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Virology Topics: What are Koch’s Postulates?
By what formal criteria are viruses demonstrated to cause human disease?
Name three viruses that cause diseases in man that do not fulfill Koch’s postulates. How was
viral causality demonstrated in these cases?
What is the difference between lysogeny and latency?
What is the Hershey-Chase experiment?
How did the study of lysogenic bacteriophages influence the concept of inducible enzyme
expression and the operon theory of coordinate gene expression?
What is tranduction? Is transduction observed with mammalian viruses, why or why not?
Why did scientific understanding of bacteriophages exceed those involving animal viruses even
though the latter were known to be major causes of death?
How are viruses organized into families?
What are the common forms of genome organization?
What is the range of genome sizes among viruses?
What is the range of virion sizes among viruses?
How are viruses typically cultured?
What is CPE? What are some examples of CPE?
How is virus replication quantified?
What is M.O.I.?
How can you calculate the probability that an individual cell will not be infected when adding a
virus to cells?
What is a one-step growth experiment?
What questions are answered using forward or classical viral genetics?
Define the following types of mutants: Temperature sensitive, Host range Nonsense, Conditional,
Null, Leaky
How might you engineer cell lines to support the growth of viral mutants.
What is genetic complementation?
What is reassortment?
What is marker rescue?
What are the basic requirements (features of the virus) for reverse genetics?
What is a defective interfering (DI) virus? How do they arise?
What common features (or requirements) of virus structure are necessary for the virus life cycle?
How is virus structure studied?
What is the difference between shape and symmetry?
What is meant by 3-fold or 5-fold axis of symmetry?
Why is an icosahedron more efficient for a virus than a tetrahedron of the same volume?
What is a packaging signal?
What kinds of viruses contain membranes?
How are viral membranes usually acquired?
Do viral membranes always contain cholesterol? Why or why not?
How do enveloped viruses enter cells? What viral proteins are required for entry? How do viral
proteins induce membrane fusion?
How do nonenveloped viruses enter cells? What viral proteins are required for entry?
What is neuraminidase?
What are the six major steps in the virus life cycle?
What is the difference, if any, between attachment factor, receptor and coreceptor?
What types of cellular molecules serve as attachment factors, receptors and coreceptors? Do all
of these molecules interact with virus with high affinity? What functions do these proteins
perform in viral life cycles? How do these proteins influence virus biology and pathogenesis?
What are the major pathways of viral entry by endocytosis? How are these different portals
distinguished experimentally?
What is the significance of a low pH dependence for virus infectivity?
What is viral uncoating? What evidence suggests that uncoating is an active process?
What strategies do viruses employ to traffic to the following cellular compartments after entering
cells: endosomes, endoplasmic reticulum (ER) and nucleus?
What are the different strategies employed by viruses with the following types of genomes:
dsDNA, ssRNA (- strand), ssRNA (+ strand), dsRNA, retroviral genomes (ssRNA + strand)
What are the implications of the above genome types with regard to:(i) subcellular sites of
genome replication (ii) fidelity of genome replication (i.e. mutation rates), (iii) reliance on host
processes for viral genome replication and conversely need for virus encoded proteins, (iv)
balance between synthesizing mRNA and genome sequences that are packaged into virions (v)
reverse genetics.
What is the end-replication problem and how do different viruses solve the problem?
What processes do SV40 T antigen and HIV Rev employ to be actively imported into or
exported out of the nucleus?
What are the size limits for proteins to diffuse in and out of the nucleus without being actively
transported?
Why do cellular carrier proteins involved in nuclear import/export work only in one direction
only?
How are proteins like HIV Envelope (Env) expressed on the surface of cells?
What are the essential requirements for the assembly of enveloped and non-enveloped viruses?
What is virus maturation and what does maturation involve in the case of HIV?
What basic cellular mechanisms have been discovered from the study of viruses, noting in
particular (1) the chemical nature of genetic material, (2) DNA structure and replication, (3)
transcription, (4) translation, (5) cell growth control and (6) transport of molecules in cells?
What strategies to viruses employ to divert host cell RNA and protein synthesis to the expression
of viral RNAs and proteins?
What basic cellular functions are exploited by viruses at different steps in the virus life- cycle?
Why are viral proteins frequently synthesized as large precursor proteins?
What two cellular pathways are most commonly targeted by DNA tumor viruses? Why do DNA
viruses encode proteins that target these cellular proteins?
What are the three mechanisms responsible for retrovirus oncogenicity?
What is the historical significance of oncogenic retroviruses in understanding human cancer?
How has the study of retroviral oncogenes advanced our understanding of the signaling pathways
that regulate cell growth, differentiation and survival?
True or False: most viruses cause life threatening disease in the natural hosts they infect?
Explain.True or False: many viruses persist in their natural hosts without causing any evidence
of disease? Explain.
True or False: virus evolution selects for viruses that replicate to high titers. Explain.
What are some of the specific mechanisms for virus invasion and spread within the body?
What are some of the specific mechanisms involved in virus latency and reactivation?
What are the implications of the rates of virus evolution and (1) efforts to develop viral vaccines,
(2) efforts to develop anti-viral drugs, (3) the ability of viruses to evade host anti-viral defense
mechanisms and (4) emergence of new viral diseases?
What is epidemiology?
How is epidemiology used to understand virus-host interactions for example (1) establishing an
etiologic role for viruses in human cancer, (2) establishing the effectiveness of a new vaccine (3)
determining the importance of life style, environmental or genetic factors in viral disease
susceptibility?
What is the difference between a prospective and a retrospective study?
What epidemiologic factors make the eradication of some viruses easier than others?
Why have anti-viral drugs been more difficult to develop than antibiotics?
What anti-viral targets are considered most “drugable”
What are some examples of anti-viral drugs and what targets do they inhibit?
What social changes associated with human settlement and civilization fostered the emergence of
new viral diseases and/or epidemics? (B) How have these affected human evolution?
What is a zoonotic virus?
KEY CONCEPTS IN BACTERIOLOGY-­‐FOUNDATIONS 2013 Below is a list of key concepts that should be understood by all students in the Graduate Program of Microbiology and Immunology. Your understanding of these concepts will be evaluated in an in-­‐class Final Exam at the end of the Bacteriology Section of Foundations General Bacteriology The structure and organization of bacterial cells Characteristics that distinguish a bacterial cell from a eukaryotic cell Bacterial phylogeny, particularly as it pertains to pathogenic bacteria Characteristics that define environmental bacteria, commensal bacteria, or pathogenic bacteria Mechanisms of bacterial signal transduction Bacterial secretion systems Regulation of bacterial gene expression Genetic exchange in bacteria Bacterial transcription and translation Bacterial communities with an emphasis on biofilms Mechanisms of bacterial motility Mechanisms of bacterial cell division and sporulation Mechanisms of host colonization Medical Bacteriology The major bacterial pathogens and the diseases they cause The definition of a virulence factor and some classic examples Characteristics that distinguish intracellular and extracellular pathogens The major types of bacterial toxins and some classic examples Defense against bacteria Major classes of antibiotics and their mechanisms of action Mechanisms of antimicrobial resistance to antibiotics The contribution of the normal flora to immune system development Mechanisms by which bacteria evade phagocyte-­‐mediated killing Mechanisms by which bacteria evade opsonization and immune cell chemotaxis 1
KEY INFORMATION & CONCEPTS in IMMUNOLOGY
Members of the faculty have assembled a basic list of key concepts that should be
understood by all students in the Department of Microbiology & Immunology. Most of
the concepts will not be covered specifically during the Foundations course.
Nonetheless, mastery of a reasonable level of independent discourse on these subjects
is expected as a part of the transition to candidacy for the Ph.D. degree (and even
would be expected of a Masters of Science student).
General Immunology:
What are the major classes of leukocyte?
For each of the main classes of leukocyte, what are two key, functionally meaningful
features that distinguish them from other major classes?
With which phase (acute, or early vs later, or chronic) of immunity is each the major type
of leukocyte most associated?
Which types of leukocyte are most typically involved in early host defenses against
extracellular bacteria?
Which types of leukocyte are most typically involved in resolution of infection with
bacteria that replicate inside of cells?
Which types of leukocyte are most typically thought of as central to clearance of a viral
infection?
Which types of leukocyte are most typically thought of as central to clearance of a
fungal infection?
Which types of leukocyte are most typically involved in early host defenses against
extracellular parasites such as helminthic worms?
What are the most important classes of cellular receptor that ʻsenseʼ microbial ʻforeignnessʼ as part of innate immune responses?
For each of these classes of receptor, be able to sketch out central features of the
mechanisms that initiate and propagate their signaling (this requires actual names and
biochemical details).
What are the most important classes of cellular receptor in immunity that detect
antigens as part of adaptive immune responses?
For each of these classes of receptor, be able to sketch out central features of the
mechanisms that initiate and propagate their signaling (this requires actual names and
biochemical details).
What are innate humoral mechanisms, how do they ʻsenseʼ foreign-ness (how do they
discriminate between self and non-self), and how are they activated?
What are specific mechanisms by which innate immune mechanisms impact adaptive
immunity, and vice versa?
Be able to discuss (“sketch out”) the scenario or story line of an immune response to at
least a couple of different types of infection (e.g., virus; intracellular bacterium;
extracellular bacterium; Gram negative vs Gram positive, etc)
Molecular & Cellular Mechanisms:
What are the key structural features of antibody molecules and the functions of the
specific classes of Ab?
What are points of connection between antibodies and aspects of innate immunity?
In structural and functional terms, how does Ag recognition by B cells differ from that of
T cells [put a different way, how does each class “see” antigen]?
For both of these classes of lymphocyte (B cells and T cells) and Ag receptor:
What are mechanisms that create or expand diversification of the recognition repertoire
of receptors? At what sites and stages of differentiation do these mechanisms act?
In molecular & cell biological terms, what are mechanisms in two major pathways of
antigen processing and presentation?
What is ʻcross-presentationʼ and why does it matter?
What signal transduction pathways mediate activation of T and B lymphocytes?
[What are major receptors leading to lymphocyte activation, signal transduction
pathways activated by them, and key transcription factors induced by the signaling?]
Why is the repertoire of mature T cells “biased” in such a manner that microbial antigens
need “self” MHC molecules in order to be activated. Be able to answer this in both
senses of “why” [function/teleological and mechanism by which this effect arises]
What is immunological tolerance and what are the mechanisms by which each form of
tolerance is achieved? [At a minimum, be able to discuss dominant versus deletional
versus other types of tolerance.]
What are the molecular and micro-anatomical (cellular) mechanisms for collaboration
between T and B lymphocytes?
For the various classes of leukocyte that either directly or indirectly kill pathogens or
pathogen infected cells, what are the main mechanisms for killing?
Be able to name and discuss representatives from at least the following classes of
cytokine, along with main features of how the chosen cytokine signals:
TNFRSF (TNF receptor superfamily)
hematopoietin (“γc”-sharing)
chemokine receptors (can include FLR / “F-met-leu-phe receptor”)
IL-1 receptor family
Be able to name a specific bacterial pathogen and a specific viral pathogen, and major
mechanisms that each uses for evasion of humoral immunity.
Be able to name a specific bacterial pathogen and a specific viral pathogen, and major
mechanisms that each uses for evasion of cell-mediated immunity.
Medical Immunology:
What are vaccines and, in specific cellular and molecular terms, how do they work?
[Be prepared to write or talk about at least two specific examples, focusing most on
those that are currently most important for human health.]
What are cellular and molecular mechanisms of allergic responses? Viewed through the
prism of natural selection, why is the capacity for allergic disease maintained?
For at least two major autoimmune diseases, what are cellular and molecular
mechanisms involved in autoimmunity? Viewed through the prism of natural selection,
why is the capacity for autoimmunity maintained?
What is “shock” and what are two different ways by which pathogens lead to this
syndrome?