Viruses have evolved two fundamental growth strategies: an r-replication strategy and the K-replication strategy to enable them to avoid or coexist with the host immune response. Describe these strategies. What are the advantages and disadvantages of each strategy for a virus? Give an example of a specific virus and how it follows one of the strategies.
Examine the “Polio Virus Pattern of Infection” figure in assignments folder. This figure is taken from a 1959 paper on polio infections, before our modern understanding of the immune response to a viral infection. Describe the interaction of the virus with the host immune response depicted in this figure. What type of infection is depicted? What is causing the clinical symptoms (Headache, sore throat etc…)? What is likely responsible for virus levels in the throat and bloodstream?
For a virus to maintain a persistent infection, it must coexist with the host immune response. Viruses have evolved a number of ways of achieving this by modulating the adaptive immune response. Mechanisms for achieving this include immunoevasins that interfere with the function of MHC proteins, CTL escape mutants, killing of cytotoxic lymphocytes and infection of lymphocytes. Choose one of these mechanisms and describe how they facilitate the ability of the virus to evade the immune response. Give an example of a virus utilizing one of these mechanisms.
What are the features of the viral lifecycle for a latent infection? Most latent infections begin as acute infections, what are the molecular events required to switch to and maintain a latent infection? Provide specific examples with a known virus.
Read the review “Anatomy of Viral Persistence” by Michael Oldstone. What are the features of a virus and its host that contribute to a persistent infection?
As our technologies for detecting viruses improves, there will likely be more associations identified between viruses and chronic diseases. Read the review by Foxman and Iwasaki on the role of viral infections in complex diseases. Explain one of the viral associations with disease described in the article. What role does genetics of the host play in the disease? Why? Would these associations fulfill Koch’s Postulates?
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