Today we will be discussing about Flaviviridae.

~Pestivirus : Yellow Fever, Dengue, West Nile
-Hepacivirus : Hepatitis C

Lets talk abt Pestivirus

Natural host(reservoir):Allows amplification of the virus and maintain viremia to allow acquisition by the arthropod.
Host: allows infection, but not necessarily maintain viremia.
Dead-end Host: An host from which infectious agent is not transmitted on.

Properties:

-Spherical enveloped virion, 40-50 nm
-Inner core protein C
-Membrane / matrix protein M
-Envelope with glycoprotein peplomers (E)
-Single linear 11 kb positive sense ssRNA :Infectious mRNA
-3’ polyadenylated tail and 5’ cap
-Cytoplasmic replication (perinuclear)
-Polyprotein from genomic RNA cleaved
-3 structural proteins
-Several non-structural proteins

Now we will talk abt the diseases that are caused by Flaviviridae that is currently troubling the nation now...

Dengue

1. Properties
-Most important arbovirus presently
-Southeast Asia to Americas to Pacific to Africa
-Non-fatal dengue fever (DF)
-Usually fatal dengue haemorrhagic fever (DHF) / dengue shock syndrome (DSS)
-4 distinct serotypes based on neutralisation test.
-DEN-1, DEN-2, DEN-3 and DEN-4
-DEN-2 shows greatest antigenic and genotypic distance from the others
-Protective immunity after infection homotypic

News Update
2007, 1500 cases were reported in the first 19 weeks of 2007.
50% higher than 2006.
Mainly due to Dengue 2, the strain causing 60% of these case.

2.Dengue Infection Cycle


3.Dengue Fever
A.

-Many infections asymptomatic
-Acute infection resulting in fever, severe headache (frontal), retro-orbital pain, nausea and vomiting
-Severe muscle and bone pain
-Severe arthralgia (joint swelling -mainly back) break bone fever
-Maculopapular rash just before recovery

B.Dengue Haemorrhagic Fever/ Dengue Shock Syndrome

-Prior infection and age key factors in DHF and DSS
-Seldom occurs in individuals above 15 years
-Similar to yellow fever in biphasic nature:
~Initial symptoms similar to DF followed by remission
~Sudden deterioration of patent condition
-Severe prostration, hypotension, circulatory collapse, bleeding and shock
-Bleeding
~Petechiae in skin, mucous membranes (mouth)
~Injection and punction sites
~Gastrointestinal bleeding
~Haemorrhagic pneumonia
-WHO grading:
~Grade I : Fever with non-specific, constitutional symptoms and the only haemorrhagic manifestations being a positive tourniquet test
~Grade II : As for grade I, but with specific haemorrhagic manifestations
~Grade III : Signs of circulatory failure or hypotension
~Grade IV : Profound shock with pulse and blood pressure undetectable
-Pathogenesis
~Not well understood despite intensive study –2 theories
~Virulent strain theory
~Some strains more virulent than others
~Molecular studies show variations in sequences amongst different strains within serotypes
~Early evidence pointed to DEN-2
~Antibody enhancement
~Main theory for DHF / DSS
~Main cell target of DEN: monocytes / macrophages
~Most cases of DHF/DSS had prior infection or infants below 1 year had maternal Ab
~Monkey experiments showed similar enhancement
-Possible cause

~Immune system overreacting
~Sever Acute Respiratory Syndrome

-Transmission - Aedes Mosquito (Female)
-Control:
1.Use of Insecticides
2. Use of Mosquito Screen
3. Removal of Stagnant water

Yellow Fever

1.Properties
-Type species of genus flavivirus
-"flavi" –"yellow" in Latin
-Tropical disease in Latin America and Africa
2.History
-Incubation period: 3-6 days
-Viraemia, infectious, headache, malaise, nausea, lassitude, muscle ache (3 days)
-Flushing of head & neck, conjunctival injection, strawberry tongue

3.Severe Yellow Fever
-Remission after acute yellow fever
-Haemorrhagic, hepatic and renal disease
-Fever, vomiting, abdominal pain, dehydration, prostration
-Haemorrhagic / coffee-ground diathesis (black vomit)
-Bleeding from puncture sites of injections and drip needles
-Jaundice

-Massive haematemesis / haemoptysis / intra-abdominal bleeding
-Renal failure, hypotension, shock
-Virus absent from blood, but antibody titre high –implying autoimmunity may play major role
-Mortality 20-50%
-Survivors suffered extended chronic jaundice before full recovery; hepatic and renal failure may persist
4.Transmission:
5.Control:
- Attenuated Vaccine


West Nile Fever

1.History
-Originated in Uganda
-Discovered in 1937
-Common in Africa, West Asia, Europe, Middle East
-Spread in US (New York) began in 1999
-Epidemic in US in 2002
2.West Nile Fever
-Mainly mild to no symptoms
-Fever
-Headache, body aches
-Skin rash
-Swollen lymph glands
-Severe symptoms
~Crossing blood-brain barrier
~Encephalitis
~Meningitis
-Mainly in persons above 50 years
3.Transmission:

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