Micro Assessment 7 – Flashcards
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            | 1. What family is the measles virus in? | 
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        | 1. Paramyxoviridae (morbillivirus genus) | 
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            | 2. Why is Measles considered a “new” virus? | 
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        | 2. No accounts in early Greek, Required population >100,000, Trade route opened avenue for transmission | 
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            | 3. What 3 viruses cause multi-system infections and humans are the only known host? | 
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        | 3. Measles, Mumps, Rubella | 
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            | 4. How is Measles different from other paramyxoviruses? | 
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        | 4. Lacks neuraminidase activity, has H protein instead of HN; Receptors are CD46 and SLAM; Forms intracellular inclusion bodies | 
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            | 5. What is a distinctive feature of cytopathology for Measles? | 
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        | 5. Intracellular inclusion Bodies | 
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            | 6. What is the Entry and Replication strategy for Measles? | 
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        | 6. 1. MV binds receptor (CD46, SLAM), 2. Binding activates F protein, causes membrane fusion (entry). 3. Replication and assembly similar to other negative-strand RNA viruses | 
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            | 7. Who typically is infected by Measles? | 
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        | 7. Children | 
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            | 8. How is Measles spread? | 
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        | 8. Respiratory route | 
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            | 9. What is the main cause of mortality from measles? | 
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        | 9. bacterial pneumonia | 
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            | 10. How long does the latent period of measles last? Are there symptoms? | 
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        | 10. 10-14 days; No | 
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            | 11. What are the symptoms following the latent period of measles? | 
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        | 11. 2-3 day prodrome of high fever (101-105), cough, conjunctivitis (Photophobia), rhinorrhea | 
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            | 12. What kind of rash develops after the initial symptoms? | 
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        | 12. maculopapular rash | 
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            | 13. What does the maculopapular rash of measles coincide with? | 
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        | 13. a strong cell-mediated immune respone and virus clearance | 
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            | 14. What viruses do not use sialic acid and don’t have neuraminidase? | 
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        | 14. Measles, RSV, Rhino (class clicker question) | 
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            | 15. What is the Clinical Case Definition of Measles? | 
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        | 15. 1. Rash >3 days, 2. Temperature >38.3C(101F), 3. Cough, rhinorrhea, and/or conjunctivitis. | 
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            | 16. When do cases of measles need to be reported? | 
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        | 16. If symptoms are epidemiologically linked to another confirmed case of measles. | 
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            | 17. Where is the initial site of measles infection? | 
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        | 17. Tracheal and bronchial epithelia | 
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            | 18. After 2-4 days how does measles spread to the lymph nodes? | 
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        | 18. carried by pulmonary macrophages | 
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            | 19. What are Warthin-Finkeldey cells? | 
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        | 19. Reticuloendothelial giant cells that are created by measles virus replicating in the lymphoid tissue | 
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            | 20. What does amplification of measles in the lymph nodes result in? | 
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        | 20. Viremia and infection of other tissues and organs | 
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            | 21. What are the primary cells infected by measles in the blood? | 
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        | 21. Monocytes (other major cell types – epithelial, endothelial, macrophages) | 
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            | 22. When is the patient with measles infectious? | 
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        | 22. 1-2 days before symptoms of viremia occur (Rash and Koplik spots) | 
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            | 23. How long after exposure to measles is a person infectious? | 
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        | 23. 10-20 days | 
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            | 24. Where can measles be cultured? | 
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        | 24. mucous membranes of nasopharynx, conjunctivia, mouth, and blood | 
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            | 25. What are small red spots with blue-white center found in upper lip and cheek called? | 
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        | 25. Koplik spots | 
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            | 26. How does the Maculopapular Measles rash spread? | 
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        | 26. Starts on the back of the neck or forehead and spreads to extremities | 
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            | 27. What does the Measles rash result from? | 
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        | 27. infection of the dermal endothelial cells followed by spread to the overlying epidermis | 
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            | 28. When are Koplik’s spots usually seen? | 
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        | 28. Before the rash | 
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            | 29. What is a complication of the measles virus? | 
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        | 29. Immune suppression – Delayed-type hypersensitivity responses are suppressed, impaired production of antibody and cellular immune responses | 
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            | 30. What is the primary cause of measles virus-induced immune suppression? | 
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        | 30. infection of monocytes and other immune effector cells | 
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            | 31. What 3 things can be neurological MV complications post infection? | 
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        | 31. 1. Postinfectious encephalomyelitis (PIE), 2. Measles Inclusion Body Encephalitis (MIBE), 3. Subacute Sclerosing Panencephalitis (SSPE) | 
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            | 32. What is an autoimmune demyelinating disease caused by MV complications? | 
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        | 32. PIE (postinfectious encephalomyelitis) | 
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            | 33. What diseases result from the establishment of persistent infections in the brain after MV? | 
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        | 33. MIBE and SSPE | 
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            | 34. What is the vaccine for measles? | 
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        | 34. Live-attenuated measles virus vaccine provides “life-long” immunity | 
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            | 35. When do Children receive the measles vaccine? | 
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        | 35. at 12-15 months, 2nd dose at 4-6 years, subcutaneously | 
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            | 36. Why is the MMR vaccine so effective? | 
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        | 36. MMR are antigenically stable monotypic viruses | 
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            | 37. Are there different strains of MV? | 
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        | 37. Yes, but neutralizing antibody to one strain protects an individual against all circulating strains | 
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            | 38. How are the different strains of MV defined? | 
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        | 38. by amino acid differences in the H or HN proteins | 
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            | 39. Why is measles an ideal candidate for eradication? | 
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        | 39. 1. only one serotype, 2. clinically identifiable, 3. no animal reservoir, 4. eradication requires “herd immunity” | 
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            | 40. What is the most common cause of MV resurgence? | 
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        | 40. Parents choosing not to vaccinate | 
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            | 41. What are the contraindications for measles vaccination? | 
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        | 41. Allergic reaction to gelatin or neomycin. Moderately or severely ill at the time of vaccination. Pregnant Women. Anyone on immunosuppressive drugs. | 
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            | 42. How long should women wait to get pregnant after receiving the Measles vaccine? | 
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        | 42. 4 weeks | 
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            | 43. What family is the Mumps virus a member of? | 
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        | 43. Paramyxoviridae family (rubulavirus genus) | 
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            | 44. Where does Mumps initially infect? | 
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        | 44. Nasal mucosa and upper respiratory tract epithelium | 
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            | 45. Which is more infectious, Measles or Mumps? | 
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        | 45. Measles | 
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            | 46. How long is the incubation period for Mumps? | 
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        | 46. ~18days | 
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            | 47. What causes the “chipmunk” look of a mumps infection? | 
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        | 47. Spread to the draining lymph nodes, Infection of the Parotid Gland | 
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            | 48. What is the first clinical sign of a mumps infection? | 
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        | 48. Infection of the parotid gland causes “chipmunk” look | 
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            | 49. When is virus shed? | 
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        | 49. begins ~6 days before onset of clinical disease | 
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            | 50. What does half of mumps infection result in? | 
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        | 50. Virus replication in the CNS | 
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            | 51. What can virus replication in the CNS lead to? | 
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        | 51. Aseptic meningitis, Deafness | 
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            | 52. If you see a truck with some disturbing appendages hanging off the back, what complication did they probably have with the mumps virus? | 
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        | 52. symptomatic gonadal involvement | 
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            | 53. What is a major complication of Mumps in post-pubertal men? | 
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        | 53. symptomatic gonadal involvement – testes swell, can cause sterility | 
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            | 54. What infection has a correlation with the development of type I Diabetes? | 
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        | 54. Mumps | 
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            | 55. What type of vaccine is there for mumps? | 
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        | 55. Live-attenuated vaccine | 
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            | 56. Which 2 RNA viruses that cause multi-system infections are (-) stranded? | 
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        | 56. Measles and Mumps | 
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            | 57. Which RNA virus that causes multisystem infections is (+) stranded? | 
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        | 57. Rubella | 
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            | 58. What is the family of Rubella? | 
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        | 58. Togaviridae family | 
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            | 59. What are the 2 genera of Togaviridae? | 
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        | 59. Alphaviruses and Rubiviruses | 
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            | 60. How are Rubiviruses distinguished from Alphaviruses? | 
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        | 60. Rubiviruses have limited host range - Humans | 
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            | 61. How does Rubella virus replicate? | 
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        | 61. 1. Enters cell by receptor mediated endocytosis, 2. Genome serves as mRNA 3. Polymerase made first 4. (-) strand antigenome is used as template for both progeny genomes and subgenomic mRNA, which encodes the viral capsid and envelope proteins. | 
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            | 62. What are the clinical manifestations of the Rubella virus? | 
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        | 62. Mild disease, Low-grade fever, conjunctivitis and sore throat, lymphadenopathy, Morbilliform Rash | 
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            | 63. How is does Rubella transmit and replicate? | 
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        | 63. aerosols, replicates initially in the mucosa of upper respiratory tract and nasopharyngeal lymph nodes | 
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            | 64. How long is the incubation period of rubella? | 
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        | 64. ~7-9 days | 
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            | 65. How long after initial exposure does the morbilliform (maculopapular) rash begin? | 
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        | 65. 16-21 days | 
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            | 66. How long can the rubella virus be shed? | 
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        | 66. Shedding begins after incubation period and continues after rash disappears, can be shed for up to a month after initial exposure. | 
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            | 67. What is the most devastating effects of Rubella infection? | 
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        | 67. in fetuses – causes congenital birth defects | 
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            | 68. When is the highest risk of rubella infections for the fetus? | 
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        | 68. 1st and 2nd trimester | 
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            | 69. Infection by Rubella in the first month of pregnancy usually results in what? | 
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        | 69. spontaneous abortion | 
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            | 70. What clinical manifestations can be found if a fetus is carried to term by a mother infected by Rubella in the first or second trimester? | 
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        | 70. Mental retardation, motor disabilities, hearing loss, congenital heart disease, cataracts | 
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            | 71. What is the primary reason for Rubella vaccination? | 
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        | 71. directed at protecting the fetus from infection | 
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            | 72. Why do measles and rubella cause rashes, while Flu, RSV, and hMPV don’t? | 
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        | 72. Flu, RSV, and hMPV don’t spread beyond Respiratory tract. (class clicker question) | 
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            | 73. What is most significant about Measles? | 
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        | 73. it’s Highly Contagious | 
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            | 74. What was the leading cause of aseptic meningitis prior to development of vaccine? | 
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        | 74. Mumps | 
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            | 75. Why is the MMR vaccine so successful? | 
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        | 75. All three viruses are monotypic, Humans are the only known reservoir | 
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            | 76. What kind of replication does Parvovirus Have? | 
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        | 76. Autonomous replication | 
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            | 77. What is the structure of parvovirus? | 
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        | 77. Linear, single-stranded DNA, Icosahedra capsid, no envelope | 
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            | 78. Where does parvovirus replicate? | 
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        | 78. nucleus | 
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            | 79. Why does parvovirus need to replicate in rapidly dividing cells? | 
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        | 79. needs active DNAase | 
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            | 80. What is “fifth disease”? | 
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        | 80. Parvo B19 | 
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            | 81. What are the symptoms of Parvo B19? | 
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        | 81. erythema infectiosum – a mild common childhood rash | 
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            | 82. How does Parvo B19 spread? | 
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        | 82. direct contact with respiratory secretions, prior to rash | 
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            | 83. What is the Biphasic pathogenesis of parvo B19? | 
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        | 83. Initial viremia – flu like symptoms; Second Phase – Rash driven by antigenic response | 
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            | 84. What are the characteristic symptoms of fifth disease? | 
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        | 84. “Slapped Cheek” rash, Lacy red rash on trunk and limbs | 
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            | 85. What symptoms can adults have from fifth disease? | 
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        | 85. Joint pain or swelling, flu like symptoms, Less rash | 
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            | 86. Who is at risk for transient aplastic crisis caused by Parvo B19? | 
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        | 86. sickle cell anemia patients | 
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            | 87. What is the risk for pregnant women who contract parvo B19? | 
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        | 87. transplacentally transmitted, can result in fetal anemia, hydrops fetalis, miscarriage | 
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            | 88. What is Parvo B19 sometimes confused with? | 
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        | 88. Rubella | 
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            | 89. When are patients most infectious? | 
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        | 89. prior to rash, difficult to prevent because diagnosis by appearance of rash | 
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            | 90. What’s the best way to prevent spread of Parvo B19? | 
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        | 90. Good Hygiene practices | 
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            | 91. What are the 2 genus of the Poxviridae Family? | 
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        | 91. Variola virus and Vaccinia virus | 
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            | 92. What is unique about the Poxviridae structure? | 
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        | 92. Large non-icosahedral complex structure, Intracellular virus, core and lateral bodies surrounded by envelope; Large double strand linear DNA with proteins | 
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            | 93. What is unique about Pox replication? | 
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        | 93. Cytoplasmic Replication, has everything it needs to replicate on it’s own. | 
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            | 94. In Pox replication, what happens in the uncoating I step? | 
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        | 94. Virus enters cell, loses outter membrane, releasing core particle into the cytoplasm | 
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            | 95. What happens in the uncoating II step of Pox replication? | 
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        | 95. After Early transcription and mRNA translation, Early proteins complete uncoating of DNA and release into cytoplasm, DNA replication begins in cyto | 
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            | 96. Where are the virus factories for Pox replication? | 
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        | 96. Cytoplasm | 
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            | 97. Where does the virus get it’s envelope? | 
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        | 97. Derived de novo, crescents with no detectable contacts with exiting membranes begin to envelope core structures | 
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            | 98. What are the pertinent infectious agents in the real world? | 
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        | 98. Extracellular enveloped virus (EEVs) | 
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            | 99. What 2 pox viruses specifically cause human disease? | 
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        | 99. Variola and Molluscum | 
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            | 100. What does variola cause? | 
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        | 100. smallpox | 
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            | 101. What are the 2 basic forms of small pox? | 
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        | 101. variola major and variola minor | 
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            | 102. How is Smallpox spread? | 
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        | 102. inhalation of virus released from ruptured mouth lesions. | 
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            | 103. Where is the generalized rash of smallpox mostly found? | 
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        | 103. Head and Limbs | 
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            | 104. How is Smallpox distinguished from chickenpox? | 
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        | 104. Small pox – febrile prodrome, firm well defined lesions (like BBs) develop pit (umbilicated), all lesions will be at the same stage. | 
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            | 105. When is smallpox most contagious? | 
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        | 105. small red spots in mouth and tongue rupture | 
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            | 106. How long are patients contagious? | 
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        | 106. until last scab falls off | 
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            | 107. What are the 2 forms of Molluscum contagiousum? | 
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        | 107. Childhood and young adulthood forms | 
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            | 108. What are the characteristics of Childhood form of molluscum? | 
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        | 108. –Lesions on face, trunk, and limbs; -spread by direct contact from skin; -mostly tropical | 
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            | 109. What are the characteristics of the Young adulthood form of molluscum? | 
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        | 109. Lower abdomen lesions, sexually transmitted | 
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            | 110. What is vaccinia? | 
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        | 110. modern day prototype of small pox, lab strain, used for small pox vaccines | 
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            | 111. What 4 key features are necessary for eradication? | 
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        | 111. 1. Humans only reservoir, 2. No healthy carriers, 3. No subclinical infections, 4. Effective vaccine afailable | 
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            | 112. Who should not receive the smallpox vaccine? | 
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        | 112. Pregnant or breast-feeding women; immunocompromised; People with eczema, atopic dermatitis, or severe acne; non-emergency situations under 18yo, heart disease patients | 
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            | 113. How can adverse reactions to the smallpox vaccine be treated? | 
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        | 113. VIG- vaccinia immune globulin | 
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            | 114. What are some non-life threatening complications of the smallpox vaccine? | 
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        | 114. generalized vaccinia, inadvertent inoculation, erythema multiforme | 
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            | 115. What are some Life-threatening complications of the smallpox vaccine? | 
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        | 115. progressive vaccinia, postvaccinial encephalitis, eczema vaccinatum, myopericarditis or MI | 
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            | 116. What can a defect in immune globulin cause in a patient receiving the smallpox vaccine? | 
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        | 116. progressive vaccinia | 
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            | 117. What family is the Polyoma virus in? | 
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        | 117. Papovaviridae | 
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            | 118. What is the structure of Polyoma virus? | 
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        | 118. circular double-strand DNA genome packaged around histones, non-enveloped icosahedral capsid | 
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            | 119. How does replication of polyoma occur in permissive cells? | 
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        | 119. replication and assembly of progeny occurs in nucleus, released by cell lysis | 
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            | 120. How does replication of polyoma occur in non-permissive cells? | 
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        | 120. infection leads to transformation of cells, integrates into host chromosome | 
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            | 121. What can transformation of non-permissive cells lead to? | 
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        | 121. tumor formation | 
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            | 122. What are the T antigens responsible for? | 
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        | 122. Transformation; Small T and large T – immortalize cells, small T and middle T – transform cells | 
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            | 123. What are the 2 known human polyoma viruses? | 
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        | 123. BK and JC | 
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            | 124. Are the human polyoma viruses oncogenic? | 
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        | 124. No | 
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            | 125. Where does polyoma initially replicate? | 
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        | 125. Respiratory of GI tract | 
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            | 126. What happens after initial infection? | 
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        | 126. Viremia, passage to kidney, lung, or brain, persistently infect kidney | 
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            | 127. Who is Polyoma a problem for? | 
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        | 127. Immunodeficient; transplant patients, AIDS | 
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            | 128. Where can BK be isolated from? | 
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        | 128. urine of AIDS patients | 
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            | 129. What is the etiologic agent of progressive multifocal leukoencephalopathy? | 
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        | 129. JC | 
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            | 130. What is PML? | 
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        | 130. demyelinating disease of CNS, Reactive JC virus infects and lyses oligodendrocytes, Culture not practical, No virus specific treatment | 
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            | 131. What is the structure of the Herpesvirus? | 
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        | 131. iscosahedral capsid surrounded by lipid envelope with virus-encoded glycoproteins | 
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            | 132. Where is Herpesvirus replicated? | 
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        | 132. Replicated and assembled in the nucleus | 
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            | 133. What Herpesviruses are neurotropic? | 
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        | 133. HSV-1, HSV-2, VZV | 
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            | 134. What herpesviruses are lymphotropic? | 
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        | 134. CMV, HHV-6, HHV-7, EBV, HHV-8 | 
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            | 135. What does the primary infection of VZV cause? | 
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        | 135. chickenpox | 
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            | 136. What are the symptoms of chickenpox? | 
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        | 136. fever, itchy rash for 1 week, Late winter/early spring, | 
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            | 137. What does a reactivated infection of VZV cause? | 
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        | 137. shingles | 
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            | 138. Where does the rash occur in shingles? | 
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        | 138. along the thoracic dermatome | 
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            | 139. Who is most at risk for CMV? | 
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        | 139. Transplant Patients! | 
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            | 140. Where is CMV found in the body? | 
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        | 140. anything wet – saliva, urine, breast milk, semen, cervical secretions, blood | 
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            | 141. What cells does CMV infect? | 
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        | 141. B-cells, causes large, puffed up lymphocyts | 
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            | 142. What is a diagnostic feature of CMV? | 
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        | 142. Large Lymphocytes | 
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            | 143. What does CMV infection in Neonates cause? | 
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        | 143. deafness and mental retardation | 
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            | 144. What is the treatment for CMV? | 
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        | 144. Ganciclovir | 
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            | 145. What does EBV cause in adolescence? | 
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        | 145. Infectious mononucleosis | 
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            | 146. What can EBV cause in AIDS patients? | 
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        | 146. hairy leukoplakia | 
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            | 147. What is Burkitt’s lymphoma? | 
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        | 147. Neoplasm of B-cels that affects bones of the jaw, caused by EBV | 
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            | 148. What 3 factors is Burkitt’s lymphoma associated with? | 
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        | 148. Early EBV infection, Activation of c-myc, Malaria | 
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            | 149. What kind of carcinoma is associated with EBV and a high salt diet? | 
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        | 149. Nasopharyngeal carcinoma | 
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            | 150. What types of Herpesvirus cause Roseola? | 
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        | 150. HHV-6 and HHV-7 | 
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            | 151. What is the principal symptom of Roseola? | 
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        | 151. High fever | 
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            | 152. What herpesvirus is associated with Kaposi’s sarcoma? | 
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        | 152. HHV-8 | 
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            | 153. What Herpesviruses are Ubiquitous in all US populations? | 
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        | 153. VZV EBV HHV-6 HHV-7 | 
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            | 154. What Herpesviruses are typically acquired in early childhood in the US? | 
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        | 154. VZV, HHV-6, HHV-7 | 
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            | 155. What Herpesviruses are sexually transmitted? | 
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        | 155. HSV-1, HSV-2, CMV, HHV-8 |