Here is the ppt for D. M.... Good luck, Saturn

1. ARBOVIRUSES:TOGAVIRUSES & BUNYAVIRUSES EDWARD-BENGIE L. MAGSOMBOL, MD FPCP, FPCC, DASNC Associate Professor, Department of Microbiology Fatima College of Medicine

2. I. INTRODUCTION New pathogenic viruses emerging due to human practices 500 known arboviruses, 100 pathogenic to humans and 50 to animals includes unrelated viruses that are arthropod-borne but now also includes non-arthropod-borne but morphologically similar viruses (Hantaan) arthropods: mosquitoes, ticks, flies. mites

3. clinical syndromes: mostly mild, acute, undifferentiated febrile illness complications: rash, hemorrhage, encephalitis, hepatitis or renal failure found in almost all parts of the world including the Arctic Ex. of outbreaks: Rift Valley Fever, Egypt (1970s) Yellow fever, West Africa (1986-1991)

4. II. VIRUS STRUCTURE AND GENETICS Families: Togaviridae, Flaviviridae, Bunyaviridae Genera: 1. Togaviridae: 4 members but Alphavirus is the only arthropod borne a. Alphavirus : ssRNA (+) stranded Spherical, 60-70 nm, enveloped 3 structural CHONs: capsid, glycosylated E2 and E1 WEE, EEE, VEE b. Rubivirus : Rubella c. Pestivirus and Arterivirus (non-pathogenic to humans)

5. 2. Flaviviridae: ssRNA, (+) stranded, 40-50 nm, enveloped 3 structural CHONs: capsid, glycosylated CHON small, membrane associated non-glycosylated CHON Ex. dengue, yellow fever, Jap B Encephalitis, St. Louis Encephalitis, Russian Spring Summer Encephalitis, Prowasan

7. 3 glycosylated CHONs enveloping virions nucleocapsid (M or middle RNA segment) (S or small RNA segment) (L or large RNA segment) no matrix proteins polymerase, other CHONs

8. alpha, flavi, and bunya viruses are all sensitive to lipid solvents and heat important survival mechanism: generating genetic diversity escape from immune responses, adaptation to new hosts, alter replication patterns 1. genetic drift = deletions, mutations and inversions (alpha, flavi, rhabdo) 2. genetic shift = genome segment reassortment (bunya, orbivirus) recombination= not known for arboviruses

9. III. DIAGNOSIS due to prior exposure, absolute Ab titers may be misleading virus-specific peptides virus-specific IgM titers helpful only in some cases most accurate method: isolation of virus from serum culture via: intracerebral inoculation of suckling mice continuous cell lines (mosquito cells)

11. Genome encodes early (non-structural) and late (structural) proteins

13. TOGAVIRUSES

14. TOGAVIRUSES: Mosquito Vectors Culex Aedes triseriatus Culiseta melanura

17. Diseases spread by animals or with an animal reservoir  zoonotic

19. Individual viruses with different tissue tropisms

21. Entire flavivirus genome translated into a single polyprotein

22. Replicate in the cytoplasm and bud at the plasma membranes

24. Humans are usually “dead-end” hosts due to absence of persistent viremia

25. Female mosquito acquire the viruses by taking a blood meal from a viremic vertebrate host

27. Urban outbreaks occur when the reservoirs for the virus are humans or urban animals.

29. Viruses establish systemic infection and viremia.

32. Flu-like symptoms correlate with systemic infection during the initial viremia

34. Vector: Aedesaegypti

36. TOGAVIRUSES: Alphaviruses Disease Mechanisms of Togaviruses & Flaviviruses

40. Infects upper respiratory tract  local LN (+ LAD)  viremia  infection of other tissues

41. Prodromal period lasts approx. 2 weeks

43. Immune complexes most likely cause the rash and arthralgia associated with the infection.

44. CMI important in resolving the infection

46. Alter normal growth, mitosis, and chromosomal structure of the fetus’s cells

47. Nature of the disorder determined by:Tissue affected Stage of development disrupted

49. Fetus at risk until 20th week AOG

52. I.P. = 14 – 21 days

53. 3-day maculopapular or macular rash + swollen glands

54. Infection in adults may be more severe

55. Arthralgia & arthritis

58. Diagnosis confirmed by the presence of anti-rubella-specific IgM

60. Broken down into four genera on the basis of structural and biochemical features

61. Unlike other negative-strand RNA viruses, they do not have a matrix protein

63. BUNYAVIRIDAE

65. Virus in arthropod can be transmitted to its eggs  allow virus to survive during winter

66. Effects:Neuronal & glial damage + cerebral edema encephalitis Hepatic necrosis (e.g. Rift Valley Fever) Leakage of plasma & erythrocytes through vascular endothelium  hemorrhagic fever

68. Virus transmitted to rodents, birds and larger animals  become reservoirs

70. Hantaviruses without arthropod vector  maintained in a rodent species specific for each virus

73. Non-specific febrile flu-like illness

75. Fever, headache, lethargy, vomiting

77. Headache, petechial rash, shock, and renal failure

79. Influenza-like symptoms followed by acute respiratory failure

81. ELISA – detect antigen to clinical specimen from patients with intense viremia