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INTRODUCTION
• Cause RTI
• Genetic variation (shift and drift)
• Estimated 40-50 million deaths
worldwide in pandemic of
1918-1919
PROPERTIES
• Classification:
- Family: Orthomyxoviridae
- Genus: Three genera according to matrix
protein and nucleoprotein:
. Influenza A, & B
A (Human & animal; moderate to
severe illness, shift and drift)
B ( Human, milder illness, only drift)
. Influenza C (Animal, rarely human)
. ‘thogoto-like-viruses’ (Animal)
ORTHOMYXOVIRUSES
HA - hemagglutinin
NA - neuraminidase
helical nucleocapsid (RNA plus
NP protein)
lipid bilayer membrane
polymerase complex
M protein
Morphology
• Helical, 100-200 nm.
• Enveloped
• Proteins:
-
-
Hemagglutinin (HA, 80%, 15 subtypes; H1-H15):
Agglutinate RBC, Attachment
Neuraminidase (NA, 20%, 9 subtypes; N1-N9):
Destroy neuraminic (Sialic) acid from the receptor
protein (Release the virus)
M2 protein: Ion channels, protons entry
Matrix protein (M): Assembly
The HA and NA
antigens of
influenza
Genome:
8 fragments of –ss RNA
Replication:
Endocytosis Nucleus Budding
Cellular replication of influenza
virus
Genetic variation
Antigenic shift: Pandamics
•
•
•
•
Decade (10 years)
Inf. A
Human strain + Animal strain
Infect same cell Genetic reassortment
Complete change
Antigenic Shift
Genetic reassortment
Genetic reassortment with
influenza A
Antigenic drift: Epidemics
•
•
•
•
Annual
Inf. A & B
Mutation (Deletion and insertion
Incomplete change
Antigenic Drift
(Mutation)
Antigenic shift and drift
Pandemics and Pandemic
Threats of the 20th Century
•
•
•
•
•
•
•
•
•
1918-19 “Spanish flu”
H1N1
1957 “Asian flu”
H2N2
1968 “Hong Kong flu”
H3N2
1976 “Swine flu” episode
H1N1
1977 “Russian flu”
H1N1
1997 “Bird flu” in HK
H5N1
1999 “Bird flu” in HK
H9N2
2003 “Bird flu” in Netherlands H7N7
2004 “Bird flu” in SE Asia
H5N1
CLINICAL ASPECTS
•
•
Incubation period: 2-3 days
Symptoms: Shivering, malaise, headache, aching,
rise T
PATHOGENESIS
Droplets URT Multiply in epith. cells Destroy cilia
•
Decreased clearance
• Risk bacterial infection
• Viremia rare
•
Secondary bacterial infection:
- S. aureus
- S. pneumonia, H. influenza, and hemolytic
streptococcus
•
Complication ( Rey`s syndrome): Often type B:
- Encephalitis
- Liver & Viscera
FATAL
IMMUNE RESPONSE
•
•
Humoral: Is not important
Cellular: TC cells & Macrophages
Vaccines:
•
Killed or inactivated (Inf. A & B):
•
•
- Whole virus: Local reaction
- Split: Less local reaction
- Subunit or surface antigen: Save
Live attenuated: Adapted to grow at less
Temp. e,g., 25o C
Reassortment genes: Under test
Subunit influenza
vaccine