returns to pre-diseased state; recovery
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28. What is meant by the “transmission”? Describe the 3 groups of transmission (and types within each group), giving examples of each.
—Transmission: from a reservoir or a portal of exit to another host’s portal of entry
—Contact transmission (Direct, indirect, or droplet), Vehicle transmission (Airborne, waterborne, or foodborne), Vector transmission(Biological or mechanical)
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29. What is a fomite? Give examples of fomites.
—Indirect transmission, non-living object that can transmit disease between hosts (toys, bedding, money, toothbrushes etc…)
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30. What is a vector? What type of animal is the most common vector?
—Animals that carry pathogens from one host to another (arthropods—fleas, ticks, and mosquitoes)
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communicable disease
Contagious disease
Noncommunicable disease
- -A disease that comes from another host, (ex: tuberculosis, influenza, herpes, HIV)
- - disease that is easily spread from one host to another, (ex: chickenpox, measles)
- -disease that is not transmitted from one host to another, many normal flora are opportunistic pathogens (ex: tooth decay)
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Local infection
Systemic infection
Focal infection
- -pathogens are limited to small area of the body
- -pathogens or their toxins are spread throughout the body by the blood or the lymph
- -local infection that causes subsequent infection or symptoms in other parts of the body, (tetanus)
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Primary infection
Secondary infection
Subclinical infection
- -acute infection that causes initial illness
- -infection caused by an opportunistic pathogen after the primary infection has weakened the body’s defenses (ex: pneumonia from influenza)
- -does not cause noticeable illness
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Acute disease
Chronic disease
Subacute disease
Latent disease
- -develops rapidly but lasts only a short time, either resolving or causing death of the host, ex: cold
- -develops slowly but is continual or recurrent, ex: TB
- -have durations and severities that lie somewhere between acute and chronic.
- -pathogen remains inactive for a long period of time before producing signs and symptoms, ex: herpes
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Epidemiology
Incidence
Prevalence
- -the study of the location, course, and transmission of diseases within populations
- -Number of new cases of a disease in a given area during a given period of time
- -Number of total cases of a disease in a given area during a given period of time
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Sporadic disease
Endemic disease
Epidemic disease
Pandemic disease
- -disease that occurs occasionally in a population; usually just a few scattered cases (ex: typhoid fever)
- -disease that normally occurs continuously in a population at predictable incidence rates
- -disease occurs at a greater frequency than what is usual within a population
- -worldwide epidemic, AIDS
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Morbidity Rate
Mortality Rate
Notifiable disease
- -Incidence of disease (number of people affected by disease in given time period)
- -number of people that died from particular disease in given time period
- -physicians are required by law to report cases to U.S. Health Official
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32. What is a nosocomial infection? Why is it also called an HAI?
—acquired by patients or workers in health care facilities (Also called HAI’s—healthcare-associated infections—includes hospitals, dental offices, nursing homes, clinics)
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33. Describe the 3 types of nosocomial infections. What is a superinfection?
—Exogenous—Pathogen acquired from the health care environment, such as air conditioning, bed rails, etc.
—Endogenous—Pathogen arises from normal microbiota that become opportunistic due to patient, such as compromised immune system
—Iatrogenic—Results from modern medical procedures, such as surgery or catheterization
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34. Nosocomial infections (HAIs) result from interaction of what 3 factors. Describe each of these.
—microbes in hospital (lots of pathogens present), compromised host (broken skin), chain of transmission (direct contact).
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35. What are the 3 principle sites of a nosocomial infection?
—urinary tract infections, surgical site infections, lower respiratory infections
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36. What are a few ways to prevent nosocomial infections? What is the single most effective way to reduce nosocomial infections?
—aseptic technique, frequent hand washing especially between patients, careful handling, cleaning, and disinfection of fomites, where possible use of single-use disposable items, patient isolation, various institutional methods such as air filtration within the hospital, learning/awareness, prescribe antibiotics only when necessary; avoid invasive procedures if possible
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1. What is immunity? Briefly differentiate innate immunity from adaptive immunity.
—Immunity is resistance, which is the ability to ward off disease.
—Innate is non-specific, fast response immunity and defends against any pathogen, whereas adaptive immunity is slow response, defense against a specific pathogen (requires specific recognition of a pathogen when breaches innate immunity defenses).
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2. What is the first line of defense in innate immunity? Describe several physical, chemical, and biological factors related to the first line of defense.
—First line of defense innate immunity: Physical barriers (skin, mucous membranes, lacrimal apparatus—tears), chemical barriers (sebum, lysozyme, perspiration, transferring), biological barriers (normal flora—microbial antagonism)
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3. What is the second line of defense of innate immunity? Don’t list the details, but summarize what cells/process are involved.
—second line of defense: cells, chemicals, inflammation, fever
—processes: components of blood (plasma, leukocytes), phagocytosis (phagocytes like macrophages or neutrophils all part of defense
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4. List the 5 types of leukocytes below. Describe their functions.. Note which ones are capable of phagocytosis.
* 1. neutrophils (granulocytes)—first responds to infection, can perform diapedesis (leave blood and go into tissue)
* 2. basophils (granulocytes)—release histamine, important during inflammation and allergic response
* 3. eosinophils (granulocytes)— produce toxic proteins against helminths; respond in allergic reactions; capable of phagocytosis
* 4. monocytes (agranulocytes)—phagocytic, capable of diapedesis
* 5. lymphocytes (agranulocytes)—T cells and B cells, natural killer cells that kill weird cells like tumor cells
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5. What are natural killer cells? What is their function? What line of defense are the part of?
—cells that are part of innate immunity that are found in blood, spleen, lymph nodes, red bone marrow
—kill abnormal cells, tumors
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6. What is leukocytosis? Describe how increases in certain leukocytes indicate different types of infections. What is leukopenia?
— Leukocytosis: increase in the number of white blood cells
— Increased eosinophils indicate allergies or parasitic worm infection
—Bacterial infections show an overall increase in leukocytes, especially neutrophils
—Viral infections show increase in lymphocytes
— Leukopenia: decrease in the number of white blood cells
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7. Define phagocytosis. What cells are capable of phagocytosis and in what order do they respond?).
—Cells capable of effecting phagocytosis are called phagocytes, neutrophils and the macrophages
— phagocytosis results in the ingestion and subsequent killing of the pathogen
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8. Describe each of the 6 steps of phagocytosis (making sure you identify terms such as lysosome, phagosome, phagolysosome).
* 1. chemotaxis: Phagocytes are attracted to chemicals, use pseudopods to move, mostly these chemicals are soluble proteins and phagocytes follow the protein gradient (toward the concentration gradient) to the site, chemotactic factors include microbial products (made by the microbe) and Chemokines, chemical signals released by leukocytes at site of infection that cell that attracts cells to site of infection
* 2. adhesion: Contact between phagocyte & microbe, inhibited by capsules and facilitated by proteins called opsonins (opsonization: coating microbe with opsonins, that aid in adherence of phagocytes)
* 3. Injestion: Cell projections (pseudopods) surround & enclose microbe in a phagosome, phagosome: vesicle in which the pathogen is present within a phagocyte
* 4. Maturation: The phagosome fuses with a lysosome, lysosome: an organelles that contains digestive enzymes (intracellular digestion), phagolysosome: Phagosome (containing microbe) + lysosme (containing digestive enzymes)
* 5. Microbial killing: H+ ions are pumped into the phagolysosome creating an acidic environment and digestive enzymes activated (Lysozome (breaks down cell wall), Lipases (digests fat), Proteases (digests proteins), Nucleases (breaks down DNA), enzymes that produce superoxide dismutase and hydrogen peroxide (toxic oxygen radicals), Acids which create a pH of about 5.5, Most pathogens are dead within 30 minutes.
* 6. Elimination: Digested pathogens are subsequently secreted via exocytosis, sometimes, components of the pathogen become attached to the cell membrane of the phagocyte, playing an important role in adaptive immunity
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9. What are chemokines?
—chemical signals released by leukocytes at site of infection that cell that attracts cells to site of infection
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10. What is meant by opsonization? What is its function?
— Opsonization: coating microbe with opsonins, that aid in adherence of phagocytes (Opsonins are components of complement and antibody molecules)
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11. Describe 3 ways that microbes escape phagocytosis.
—1.Prevent of adherence (M proteins: Streptococcus pyogenes)
—2. Capsules (Kill phagocytes)
—3. Produce leukocidins (e.g., Staphylococcus)
—4. Membrane Attack Complexes: lyse phagocyte
—5. Survive within phagocyte (Escape from phagosome (Listeria, Shigella) and prevent fusion with lysosome and multiply within phagocyte (TB, HIV, Chlamydia))
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12. What are Interferons? How are they used to stop viral infections? Why are they not commonly used as an antimicrobial medication?
—Interferons: released by host cells to nonspecifically inhibit the spread of viral infections
—types: alpha and beta type I, gamma type II
— Both -interferon and -interferon are secreted by virus-infected cells; these molecules bind to other body cells, stimulating those cells to produce antiviral proteins, which act to prevent vial infection of those susceptible cells
—Not used because:
—Side effects: nasusea, fatique, heaches, vomiting, fever
—High concentrations are toxic to heaing, liver, kidneys, and red bone marrow
—No effect on cells already infected by virus
—Some viruses resistant to antiviral proteins
—That said, some interferon-based drugs existed
—α-IFN used to treat genital herpes and hepatitis
—β-IFN used to slow MS
—Research into using IFNs to slow development of AIDS
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13. What is complement? What are the 3 effects (outcomes) of complement?
—Consists of over 30 plasma proteins produced by liver (Named in order of their discovery
—triggers inflammation (and fever), release of histamine by mast cells
—increases phagocytosis, by releasing opsinins (proteins that coat a pathogen allowing adherence by phagocytes)
—cytolysis, forms a membrane attack complex (MAC)
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14. What is the goal(s) of inflammation? Is it a systemic or local response to an infection?
—inflammation is a defense response to protect damaged tissues
—local response from infection or damage from heat, chemicals, sunburns etc..
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15. What are the 4 signs/symptoms of inflammation?
—redness, pain, heat, swelling
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16. Describe the 3 stages of inflammation.
• 1. Vasoldilation:
Dilation of blood vessels
• Increases blood flow to area which brings in more phagocytes
• Causes redness and heat
o Increases permeability of blood vessels (for phagocytes)
• This causes fluid to leak, leading to swelling (and pain)
o Bring in clotting factors (fibrinogen)
• Sometimes leading to an abscess (clotting factors trap pathogens and leukocytes; pus formation)
o Some chemicals involved:
• Histamine : released by damaged cells and basophils; cause vasodilation
• Bradykinin: in blood; important for chemotaxis of neutrophils
• Prostaglandins:increase permeability of vessels and help phagocytes move thru capillary walls
• Leukotrienes: increase permeability of blood vessels and help attach phagocytes to pathogens
• 2. phagocytic migration:
o Increased blood flow to site of infection brings in phagocytes
o Phagocytes adhere to capillary wall (margination)
o Next, they squeeze between cells of capillary wall into damaged area (diapedesis)
o Phagocytes begin destroying pathogens
o Neutrophils arrive first, followed by monocytes
o Monocytes enlarge into wandering macrophages, which actively devour pathogens, damaged tissue cells, and dead neutrophils leading to formation of pus
• 3. Tissue repair:
o Involves the delivery of extra nutrients and oxygen to the site
o Involves process of mitosis
• Tissue cells begin dividing to replace dead cells
o The ability of tissue to regenerate depends on:
• Extent of damage
• Type of tissue
• Skin and mucous membranes repair rapidly
• Sometimes, a loss of function results
• Depending on amount of scar tissue
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17. What is the role of basophils and histamine in inflammation?
—histamine causes vasodilation, released by damaged cells and basophils
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18. What is margination? What is diapedesis?
— margination: phagocytes adhere to capillary wall
| —diapedesis: when phagocytes squeeze between cells of capillary wall into damaged area
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19. What is fever? Is it a systemic or localized response to an infection?
—a body temperature above 37 °C
• Recall that inflammation is in response to a localized infection, systemic inflammatory responses would result in a body-wide vessel dilation and leakage, resulting in shock.
• Therefore, fever is the preferred systemic response to an infection
• Side effects: malaise, body aches, and tiredness
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20. Briefly describe the steps involved in fever (include a definition and examples of pyrogens).
—Hypothalamus normally set at 37°C, certain chemicals called pyrogens can “reset” the thermostat (Bacterial toxins, Cytoplasmic contents of bacteria released by lysis, Antibody-antigen complexes, Chemicals released by phagocytes after they have phagocytized a bacteria)
—In response to pyrogens, the hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature.
—This initiates nerve impulses that produce rapid muscle contractions (shivering), increased metabolic rate, and constriction of blood vessel
—This essentially raises the body temperature to its new setting (called chill stage of fever)
—When pyrogens are eliminated (as infection comes under control), the temperature setting falls back to 37°C
—The body now works to cool itself: perspiration, lower metabolism, dilating blood vessels (called crisis stage of a fever); a sign that the infection has been overcome
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21. What are some benefits and disadvantages of fever?
— Benefits of moderate fevers (enhances the effects of interferons, inhibits multiplication of pathogens (unfav temp), enhances performance of phagocytes and antibodies, increases metabolic activity, which speeds up tissue repair)
—Dangers of sustained high fevers (denatures critical proteins, nerve impulses are inhibited (leading to hallucinations, coma, death; dehydration)
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1. What is meant by adaptive immunity? What line of defense is it?
—Adaptive immunity: Aka: induced immunity; specific immunity, involves activity of lymphocytes, Two main types of lymphocytes (B Lymphocytes, Mature in the bone marrow; T Lymphocytes, Mature in the thymus)
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2. Describe the 5 characteristics of adaptive immunity.
—specificity: any particular adaptive immune response acts against only one particular antigen and NOT against others
—inducibility: cells of adaptive immunity activate only response to specific pathogen
—clonality: once induced, cells of adaptive immunity proliferate to form many clones (identical copies) of itself
—unresponsiveness to self: as a rule, adaptive immunity does not act against normal body cells (i.e., self tolerance)
—memory: immunological memory; allows for a quick and efficient response upon re-exposure to same pathogen
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3. Briefly describe the 2 branches of adaptive immunity (what it is/what type of cells/etc).
— humoral immunity: antibody immune response, antibodies produced, B lymphocytes
— cell-mediated immunity: T-lymphocytes, helper t cells
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4. What are antigens? What are epitopes of antigens?
—antigens: immunogens, antibody generators
| — epitope: the region of an antigen that elicits an immune response, recognize and react site for antibody
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5. Differentiate/describe the following:
a. Exogenous antigens— Inlcude toxins and other secretions, components of cell wall, membranes, flagella, and pili
b. Endogenous antigens— Some pathogens (such as viruses) reproduce inside a host cells and produce internal antigens
c. Autoantigens— derived from normal cellular processes; should not normal elicit an immune response, Self tolerance
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6. How do cells distinguish “self” from “non-self”? Describe the MHC complex and the 2 basic types.
—Antigens on the surface of cells known as major histocompatibility antigens , how the body can distinguish “self” from “nonself” (MHC is a cluster of genes located on each copy of chromosome 6 (in humans) which codes for the major histocompatibility antigens
o Class I MHC proteins—found on the cytoplasmic membrane of all cells except red blood cells
o Class II MHC proteins—found only on special types of cells called antigen-presenting cells
• Macrophages, dendritic cells
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7. How do cells process antigens? Discuss 2 basic ways (and the role of APC’s and MHC).
—antigens must be processed before MHC proteins can display epitopes.
—processing Endogenous Antigens
• Small amounts of proteins produced inside cells are catabolized into small peptides.
• These bind to MHC class I molecules
• The MHC I-epitope complexes are transported to the cytoplasmic membrane where they are displayed on the surface.
—Processing Exogenous Antigens.
• Antigen-presenting cells internalize exogenous antigens by phagocytosis and catabolize the molecules to produce peptide epitopes.
• MHC class II bind to epitopes. The MHC II-epitope complexes are then transported to and displayed on the cell’s surface.
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8. What are antibodies? Briefly describe the structure of an antibody.
—antibodies: immunoglobulins (A protein produced by B-lymphocytes in response to the presence of an antigen, in particular, an antibody binds on epitopes of an antigen)
— Structure of a Monomer
o Composed of 4 polypeptide chains
• 2 heavy chains & 2 light chains
• Chains joined together by disulfide bonds
o 2 areas
• variable portion (V)
• combines with epitope
• different in each specific antibody
• constant portion (C)
• same for all antibodies in each of the 5 classes
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9. What are the 5 outcomes of an antigen-antibody complex? Unless you know what they mean, make sure you describe them as well as list them.
• Recall: the complement system help destroy microbes by enhancing phagocytosis, promotes inflammation by signaling basophils to release histamine , and promostes cell lysis
2. neutralization
• IgG’s inactivate viruses by blocking their attachment to host
• Viruses are worthless if they are not within a host cell
• IgA blocks adhesion of microbes to mucous membranes
• Neutralize toxins by blocking active site
• Actis as an antitoxin
3. opsonization
• Antibodies can coat a microbe enhancing phagocytosis
4. agglutination
• Each monomer has 2 binding sites, so can bind 2 at 1 time
• Some larger antibodys (e.g., IgM) are made of 5 monomers so can clump 10 antigens at 1 time
• Essentially decreases the number infectious agents to be dealt with
5. Antibody-dependent cellular cytotoxicity (ADCC)
Activates Natural Killer Cells, which release chemicals (such as perforin and granzyme) which lead to apoptosis (programmed cellular death)
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10. Briefly describe the 5 different types of antibodies (structure, function, abundance).
```
o immunoglobulin G (IgG)
o immunoglobulin M (IgM)
o immunoglobulin A (IgA)
o immunoglobulin D (IgD)
o immunoglobulin E (IgE)
```
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11. Describe the structure and function of B-cells. Where are they produced? Where do they mature? What are BCR’s?
—Humoral immunity B cells: A type of lymphocyte that produces antibodies
o Produced and mature in red bone marrow
o Unlike T-cells that migrate to the thymus gland to mature
o Found in the spleen, lymph tissue, some circulate in blood
—specificity of B-cells
o We have millions of distinct B-lymphocytes
o The surface of each B cell is covered with about 500,000 identical copies of the B cell receptor unique to that cell.
• A BCR is a type of immunoglobulin (Ig).
• Typically an IgD
—Each unique B cell recognizes only one antigen, due to its specific BCR (BCR-antigen specificity), clonal section
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12. In detail, describe the theory of clonal selection of B-cells. Use the terms B cells, clones, , antibodies, plasma cells and memory cells. How does it lead to primary response? Secondary response? Draw it out (and describe) if it helps.
—binding of an antigen to one of these B-cell receptors activates the B-cell
—This selected clone (activated B-cell) starts to rapidly proliferate
o Results in the production of a clones of identical cells
o Most of these cells differentiate into plasma cells
• Those B cells that can immediately produce and secrete antibody molecules into blood or nymph
• This is primary response
o Other cells become long-lived memory cells
• long-term, stable B cells
• Become activated into plasma cells when encounter same antigen from previous encounter
• Provides a quick and strong response (secondary immune response)
• Some can last for more than 20 years
— primary response
o Upon initial exposure to an there is a 10 to 17 day lag before the peak in antibody concentration
• Recall that IgM is first to the scene, followed by IgG
• Do not confuse these with phagocytes (neutrophils and macrophages)
—secondary response
o The second (or later) time an antibody is exposed to an antigen there is only a 2 to 7 day lag before the peak in antibody concentration
o This is why your body is able to rapidly defeat many of the pathogens to which you have been previously exposed
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13. What is the purpose of clonal deletion? How does clonal deletion of B-cells work?
—clonal deletion: tolerant B cells leave the bone marrow, undergo further maturation in spleen and travel in blood and lymph.
—lymphcytes can react with auto antigens, but are destroyed before leaving bone marrow
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14. Differentiate primary and secondary response of the immune system?
—primary response is immediate, secondary is slow.
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15. How is cell mediated immunity different than humoral immunity? What sort of cells are involved? How are T-cells similar to B cells? How are they different?
— Cell-mediated immunity: mediated by T cells rather than via secreted antibodies, cell-mediated immunity is particularly effective against endogenous antigens
—Humoral immunity: B cells, lymphocyte that produces antibodies, recognizes one antigen
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16. cells. Differentiate Helper T-cells from Cytotoxic T-cells. Make sure you also understand CD4 and CD8 as it relates to T-cells and HIV.
1. Helper T cells (Th cells, CD4 cells)
• Release cytokines (chemical signals) that regulate the activity of B cells and cyototoxic T-cells
o Help cytotoxic T-cells (and macrophages) in cell-mediated immunity (Type 1 Helper T-cells)
o Help B-cells produce antibodies in humoral immunity (Type 2 Helper T-cells)
• CD4 refers to a glycoprotein receptor on the surface of Helper T-cells (in addition to TCRs)
o CD4 is also a primary receptor used by HIV to gain entry into host T cells.
2. cytotoxic T cells (Tc cell, CD8)
• have ability to recognize and kill target cells that have identified as non-self
• CD8 is a glycoprotein receptor on the surface of Tc cells and NK cells
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17. Describe the process of clonal deletion of T-cells?
— Cells with receptors that respond to autoantigens are selectively eliminated via apoptosis in a process known as clonal deletion
o because potential offspring—clones—are deleted
• Clonal deletion of T cells occurs in the thymus, where thymus cells process and present all the body’s autoantigens to young T cells
o For B-cells, happens in bone marrow
• T cells that do not recognize MHC are also deleted.
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18. Briefly describe the activiation of cytotoxic T-cells. In your discussion, discuss the role of APC’s, helper T-cells, cytotoxic T cells, and memory cells (basically, this is clonal selection of T-cells, similar to B cells).
• antigen presentation
o An antigen presenting cell (APC) degrades an endogenous antigen into fragments (a peptide series)
o The antigen fragment is then presented on the surface of the APC in association with MHC -I
• helper T cell differentiation
o The APC displays antigen to TH cell (TCR of helper T cells binds to antigen-MHC complex on APC
o IL-2 (interleukin) stimulates the newly activated cell to become a Th-1 cell.
• Activation of cytotoxic T cells
o This stimulates the Th-1 cells secrete cytokines that activate Tc lymphocytes
• Once activated, theTc lymphocyte begins to proliferate (clonal selection)
o Activated cytotoxic T cells destroys target cells (with the MHC-epitope complex)
o Some T-cells become long-lived memory cells
• Quick and efficient respons
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19. How do Tc Cells work? How is this different than natural killer cells? Make sure to specifically discuss the differences between the roles of Tc cells and Natural killer cells.
• Tc Cells have the ability to recognize and kill non-self cells
o Non-self cells are those with altered function, such as virus-infected cells, tumors cells, transplanted foreign tissues
• How do they know when cells are non-self?
o They look for MHC holding an antigen/epitope
o This indicates the cell is infected….ATTACK!
o In contrast, non-specific Natural Killer cells attach cells showing no MHC (or an abnormal MHC)
• Tc cells attack by releasing perforin and granzyme
o Perforin: proteins that produces pores in cell membrane
o Granzyme: enter cells and activate apoptosis
• Leads to apoptosis
o Programmed cell death
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20. What is perforin and granzyme? What is apoptosis?
o Perforin: proteins that produces pores in cell membrane
o Granzyme: enter cells and activate apoptosis
• Leads to apoptosis: Programmed cell death
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21. Discuss the process of T-dependent antibody immunity (the role of helper T-cells in B cell activation).
• T-dependent antibody immunity
o requires the assistance of type 2 helper T (Th2) cells to activate B-cells
o involves a series of interactions among antigen-presenting cells, helper T cells, and B cells, which are mediated by cytokines
• Antigen presentation for Th activation and cloning.
o APCs present exogenous epitopes on MHC II molecules to Th using the complementary TCR.
• Differentiation of helper T cells into Th-2 cells.
o IL-4 (interleukin) stimulates the newly activated cell to become a Th-2 cell.
• Activation of B cell
o The Th-2 cell interacts with B cells (with matching MHC-antigen complex)
o The activated B cell proliferates rapidly and the clones differentiate into either memory B cells or plasma cells
o plasma cells produce antibodies; memory cells long lived
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22. Contrast actively and passively acquired immunity. Contrast natural and artificial immunity. Give examples of each type (naturally acquired active, naturally acquired passive, artificially acquired active, artificially acquired passive).
• Naturally Acquired Immunity
o active
• Person is exposed to antigens, becomes ill, body produces antibodies and specialized lymphocytes
• typically long-lasting (life-long or several years)
o passive
• Natural transfer of antibodies from mother to infant across the placenta (transplacental transfer…IgG) or thru breastmilk (IgA)
• Effective immediately but provides temporary immunity
• Weeks to months, until baby’s immune system kicks in
• Artificially Acquired Immunity
o active
• Thru vaccinations (immunizations)
• vaccine: suspension of organisms or fractions of organisms that is used to induce immune response
• Whole pathogenic microbes that have been killed or weakened
• Fragments of microbes, such as viral capsids or naked DNA
• Inactivatd bacterial toxins
• Long-lived
o passive
• Injection of antibodies rather than antigens
• Effective immediately but Short-lived
• e.g, tetanus shot
