1. Viral Disease Slackers Facts by Mike Ori

2. Disclaimer The information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes. The document can mostly be used forward and backward. I tried to mark questionable stuff with (?). If you want it to look pretty, steal some crayons and go to town. Finally… If you’re a gunner, buck up and do your own work.

3. What are the three types in Orthomyxoviruses

4. A, B, C

5. Seasonal flu is what type?

6. Type A

7. Describe the genome of orthomyxovirus

8. Segmented ssRNA (-)

9. To what do H and N refer to

10. Hemagglutinin and neuraminidase spikes on the viral surface

11. In which portion of the cell orthomyxovirus replicate and why?

12. In the nucleus because they cannot prime their RNA strands

13. Why is the seasonal flu shot seasonal?

14. A new vaccine is required each year because of antigenic drift due to polymerase errors

15. Why does bacterial pneumonia often follow influenza?

16. 1.The virus causes destruction of ciliated respiratory epithelium in the upper respiratory tract. This degrades the mucociliary elevator and prevents efficient clearance of bacteria. 2.General immune system down regulation occurs as the influenza infection is controlled.

17. What is the basis for the increased virulence seen in H1N1 of swine origin

18. Antigenic shift has substantially altered the virus to reduce its antigenic similarity to previous strains and to allow it to replicate in both the upper and lower respiratory tract.

19. Why are people over 50 less likely to get sick from H1N1 swine origin.

20. 1.An similar pandemic occurred within their lifetime. 2.They do not have as robust an immune system and cannot generate as much of a cytokine storm

21. Why is avian flu H5N1 difficult to get

22. Currently the strain’s H antigen interact with sialic acid alpha 2,3 gal receptors which are situated in the lower respiratory tract. Thus it take larger exposures to transmit the disease.

23. What would occur if H5N1 reassorts in swine

24. Why are swine important intermediates in the assortment of avian and human influenza?

25. Swine upper respiratory epithelium contains sialic a2,3 gal and sialic a2,6 gal receptors thus they can be easily coninfected with both human and avian virus. This allows nature to tinker. Idle goddesses are the devils workshop.

26. What will happen if H5N1 reassorts or mutates to efficiently infect both upper and lower respiratory epithelium.

27. The potential for significant mortality

28. What are the requirements of a pandemic influenza

29. 1.New human type A strain 2.Causing serious illness 3.Easily spreads person to person

30. What diseases are caused by paramyxovirus

31. Mumps Parainfluenza and croup Rubeola (5 day measles) Respiratory syncitial virus

32. Describe the paramyxovirus spikes

33. Combined H and N on single spike (para=next to hence H is para to N) Fusion (F) protein on second spike

34. What is a syncitia and why do they form

35. A syncitia is a giant cell that forms by fusion of multiple cells. Paramyxovirus tends to form syncitia through the action of F protein deposited on cell surfaces.

36. Distinguish parainfluenza from Respiratory syncitial virus

37. Parainfluenza = bronchitis RSV = bronchiolitis

38. Describe RSV epidemiology

39. Occurs from the late fall to the spring. Predominantly affects small children < 1 yo.

40. Describe RSV immunity

41. Immunity is incomplete. Repeated infections occur with lessened severity but its unclear if there is an immune basis.

42. RSV diagnosis

43. Immunofluorescence of nasal swabs

44. RSV prophylaxis

45. Injection of monoclonal antibody against factor F is indicated in high risk children

46. Its flu if?

47. It looks like a cold but also has Myalgia/arthralgia Fever

48. Adenovirus structure

49. Linear dsDNA

50. Adenovirus disease

51. URI particularly in children

52. Adenovirus persistence

53. DNA virus can establish latent/carrier state

54. What viruses are responsible for the common cold?

55. Rhinovirus Coronavirus Reovirus

56. What is a exanthema?

57. Circle the correct answer Choose wisely grasshopper A.A widespread rash B.An out of date national anthem. C.Last years skirt lengths

58. List the common exanthem viruses and families

59. IllnessGenusfamily MumpsParamyxovirusparamyxoviridae MeaslesMorbillivirusparamyxoviridae RubellaRubivirustogaviridae Roseola infantumHHV6, adenovirus, coxackie virus, echovirus Erethema InfectiosumParvovirus B19

60. What is the basis of the vaccine for these diseases

61. Combined attenuated vaccine for measles, mumps, and rubella. This avoids a rash of shots.

62. Mumps time course

63. 16 day incubation 7 day clinical disease

64. Mumps complications

65. Orchitis Meningitis Encephalitis

66. Rubeola (Measles) time course

67. 10 day incubation 5 days of rash Koplik spots 1-2 days prior to exanthema

68. Rubeola epidemiology

69. Occurs in unimmunized people typically in childhood or teens during the winter and spring.

70. What is unique about morbillivirus spikes

71. Even though they are paramyxoviridae they lack N activity. Thus they have H and F spikes as opposed to H/N and F typical of other paramyxoviridae.

72. What are koplik spots

73. Small bluish yellow spots that appear on the oral mucosa in advance of the rubeola rash

74. Rubeola complications

75. Post infectious encephalitis in near term SSPE (encephalitis) in 2-10 years

76. Rubeola sx

77. Progressive rash extending from head to toe. High fever Delirium Photophobia Conjunctivitis

78. Rubella time course

79. Incubation period 16 days Exanthema for 3 days Contagious -7 to +7 from rash

80. Rubella epidemiology

81. Occurs in unimmunized people usually in the winter and spring

82. Should pregnant women receive MMR vaccine?

83. No, MMR is a live vaccine and rubella is a transplacental infective agent. Reversion of rubella to a virulent form could lead to congenital rubella in the child.

84. Congenital rubella sx

85. Cataracts Cardiac defects Reticuloendothelial defects (liver, spleen, thrombocytes) Mental retardation

86. What is the mechanism of spread for MMR?

87. All enter the respiratory tract to cause viremia before moving to their tropic tissue

88. What are the tropic tissues for MMR?

89. Mumps – salivary glands, testes, ovary, CNS? Measles – skin and Lymph nodes? Rubella – skin and lymph nodes?

90. What is agent for Erythema Infectiosum?

91. Parvovirus B19

92. Where does the exanthema appear?

93. On the face. It has a characteristic slapped face appearance.

94. What is the alternative name for Erythema Infectiosum?

95. Fifth disease

96. A child presents with a faint rash and convulsions. What is a likely diagnosis?

97. Roseola infantum

98. Describe the structure of Enteroviruses

99. They are small naked icosahedral virus with ssRNA (+) in picornaviridae Pico = small rna = RNA

100. What is the transmission path for enterovirus

101. Fecal-oral

102. Describe the stability of enterovirus

103. They are very stable and are resistant to acidic pH, detergents, disinfectants, and alcohol

104. Describe the epidemiology of enterovirus

105. Summer and fall in temperate climes. Year round in the tropics. Transmitted by direct or indirect fecal-oral contact. Vectors occasionally spread the virus.

106. What are the picornaviridae genus?

107. Polio Echo Rhino Coxsackie Hep A (PERCH)

108. What are the three possible outcomes of polio infection

109. Abortive poliomyelitis Aseptic meningitis Paralytic poliomyelitis

110. What is the entry point tissue for polio

111. Oropharynx. Resulting viruses swallowed and infect intestines. Then infect CNS

112. What vaccines are available for polio

113. Salk = killed Sabin = Attenuated

114. Polio diagnostic

115. Viral visualization Ab titer

116. What is the potential contagious period for polio

117. Intestinal shedding can occur for weeks even in the face of effective immune response

118. What is the structure of papillomavirus

119. dsDNA circular. Naked icosahedral

120. How many genotypes of HPV are known

121. 70+

122. What is the transformation potential of HPV

123. It’s a DNA virus and thus can be stabilized in the cell. Higher stain numbers are more oncogenic (?). Malignant strains seem to insert DNA into host genome.

124. HPV Transmission Routes

125. Occupational exposure (meat packers) Sexual contact Public showers/swimming pools (suspected) Perinatally

126. List the diseases associated with common HPV genotypes

127. 1,2 – common warts 7 – meat handler warts 6,11 – benign genital warts 16,18,31,45 – warty lesions with malignant potential in the nethers

128. What percent of females in US are HPV positive?

129. 20%-60%

130. Where does HPV replicate?

131. Nucleus – it’s a DNA virus

132. How is HPV typically diagnosed in females

133. Detected by cytoplasmic vacuolization and nuclear enlargement on routine pap smear

134. What is cryotherapy

135. Removing HPV infected epithelium with extremely cold substances such are liquid nitrogen

136. Describe PML

137. Degenerative brain disease that causes focal areas of demyelination surrounded by bizarre astrocytes.

138. What is the virus of PML?

139. The JC Polyomavirus

140. What is a likely comorbidity in PML PT?

141. HIV

142. A bone marrow transplant patient presents a few weeks after discharge with hemorrhagic cystitis. What is the likely agent

143. BK polyomavirus

144. What is the tropic tissue for BK virus?

145. Kidney

146. What are the general sx of arbovirus

147. Encephalitis Hemorrhagic fever

148. What is the characteristic of an arbovirus?

149. They are all transmitted via insect vectors such as mosquitoes or ticks.

150. What is the family for arboviruses involving horses?

151. Togavirus

152. What commonly togavirus is commonly vaccinated for?

153. Rubella

154. What is the distribution of western, eastern and St Loius encephalitis

155. Western – western us Eastern – Eastern US St Louis – central US?

156. Describe a typical WEE,EEE victim

157. People in association with horses where mosquitoes are present

158. What is the age range for St Loius and West Nile Virus

159. St Loius > 40 West Nile > 50

160. What is the classic distribution for yellow fever

161. Caribbean and south and central america

162. What is the classic distribution of Dengue

163. World wide. Middle east, far east, Africa, Caribbean

164. What is the vector for yellow fever and dengue

165. Aedes aegypti

166. Describe Yellow Fever SX

167. Fever, chills, headache, hemorrhage, jaundice, and shock

168. Describe Dengue sx

169. Severe back and joint pain, fever, rash.

170. What is the reservoir for west nile

171. Birds

172. What is the vector for west nile?

173. Mosquitoes

174. West nile sx

175. Flu-like, Rash on torso and upper extremities

176. Describe the morphology of bunyavirus

177. ssRNA (-), enveloped, spherical, segmented

178. California virus family and sx

179. Bunyavirus Encephalitis with seizures In north central mid west states

180. Hantavirus family

181. Bunyavirus

182. Hantavirus epidemiology

183. Direct exposure to rodent feces. Occurs in the southwestern US

184. Hantavirus sx and mortality

185. Fulminant respiratory disease with > 50% mortality.

186. Reovirus arbovirus disease

187. Colorado tick fever

188. Arenavirus morphology

189. Spherical enveloped ssRNA (+/-) segmented

190. Arenavirus unique characteristics

191. Ambisense (+/-) RNA Presence of host cell ribosomes within virus

192. Filovirus morphology

193. Enveloped ssRNA (-)

194. Filovirus sx

195. Hemorrhagic disease

196. Famous filovirus diseases

197. Marburg and ebola

198. What disease is cased by a rhabdovirus

199. Rabies

200. Rabies virus morphology

201. Bullet shaped enveloped helical ssRNA (-)

202. What is the initial tx for rabies

203. Injection of IgG near bite. Vaccination with killed attenuated virus.

204. Describe the timecourse of rabies

205. Occurs from 10 days to one year depending on inoculum size

206. Classify the final stages of rabies infection

207. Prodrom Acute neurologic phase Coma Death

208. What is the mortality of rabies

209. 100% (only a few exceptions are known)

210. What is the furious phase of rabies infection?

211. Occurs during the acute neurologic phase. Patients are often aggressive and disoriented

212. What is the dumb phase of rabies infection

213. Occurs during the acute neurologic phase. Patients are lethargic and paralytic.

214. Why isn’t everyone vaccinated against rabies

215. The vaccine is a killed attenuated vaccine so people receiving it are double protected form conversion but the protection does not last long so repeated vaccine would be necessary. Rabies is uncommon with proper precautions

216. Rotavirus family

217. Reoviridae

218. Rotavirus structure

219. Small wheel shaped ssRNA (+). 1 segments

220. What are the segmented virus

221. Bunya Orthomyxo Arena Reo (BOAR)

222. What is the epidemiology of rotavirus

223. Infection during cooler months in children < 2 years old. Highly contagious and spreads rapidly in institutions and families

224. Describe Rotavirus disease

225. 1-3 day incubation period followed by abrupt onset of vomiting. Subsequent diarrhea lasting 5-8 days. Virus shedding for 2-12 days

226. Rotavirus prevention

227. Hand washing. Vaccine in development.

228. Rotavirus death factors and numbers

229. Malnutrition and immunodeficient children 600K die worldwide

230. Norwalkvirus family

231. Calcivirus

232. Calcivirus morphology

233. Naked small round ssRNA (+)

234. Norwalk disease

235. 1-2 day incubation 1-2 day vomiting and diarrhea

236. Other diarrhea agents

237. Astrovirus (star shaped naked) Adenovirus