Basic Virology. Martinez J. Hewlett

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      Hepatitis delta (D) virus is a defective virus that cannot replicate without the aid of another virus, the hepatitis B virus. Rates of hepatitis D and B virus coinfection vary widely throughout the world. Hepatitis D and B virus coinfection in the same individual, however, leads to a higher incidence of chronic liver disease than does infection with hepatitis B virus alone. Hepatitis D virus infection can be prevented by use of the hepatitis B vaccine, since hepatitis D virus replication is dependent on the presence of hepatitis B virus.

      Like HAV, hepatitis E virus is spread in the developing world by contaminated water and possibly by food. It is found throughout the world and has caused significant epidemics in India and Russia through problems with drinking water. In the developed world, hepatitis E virus is spread from animal reservoirs, primarily domestic pigs. The disease caused by this virus is usually mild, but can have high mortality rates in pregnant women. Recovery from acute infection is generally complete. Chronic infection occurs in immune‐compromised individuals.

      1 The disease SSPE is a complication that may follow infection with measles virus. Discuss the possible mechanisms occurring during development of this rare disease.

      2 What features of pathogenesis are shared by measles virus, varicella zoster virus, and variola virus?

      3 What are some of the unique features of infection by rabies virus?

      4 What features distinguish an acute from a persistent infection?

      5 Distinguish encephalitis produced by herpesvirus from that resulting from infection with an arbovirus such as La Crosse encephalitis virus.

      1 This part described the various patterns of viral infection that can be observed, among them acute, persistent, and latent. What common features may exist among these three types of infection? What are the distinguishing characteristics of each of these three types of infection?

      2 The five hepatitis viruses have the same tissue tropism (the liver), and yet each is in a different virus family. One of them (hepatitis D or the delta agent) is actually a defective virus, sometimes called a subviral entity.In the table below, indicate the mode of transmission of each of these agents:AgentTransmitted byHepatitis A virusHepatitis B virusHepatitis C virusHepatitis D (delta) agentHepatitis E virusWhat functions of the liver may allow all of these agents to have a common tissue tropism, despite their differing modes of transmission?

      3 As part of a larger project, you have been given five unknown viruses to characterize. Your job is to determine, given the tools at your disposal, the host range and tissue tropism of these unknown viruses. You will be using two kinds of cells: human and mouse. In each case, you have a cell line that grows continuously in culture and is therefore representative of the organism, but not of a particular tissue (human: HeLa cells; mouse: L cells). In addition, you have cells that are derived from and still representative of specific tissues: muscle or neurons. For each virus, you have an assay system that indicates if the virus attaches to (“+”) or does not attach to (“−”) a particular type of cell. Using the data in the table below, determine, if possible, the host range and tissue tropism of each unknown virus.HumanMouseVirusHeLaMuscleNeuronLMuscleNeuron#1+−−−−−#2++−++−#3−−−+++#4−−−−−−#5+−+−−−Here is the report form you will send back with your results. Indicate with a check mark (✓) what your conclusions are for each of the unknown viruses.Virus#1#2#3#4#5Host rangeHumanMouseBothNeitherTissue tropismMuscleNeuronNo tropismCannot be determined from data

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      2 Baer, G.M. and Tordo, N. (1994). Rabies virus. In: Encyclopedia of Virology (eds. R.G. Webster and A. Granoff), 1180–1185. New York: Academic Press.

      3 Barry, J.M. (2004). The Great Influenza: The Epic Story of the Greatest Plague in History. New York: Viking.

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      10 Haase, A.T. (1997). Methods in viral pathogenesis: tissues and organs. In: Viral Pathogenesis (ed. N. Nathanson), 465–482. Philadelphia: Lippincott‐Raven.

      11 Koff, R.S. (2004). Hepatitis C. In: Infectious Diseases (eds. S.L. Gorbach, J.G. Bartlett and N.R. Blacklow), 2072–2074. Philadelphia: W.B. Saunders.

      12 Koff, R.S. (2004). Hepatitis E. In: Infectious Diseases (eds. S.L. Gorbach, J.G. Bartlett and N.R. Blacklow), 2074–2076. Philadelphia: W.B. Saunders.

      13 Koff, R.S., Hepatitis, B., and hepatitis, D. (1998). Infectious Diseases (eds. S.L. Gorbach, J.G. Bartlett and N.R. Blacklow) chap. 91. Philadelphia: W.B. Saunders.

      14 Kolata, G. (2001). Flu: The Story of the Great Influenza Pandemic. New York: Touchstone.

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      16 McNeill, W. (1996). Patterns of disease emergence in history. In: Emerging Viruses (ed. Morse), 29–36. New York: Oxford University Press.

      17 Morse, S.S. (1996). Examining the origins of emerging viruses. In: Emerging Viruses (ed. S.S. Morse), 10–28. New York: Oxford University Press.

      18 Nathanson, N. (2001). Epidemiology. In: Virology, 4e (eds. B.N. Fields and D.M. Knipe) chap. 14. New York: Raven Press.

      19 Nathanson, N. and Tyler, K.L. (1997). Entry dissemination, shedding, and transmission of viruses. In: Viral Pathogenesis (ed. N. Nathanson) chap. 2. Philadelphia: Lippincott‐Raven.

      20 Oldstone, M.B.A. (1998). Viruses, Plagues, and History. New York: Oxford University Press.

      21 Porterfield, J.S. and Htraavik, T. (1994). Encephalitis viruses. In: Encyclopedia of Virology (eds. R.G. Webster and A. Granoff), 362–371. New York: Academic Press.

      22 Preston, R. (1994). The Hot Zone. New York: Random House.

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