Pathogenic Microbiology
Final Exam Questions
Course Introduction
Pathogenic Microbiology explores the biology, ecology, and impact of microorganisms that cause diseases in humans. This course covers the mechanisms of pathogenesis, host-pathogen interactions, and the molecular, cellular, and epidemiological aspects of disease-causing bacteria, viruses, fungi, and parasites. Students will examine methods for identifying and controlling pathogens, the immune response to infection, and current challenges in the prevention and treatment of infectious diseases. Through lectures, laboratory experiences, and case studies, students gain a comprehensive understanding of microbial virulence, diagnostic techniques, and the public health implications of infectious agents.
Recommended Textbook
Fundamentals of Molecular Virology 2nd Edition by Nicholas H. Acheson
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Chapter 1: Introduction to Virology
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Q1) Which of the following is an enzyme that most RNA viruses encode in their genome?
A) DNA-dependent-RNA-polymerase
B) RNA-dependent-RNA-polymerase
C) DNA-dependent-DNA-polymerase
D) RNA-dependent-protein-synthetase
Answer: B
Q2) If the genome of a positive-strand RNA virus, which has been purified away from all of the virion proteins, was injected into the cytoplasm of an appropriate host cell, what would happen first?
A) The genome would be copied into complementary negative RNA.
B) The genome would be translated by cellular ribosome's.
C) The genome would be transcribed by a cellular RNA-dependent-RNA-polymerase.
D) The genome would be transcribed by a viral RNA-dependent-RNA-polymerase.
E) None of the above.
Answer: B
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3
Chapter 2: Virus Structure and Assembly
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Q1) Which of the following is a description of a scaffolding protein?
A) A cellular protein that acts as a chaperone during assembly of a helical capsid.
B) A viral protein that is used on the outside of an icosahedral capsid during assembly.
C) A viral protein used on the inside of an icosahedral capsid during assembly and then removed.
D) A protease that trims the proteins during assembly of an icosahedral capsid.
E) A energy dependent motor used to package the genome into larger icosahedral capsids.
Answer: C
Q2) In a helical nucleocapsid, which of the following MOST affects the LENGTH of the capsid?
A) the (mu) value
B) the (rho) value
C) the size of the genome and the P (pitch) of the helix
D) the size of the capsid protein
E) None of the above.
Answer: C
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Chapter 3: Virus Classification: The World of Viruses
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Q1) Which of the following is a type of nucleic acid NOT found as the genome of a virus that can infect vertebrates?
A) ssDNA
B) dsDNA
C) ssRNA
D) dsRNA
E) All of the above are found.
Answer: E
Q2) What is a ribozyme?
A) A molecule of RNA that is independently capable of replicating without cellular enzymes.
B) A molecule of RNA that codes for an enzyme.
C) Another name for a small infectious molecule of RNA
D) A virus that uses a small piece of RNA as its genome.
E) A molecule of RNA that can carry out an enzymatic process.
Answer: E
Q3) Viroids do not require a helper virus in order to replicate and cause disease.
A)True
B)False
Answer: True
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Chapter 4: Virus Entry
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Q1) Adenoviruses use which of the following entry mechanisms?
A) The fibers on the virion can penetrate the endosome membrane can cause it to lyse open.
B) An interaction between the penton base of the virus and the cellular integrin proteins causes the endosome membrane to lyse open
C) The capsid forms a pore through the cell membrane and extrudes the genome into the cytoplasm
D) The viral envelope fuses at the plasma membrane after binding to the host integrin protein.
E) The viral envelope fuses with the nuclear membrane after binding to the nuclear pore complex.
Q2) The diameter of the opening in the nuclear pore complex is much too narrow to allow passage of any virus particles directly into the nucleus.
A)True B)False
Q3) Describe what a fusion peptide is and how it is involved in mediating membrane fusion between the viral envelope and the cell membrane?
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Chapter 5: Single-Stranded RNA Bacteriophages
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Q1) Site directed mutagenesis of the MS2 genome was carried out to abolish the MJ stem structure that is just upstream of the start codon of the replicase gene.Which of the following describes the result of this experiment?
A) The coat protein was unable to bind to the viral genome.
B) The maturation protein was unable to bind to the stem-loop.
C) The ribosome could no longer bind to the start codon for the replicase gene.
D) The replicase protein was unable to bind to the viral genome.
E) Translation of replicase gene increased in the absence of coat protein translation.
Q2) In the ssRNA phage MS2, the replicase protein binds to the start codon of the coat protein gene.Which of the following describes the reason for this binding?
A) It prevents replication and translation from occurring simultaneously.
B) It initiates synthesis of the minus-strand copy of the genome.
C) It enhances binding of the ribosome to the coat protein gene.
D) It disrupts the stem-loop structure that prevents replication of the viral genome.
E) It exposes the 3' end of the genome which allows the replicase to begin RNA synthesis.
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Chapter 6: Microviruses
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Q1) Which of the following processes was studied by working with the phage X174?
A) Transcription of mRNA
B) Splicing of mRNA
C) Translation of mRNA
D) Replication of DNA
E) Lysogeny
Q2) Several different mRNAs are produced from the X174 genome using which of the following mechanisms?
A) Multiple transcription promoters
B) Multiple transcription terminators
C) Multiple translation start sites
D) Multiple stop codons
E) Both a and b are correct
Q3) Which of the following describes the first step in the replication cycle of the phage X174?
A) Conversion of ssDNA into dsDNA.
B) Translation of the viral genome into protein.
C) Transcription of the viral DNA by the cellular RNA polymerase.
D) Transcription of the viral DNA by the viral RNA polymerase.
E) Integration of the viral DNA into the host chromosome.
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Chapter 7: Bacteriophage
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Q1) Which of the following enzymes is NOT involved in replication of the bacteriophage T7 genome?
A) Single-Strand DNA binding protein
B) Lysozyme
C) DNA ligase
D) RNA polymease
E) RNA primase/helicase
Q2) The RNA polymerase from bacteriophage T7 has become a useful tool in molecular biology.Which of the following describes how it can be used?
A) To express high levels of a foreign protein in a bacterial cell.
B) To measure small amounts of target RNA molecules in a sample.
C) To measure the levels of pathogenic viruses in drinking water.
D) To amplify DNA molecules in a sample.
E) To fuse two pieces of RNA together.
Q3) Describe how the RNA polymerase from bacteriophage T7, along with specific DNA sequences taken from the late T7 genes, can be used to produce high levels of a foreign protein in a bacterial cell.
Q4) How does the bacteriophage T7 inhibit the host cell RNA polymerase and why is this advantageous to the virus?
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Chapter 8: Bacteriophage Lambda
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Q1) The N and Q proteins from phage both have which of the following functions?
A) Recombination of the viral genome
B) Repressors of transcription initiation
C) Activators of transcription initiation
D) Repressors of transcription termination
E) Unwinding of the viral genome
Q2) What is the function of the Int protein from phage?
A) It mediates site specific recombination between attP and attB.
B) It ligates the ends of the viral chromosome.
C) It binds to multiple sites within the origin or replication.
D) It recruits the cellular DNA replication enzymes to the viral genome.
E) It acts as a scaffolding protein for virion assembly.
Q3) The phage will lysogenize the host cell if which of the following proteins is produced in sufficient levels during infection?
A) N
B) CI
C) Q
D) Integrase
E) Cro
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Chapter 9: Viruses of Archaea
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Q1) Which of the following characteristics is common to many of the viruses that infect archaeal cells and distinguishes them from the phages that infect bacteria.
A) They release mature virions without lysing the host cell.
B) Their viral genomes are very high in AT basepairs.
C) Their viral genomes are linear.
D) Their viral genomes are composed of double-stranded RNA.
E) Their virions are composed of icosahedral capsids.
Q2) Even though the two archaeal viruses HHPV-1 and HRPV-1 are clearly related to each other, based on genome and virion structures, they have one major difference.Which of the following describes this difference?
A) One can undergo lysogeny while the other can only carry out lytic infection.
B) One infects hyperthermophilic hosts while the other infects a hyperhalophilic host.
C) One packages a dsDNA genome while the other packages a ssDNA genome.
D) One appears to encode an obvious DNA polymerase while the other does not.
E) One has a linear genome while the other has a circular genome.
Q3) Archaea cells contain a nucleus like eukaryotic cells.
A)True
B)False
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Chapter 10: Cucumber Mosaic Virus
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Q1) In an infected plants, the cucumber mosaic virus replicase complex is associated with the membrane surrounding which of the following cellular organelles?
A) Golgi apparatus
B) Nucleus
C) Mitochondria
D) Central Vacuole
E) Chloroplast
Q2) Which of the following has been used as a system to study brome mosaic virus replication?
A) Bacterial cells
B) Yeast cells
C) Insect cells
D) Animal cells
E) Human cells
Q3) In cucumber mosaic virus, productive infection requires simultaneous entry of all three major RNA segments, each packaged into a separate virion.
A)True
B)False
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Chapter 11: Picornaviruses
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Q1) The ability of picornaviruses to cause pathogenesis in specific tissues can be localized to which of the following regions of the viral genomic RNA?
A) The RNA-dependent RNA polymerase coding region.
B) The 3' noncoding region.
C) The non-structural protein coding region.
D) The capsid protein coding region.
E) The 5' noncoding sequence.
Q2) Instead of a 5' cap on the viral genomic RNA, genomes of the picornaviruses have a covalently bound protein.In addition, the viral 3C protease cleaves a major component of the cap binding complex.This situation should inhibit translation initiation of the picornaviral RNA into protein.Explain how the virus "solves" this problem.
Q3) Which of the following describes the source of the protease that cleaves the picornavirus polyprotein into individual functional proteins?
A) It is a cellular protease.
B) It is brought into the host cell with the virion.
C) It is part of the polyprotein.
D) It is one of the capsid proteins.
E) It is a complex of a viral and a cellular protein.
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Chapter 12: Flaviviruses
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Q1) Which of the following techniques was used to isolate the flavivirus Hepatitis C virus?
A) Molecular cloning of the viral cDNA
B) Purification of virus particles
C) Antibody staining with patient serum
D) Plaque assay
E) Southern blotting
Q2) A cloned DNA copy of the yellow fever virus can be used to produce infectious viral RNA.
A)True
B)False
Q3) Which of the following describes the reason why the precursor to the capsid protein from flaviviruses has a membrane spanning domain?
A) So that it is localized on the membranes where viral RNA replication takes place.
B) So that it islocalized on the membranes where the virions obtain their envelope.
C) So that it is close to where the other structural proteins are localized.
D) So that it will be translated by ribosomes associated with the ER.
E) All of the above are correct.
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Chapter 13: Togaviruses
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Q1) The production of the subgenomic mRNA allows togaviruses to synthesize 10 times more structural proteins than non-structural proteins.
A)True
B)False
Q2) How are the structural proteins in togaviruses expressed?
A) They are translated from the negative-sense strands after genome replication.
B) They are translated directly from incoming genomes.
C) They are translated from a subgenomic RNA.
D) They are only translated from newly synthesized full-length genomes.
E) None of the above are correct.
Q3) Which of the following components of the togavirus virion bind to the host cell receptor?
A) Lipid envelope
B) Capsid protein
C) HA protein
D) E1 glycoprotein
E) E2 glycoprotein
Q4) There are two proposed mechanisms for how togaviruses assemble their virions.Describe the two mechanisms and any available evidence that supports them.
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Chapter 14: Coronaviruses
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Q1) The subgenomic mRNAs in the coronaviruses are synthesized from subgenomic negative-strand templates.
A)True
B)False
Q2) The membrane proteins of coronaviruses are glycosylated in which of the following cellular compartments?
A) Cytoplasm
B) Endosome
C) Lysosome
D) Smooth ER
E) Golgi apparatus
Q3) Enveloped virus-like particles can be formed in cells when only the M and E protein from a coronavirus are expressed.What does this indicate?
A) That these proteins can not associate with the nucleocapsid.
B) That these proteins can not associate with each other.
C) That these proteins are sufficient for assembly and budding of virions.
D) That these proteins require HE and S for virion formation.
E) All of the above are correct.
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Chapter 15: Paramyxo-Viruses and Rhabdoviruses
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Q1) Subacute sclerosing panencephalitis (SSPE)is a common complication of measles where the virus infects the nervous tissue immediately after causing the typical measles virus symptoms.
A)True
B)False
Q2) What is the function of the neuraminidase enzyme during infection with Sendai virus, a member of the paramyxovirus family?
A) It helps the assembly of the envelope.
B) It attaches to the host cell receptor.
C) It is involved in evasion of the host immune system.
D) It facilitates exit of the virions.
E) It is involved with transcription of viral mRNAs.
Q3) The F protein of the paramyxovirus measles is responsible for both binding and fusion of the virion to the host cell.
A)True
B)False
Q4) Describe the two models that explain how the monopartite negative-strand RNA viruses produces individual mRNAs.Which of the two models does the experimental evidence support?
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Chapter 16: Filovirouses
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Q1) The GP protein of Ebola virus is unusual from the glycoproteins from other negative-strand RNA viruses in two major ways.Describe these differences.
Q2) Marburg virus, a member of the filovirus family, has a higher mortality rate than either Ebola Zaire or Ebola Sudan.
A)True
B)False
Q3) During an outbreak of Ebola virus, which of the following as NOT been shown to be a major source of transmission between individuals?
A) Preparation of bodies for burial.
B) Reuse of needles and syringes.
C) Sexual transmission.
D) Aerosol droplets.
E) Contact with contaminated blood.
Q4) Labs that have Biosafety Level 2 are allowed to work with live infectious filoviruses.
A)True B)False
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Chapter 17: Bunyaviruses
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Q1) Which of the following describes an interesting feature of the envelope glycoproteins from bunyaviruses?
A) They are exported out to the plasma membrane of the cell.
B) They are retained in the Golgi membrane.
C) They are not glycosylated.
D) They are cleaved into three segments.
E) 80% of the proteins made are secreted out of the cell.
Q2) Bunyaviruses remove the 5' ends of cellular mRNAs.Describe the mechanism that these viruses use to do this and how the virus uses these RNA fragments.What advantage does this provide to the virus?
Q3) What do bunyaviruses use to prime the transcription of their viral mRNAs?
A) A cellular protein
B) A viral protein
C) Fragments of cytoplasmic capped mRNAs.
D) Fragments of nuclear capped mRNAs.
E) The do not use primers for mRNA transcription.
Q4) Explain how genetic drift and shift can lead to the emergence of new strains of bunyavirus that are pathogenic in humans.
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Chapter 18: Influenza Viruses
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Q1) Influenza is unusual for an RNA virus because it replicates in the nucleus.
A)True
B)False
Q2) The abundance of which of the following proteins from influenza virus controls whether the virus is producing mRNAs or full-length positive antigenomes.
A) PB1 protein
B) PB2 protein
C) PA protein
D) Nucleocapsid protein.
E) Matrix protein
Q3) Many of the symptoms caused by infection with the influenza virus, including fever, headache and malaise, are actually the result of which of the following?
A) Factors produced by the virus during infection.
B) Direct damage to the cells of the lung.
C) Infection of the liver.
D) Loss of ciliated epithelium.
E) The effect of cytokines induced by the virus.
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Chapter 19: Reoviruses
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Q1) There is evidence that the noncoding sequences on reovirus genome segments are highly conserved.
A)True B)False
Q2) Reovirus capsid proteins assemble around positive-strand RNA segments before completion of genome replication.
A)True B)False
Q3) Which of the following reovirus proteins is implicated in selective inhibition of PKR activation in infected cells?
A) 1
B) 3
C) 1
D) 2
E) 1
Q4) Some reoviruses are transmitted by insects and are therefore examples of arboviruses.
A)True B)False
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Chapter 20: Parvoviruses
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Q1) Eukaryotic cellular chromosomes use the same mechanism as the parvoviruses to maintain the ends of their linear DNA.
A)True
B)False
Q2) Parvoviruses can only productively infect cells that are NOT going through the cell cycle.
A)True
B)False
Q3) Which of the following does NOT explain why parvoviruses replicate better in tumor cells than in normal cells?
A) Tumor cells have a reduced interferon response than normal cells.
B) Tumor cells bind to more parvovirus virions than normal cells.
C) Tumor cells have reduced DNA damage response than normal cells.
D) Tumor cells go through the cell cycle more quickly than normal cells.
E) None of the above.
Q4) The dependoviruses, which are a group of parvoviruses, require coinfection with an adenovirus or herpesvirus to undergo a productive infection.
A)True
B)False
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Chapter 21: Polyomaviruses
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Q1) The polyomavirus SV40 has been used as an in vitro model for studying the biochemistry of DNA replication in mammalian cells.Explain why SV40 is a good model for studying this process.
Q2) Under which of the following conditions do polyomaviruses cause tumors in their hosts?
A) Injection of high titers in young animals.
B) Injection of high titers in older animals.
C) Exposure to the virus via an aerosol.
D) Exposure to particularly tumorigenic strains of the virus.
Q3) Polyomaviruses are a major infectious cause of human cancers.
A)True
B)False
Q4) Which of the following cellular proteins are packaged into the polyomavirus virions?
A) Tubulin monomers.
B) Actin monomers.
C) Histone octomers.
D) Myristylated proteins.
E) Transcription factors.
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Chapter 22: Papillomaviruses
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Q1) The E7 proteins from the oncogenic strains of papillomaviruses bind to pRb more tightly than the E7 proteins from nononcogenic strains of the virus.
A)True
B)False
Q2) Which of the following describes the mechanism used by the E6 protein of papillomaviruses to remove the p53 protein.
A) It causes the p53 protein to be exported out of the cell.
B) It causes the p53 protein to be targeted to the lysosome.
C) It causes the p53 protein to become ubiquinated.
D) It acts as a protease to directly degrade the protein.
E) It phosphorylates p53, which causes it to be degraded by the proteasome.
Q3) Mutations in the p53 gene are seen in over 50% of human tumors.
A)True B)False
Q4) Very few cases of cervical cancer are caused by infection with papillomavirus.
A)True B)False
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24
Chapter 23: Adenoviruses
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Q1) The tripartite leader found on all of the transcripts produced from the major late gene of adenovirus carries out which of the following functions?
A) It makes the mRNA more stable.
B) It binds to the eIF4F translation factor.
C) It shunts the ribosome to the correct AUG on the mRNA.
D) It assists with transport of the mRNA out of the nucleus.
E) It improves the efficiency of mRNA splicing.
Q2) A strain of adenovirus, called ONYX-015, that does not express the E1B 55K protein, is being studied as a treatment for cancer.Why does the lack of E1B 55K allows this virus to spread and kill cancer cells but not normal cells?
Q3) During the cell cycle in an uninfected cell, the cellular protein Rb represses S phase genes by doing which of the following?
A) Localizes histone deacetylase to E2F inducible genes.
B) Binds to the adenovirus E1A protein and releases E2F.
C) Prevents binding of the cellular RNA polymerase II to E2F inducible genes.
D) Binds and phosphorylates the cyclin dependent kinase.
E) Prevents the binding of E2F to the promoters of S phase genes.
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Chapter 24: Herpesviruses
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Q1) During one round of infection with the herpes simplex virus, all four isoforms of the viral genome are produced.
A)True
B)False
Q2) Both herpes simplex virus and Epstein-Barr virus have multiple mechanisms to suppress both cellular antiviral pathways as well as allow latently infected cells to hide from the adaptive immune system.Describe two of these mechanisms used by either virus.
Q3) Which of the following describes the distinguishing features of the three types of latency exhibited by the Epstein-Barr virus?
A) Whether the viral DNA is integrated into the host chromosome or not.
B) The number of copies of the viral genome maintained.
C) The type of envelope glycoproteins on the cell surface.
D) The cell types that are latently infected.
E) The number and type of EBNA and LMP genes expressed.
Q4) Describe what happens during a primary infection with herpes simplex virus I (HSVI), how the virus enters into latency, and then how the virus can be reactivated back to a lytic infection.Your answer should focus on the cell types affected by each stage of the infection.
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Chapter 25: Baculoviruses
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Q1) Treatment of baculovirus infected cells with the toxin a-amanitin, which inhibits RNA polymerase II, does not reduce levels of the viral late transcripts.Which of the following explains why?
A) Baculoviruses use the cellular RNA polymerase III to transcribe their late genes.
B) Baculoviruses produce their own RNA-dependent RNA polymerase.
C) Baculoviruses produce their own DNA-dependent RNA polymerase.
D) Baculoviruses produce such high levels of the late mRNAs that the inhibition does not matter.
E) Insect cells do not use RNA polymerase II to transcribe their genes.
Q2) The budded virions produced during a baculovirus infection are primarily involved in which of the following?
A) Shutting down host defense mechanisms.
B) Surviving the harsh conditions of the environment.
C) Transmission via eggs laid by an infected female.
D) Transmission between different hosts.
E) Transmission of the virus between cells within a host.
Q3) Baculoviruses can infect and replicate in human but do not cause any disease.
A)True
B)False
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Chapter 26: Poxviruses
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Q1) The mRNAs of poxviruses do not undergo splicing.Which of the following explains why?
A) Poxvirus genomes are small and they need to conserve genome space.
B) Poxviruses replicate in the cytoplasm of infected cells.
C) They do not need to regulate gene expression through alternative splicing.
D) They do not encode the proteins that carry out mRNA splicing.
E) Poxvirus mRNAs do not contain exons.
Q2) If a purified poxvirus genome was heated to melt the hydrogen bonds holding the two strands of DNA together, which of the following would describe the structure of the genome?
A) Multiple pieces of single-stranded DNA
B) Two linear pieces of single-stranded DNA
C) A covalently closed circle of double-stranded DNA.
D) Two single-strand circles entwined together.
E) A circle of single-stranded DNA.
Q3) Smallpox was named in 15 century France to distinguish it from "large pox" or syphilis.
A)True
B)False
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Chapter 27: Viruses of Algae and Mimivirus
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Q1) Like most other eukaryotic viruses, the entire virion of the chlorovirus PBCV-1, a phycodnavirus, enters the host cell and releases the viral genome into the nucleus.
A)True
B)False
Q2) The coccolithoviruses encode enzymes that produce the sphingolipid ceramide.What is the proposed function of this lipid in infected cells?
A) It enhances the production of cellular membranes, which the virus requires for replication.
B) It modifies cellular membranes, which enhances binding and entry of virions.
C) It activates apoptosis, causing host cells to lyse and release virus particles.
D) It inhibits apoptosis, allowing host cells to stay alive longer.
E) It induces signaling pathways in the host cell that increase viral replication.
Q3) The genome of the giant mimivirus contains more non-coding and "junk" DNA than most other DNA viruses.
A)True
B)False
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Chapter 28: Retroviruses
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Q1) Most retroviruses cause cancers in their animal hosts.
A)True
B)False
Q2) The Gag and Pol proteins are coded for in two different reading frames in the avian retroviruses.Which of the following mechanisms is used to produce the Pol proteins?
A) Alternative mRNA splicing.
B) RNA editing.
C) Read through of a translational stop codon.
D) Ribosomal frameshifting.
E) Initiation of translation at a downstream start codon.
Q3) The double-stranded proviral genome of retroviruses is longer than the incoming single-stranded RNA genome.What is the function of this extra DNA sequence and where did it come from?
Q4) Which of the following statements about acute transforming retroviruses is TRUE?
A) They produce viral enzymes that lead to cellular transformation.
B) They cause tumors because of where they integrate into the host genome.
C) They carry a mutated or deleted version of a cellular gene.
D) They are usually competent to replicate and produce virions.
E) They only transform cells in which the provirus has not been integrated.
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Chapter 29: Human Immunodeficiency
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Q1) People who have a natural mutation in the gene encoding the CCR5 protein are resistant to infection with HIV.
A)True B)False
Q2) The majority of individuals infected with HIV develop AIDS 8-10 years after the initial infection.
A)True B)False
Q3) HIV, unlike most other retroviruses, can infect nondividing cells.Which of the following explains why?
A) The HIV reverse transcriptase enzyme can function with a lower concentration of nucleotide triphosophates.
B) The HIV integrase enzyme can work without the help of cellular enzymes.
C) The HIV matrix protein can direct the nuclear import of the HIV preintegration complex.
D) The HIV Vpr protein can interact with cellular microtubules to bring the virion close to the nucleus.
E) All of the above are correct.
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Chapter 30: Hepadnaviruses
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Q1) Which of the following describes an interesting feature of the preC and pregenomic mRNAs produced by the hepatitis B virus?
A) They are extensively spliced to produce a set of nested mRNAs.
B) They are transcribed by the cellular RNA polymerase III enzyme.
C) They are produced by the reverse transcriptase enzyme.
D) They are transcribed past a polyadenylation site near the promoter.
E) They each code for several proteins due to the use of alternative start codons.
Q2) It is recommended that people in certain professions or with certain disease should receive the hepatitis B vaccine.For which of the following individuals would it NOT be critical for them to be vaccinated against hepatitis B?
A) Zoo keeper
B) Nurse
C) Tattoo-parlor worker
D) Barber
E) Hemophiliac
Q3) Hepatitis B replication is completely limited to hepatocytes.
A)True
B)False
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Chapter 31: Viroids and Hepatitis Delta Virus
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Q1) Which of the following is NOT thought to be a mechanism by which viroids cause disease in their plant hosts?
A) By basepairing to an important cellular RNA, preventing its function.
B) By activating the dsRNA induced protein kinase.
C) By causing the degradation of cellular mRNAs via the RNAi pathway.
D) By interfering with mRNA splicing because they resemble a cellular snRNA.
E) By inhibiting the machinery that exports mRNAs out of the nucleus.
Q2) The ribozyme function found in virioids and hepatitis delta virus can be used to cleave exogenous RNA molecules.Which of the following is a requirement for the ribozyme to be recycled and cleave more than one substrate?
A) The entire length of the substrate must not be too long.
B) The structure of the ribozyme RNA must be very stable.
C) Only a short region of complementarity between the target and the ribozyme.
D) The level of magnesium ions must be low enough.
E) The temperature of the reaction must be high enough.
Q3) There is some controversy about whether the replication of the hepatitis delta virus (HDV)genome is performed by the cellular RNA polymerase I or RNA polymerase
II.Describe the evidence that supports each model.
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33
Chapter 32: Prions
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Q1) Describe how the prion hypothesis explains how there can be both an acquired and a genetic form of Creutzfeldt-Jakob disease.
Q2) Explain the observations that link new variant CJD with BSE.
Q3) The genetic forms of prion diseases result from mutations in the prion gene.What is the proposed mechanism for how these mutations cause the prion disease?
A) They cause the prion protein to become degraded in the cell.
B) They stabilize the structure of the PrP form of the protein.
C) They lead to overexpression of the prion protein in the brain.
D) They cause the prion protein to misfold more easily into the PrP form.
E) They cause the prion protein to interact with the microtubules in the neuron.
Q4) What is the nature of the infectious agent that causes the human disease kuru?
A) A positive-strand RNA virus.
B) A small RNA molecule similar to a viroid.
C) Kuru is only seen as an inherited genetic disease.
D) A single species of protein called a prion.
E) A small DNA molecule that does not code for a protein.
Q5) The PrP protein is more resistant to proteases than the PrP protein.
A)True
B)False
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Chapter 33: Intrinsic Cellular Defenses Against Virus
Infection
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Q1) The presence of double-stranded DNA in the cytoplasm is recognized by cellular receptors and initiates antiviral defenses.
A)True
B)False
Q2) When interferon binds to its receptor it stimulates an intracellular signaling pathway.Which of the following proteins is part of this signaling pathway?
A) NF-\( \kappa \)B and HMG1 proteins
B) Caspase proteins
C) Jak and Stat proteins
D) IRF-3 and IRF-7 proteins
E) Death inducing signaling complex
Q3) Why is double-stranded RNA such a potent inducer of a cell's antiviral defenses? Describe one antiviral defense system that requires double-stranded RNA in order to be activated.
Q4) Interferon is an excellent treatment for certain viral infections, like those caused by heptatitis B and C, because it has very few side effects.
A)True
B)False
Page 35
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Chapter 34: Innate and Adaptive Immune Responses to Virus Infection
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Q1) Which of the following describes the process of antibody-dependent cellular cytotoxicity?
A) An antibody activates the Fas receptor on the infected cell and causes it to enter apoptosis.
B) An antibody causes the virus to be killed by a cytotoxic T lymphocyte.
C) An antibody binds to a virus particle and it is engulfed by a macrophage.
D) An antibody binds to a virally infected cell and it is attacked by a macrophage.
E) Both "c" and "d" are correct
Q2) What happens when the T cell receptor on a CD8 positive T cell recognizes the peptide displayed in the MHC-I complex on an infected cell?
A) It attracts natural killer cells, which kill the infected cell.
B) It releases interferon g which stimulates macrophages to engulf the cell.
C) It releases IL-4 to stimulate the B cells to release antibodies.
D) It releases proteins that kill the infected cell.
E) It releases IL-12 which stimulates the production of Th1 cells.
Q3) Explain how B and T lymphocytes produced a variety of cell surface receptors that can bind a wide variety of epitopes on antigens.How is this related to the clonal selection theory?
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Chapter 35: Antiviral Vaccines
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Q1) For which of the following viruses is a vaccine NOT being currently developed?
A) Human rhinovirus.
B) Hepatitis C virus.
C) Dengue virus.
D) Respiratory syncytial virus.
E) Human immunodeficiency virus
Q2) For which of the following viruses would a vaccine that stimulates the cellular immune system be most useful?
A) Herpesviruses
B) Dengue virus
C) HIV
D) Hepatitis C virus
E) All of the above.
Q3) Which of the following has been a major technological problem with producing a vaccine to the H5N1 avian influenza?
A) It was difficult to produce a reassortant virus strain.
B) It was difficult to identify the most antigenic regions of the virus.
C) The virus can not be grown in cultured cells.
D) It was difficult to produce enough of the vaccine strain in chicken eggs.
E) The virus replicates to very low titers.
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Chapter 36: Antiviral Chemotherapy
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Q1) What is the definition of a therapeutic index when discussing an antiviral drug?
A) The amount of the drug that inhibits the virus replication.
B) The amount of the drug that is toxic to the host cell.
C) The amount of the drug that is inhibits viral replication divided by the amount of the drug that is toxic.
D) The dose that exerts 50% toxic effect divided by the does that exerts a 50% antiviral effect.
E) The amount of the drug that kills 50% of the hosts.
Q2) Which of the following viral enzymes encoded by cytomegalovirus is responsible for phosphorylating and activating the antiviral drug ganciclovir?
A) Guanine kinase
B) Cellular nucleotide kinase.
C) UL97, a serine-threonine protein kinase
D) Thymidine kinase
E) Thymidylate kinase
Q3) Describe some of the factors that make drugs to inhibit virus infections harder to develop than the drugs used to fight bacterial infections.
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Chapter 37: Eukaryotic Virus Vectors
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Q1) RNA virus vectors do not require the same enhancer/promoter sequences as DNA virus vectors.
A)True
B)False
Q2) Viruses make good gene therapy vectors because they are highly efficient at delivering nucleic acids to a particular kind of cell.
A)True
B)False
Q3) In the first generation of adenovirus vectors the E3 gene was deleted.How could the virus replicate in the absence of the E3 gene products?
A) A plasmid containing the E3 gene is transfected along with the viral DNA.
B) The cell line that the recombinant viruses are grown in carries the E3 gene.
C) The E3 gene products are not required for adenovirus replication.
D) The transgene inserted into the virus complements for the E3 gene.
E) The E3 gene products are packaged into the virions.
Q4) Virus vectors that contain large transgenes do not require a helper virus to be propagated.
A)True B)False
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