Study questions Topic 11 (Immune responses to viral infections)

Host defense

  1. What constitutes intrinsic defenses?
  2. How does the innate defense system recognize that a cell is infected with a virus? What is the difference between TLRs and RLRs?
  3. Name five primary players in innate defense (hint, 3 are cells, 2 are proteins or protein complexes).
  4. What is the inflammatory response? How does this process relate to the Th1 and the Th2 response?
  5. What are the common communicating biomolecules that link intrinsic, innate, and adaptive defenses? What processes give rise to their synthesis? Where do most of this communication take place?
  6. Describe the establishment of the anti-­‐viral state by interferon. What are redness, heat, swelling, and pain? Why is it good?
  7. Is it true that most non-­‐cytopathic viruses do not induce a strong inflammatory response? Why or why not? What is the expected outcome of a non-­‐cytopathic infection?
  8. What are the roles of B cells in viral infections? How do anti-­‐viral antibodies block infection?
  9. What do T cells do during viral infections?
  10. How is the decision made to favour T cells or antibody production during viral infection? What is immune memory? Why do we need it?

Viral evasion strategies

  1. What are virokines and viroceptors, and how do they function? Know several ways that viruses modulate IFN function.
  2. What is apoptosis? Why does it occur in virus-­‐infected cells? Why do viruses block apoptosis? How do they do it?
  3. Why and how do viruses block autophagy?
  4. Discuss how RIG I activity is remediated in response to HIV infection. Apobec is a weapon of mass deamination. Why? How does HIV defeat it? How do viruses modulate NK cell activity?
  5. What are MHCI and MHCII antigen presentations? How do viruses interfere with both?

Virus-­host interactions

  1. What is a cytopathic virus?
  2. What is viral virulence? How is it measured?
  3. Viral virulence genes fall into four classes. What are they?
  4. Give an example of immunopathology mediated by CD8+ T cells, CD4+ T cells (both Th1, and Th2), and antibodies.
  5. Why is dengue fever a big problem globally?
  6. What does this phrase mean: “Immunopathology is the price paid by the host to eliminate a viral infection”.
  7. How does a virus-like measles virus, that infects the respiratory tract, cause a characteristic skin rash all over the body? What causes the rash?
  8. What is “systemic inflammatory response syndrome”?  aka cytokine storm. What is the mechanism of immunosuppression and what are the consequences? What determines if a host is susceptible or not to viral infection?
  9. Does increasing age make humans more or less susceptible to viral infection? Why?


Think questions

  1. When we vaccinate against viral infections such as measles, mumps, rubella, poliomyelitis, and chickenpox, we inject an attenuated or inactivated form of the virus. The body responds by making antibodies that coat the surface of that virus by binding to its surface proteins or glycoproteins. Briefly describe two ways this may prevent future infections with this virus.
  2. Why do you think that a symptomatic reactivation of HSV-1, HSV-2, and VZV infections typically is associated with some immunosuppressive event?
  3. When a virus infects the body, the body responds by producing antibodies that coat the virion. Discuss briefly how this might offer protection to the body. One of the experimental approaches to preventing viral infection is to use recombinant DNA technology to artificially synthesize the host cell receptor molecule to which a specific virus would normally attach and then therapeutically administer this receptor to people prior to viral exposure. Discuss briefly how this might offer protection to the body.