Influenza
Introduction
● Subtypes: A. B, C
● Virus has many reservoirs in nature, is always present in environment
● Incubation period: 1-4 days. Causes antibody response to envelope proteins haemagglutinin (H) and
neuraminidase (N). Type of H + N determine infection severity
● H = binds to sialic acid (α2,3 or α2,6). HA1 - initial binding, HA2 - membrane fusion.
● NA = ensures effective release of progeny virus from infected cells. Cleaves HA-SA interactions. Targeted by
antiviral drugs.
● M1 = Matrix protein that forms a protective layer just under the viral envelope. Most abundant protein
● M2 = Envelope protein. Acts as an ion channel so pH in viral cytoplasm can be adjusted allowing viral and
endosomal membrane fusion and release of viral nucleic acids
● NP = Surrounds the viral genome segments so protecting them from damage. Interacts with viral and cellular
proteins to ensure effective viral gene expression.
● Human subtypes H1N1, H3N2, H1N2. Each animal has its own subtypes it can be infected with/transmit
Entry
● H binds to sialic acid on host cell. Sialic acid found on end termini of galactose. Type of galactose +
sialic acid binding (eg. α2,6 or α2,3) allows different types of H+N subtypes to bind (eg. human, avian).
This is receptor specificity
● Binding allows envelope of virus and host cell membrane to fuse. Endocytosis occurs and
virion contents released into cytoplasm → replication
Replication
● Capsid assembly → envelope protein synthesis and glycosylation in Golgi → packaged RNA
segments are enveloped by host membrane → mature virions bud out of cell membrane
● N cleaves sialic acid receptor to release progeny virus
Epidemics
● Disease incidence and RNA isolates are monitored
● If 2 virus subtypes infect same cell, reassortment can occur which gives increase viral fitness and harder to
treat and evades immune system
● A more segmented genome leads to seasonal epidemic
● Antigenic changes ie drift (mutations in epitopes) or shift (recombination forms new H subtype) can cause
pandemics. No immunity in population so spreads easily
● During major pandemics, eg 1918 Spanish flu, secondary infections are common and often confused as cause
of death
○ Is possible a novel virus with effective transmission and high pathogenicity could occur again
● Influenza will always be present. Best way to deal with it is to prepare for pandemics with surveillance
● H5N1 mutations prone to acquisition of more mutations allowing more effective transmission through ability
to easily replicate and be spread as aerosol virus
● Difficult to make vaccines for avian flu because experiments involve working with activated forms
Introduction
● Subtypes: A. B, C
● Virus has many reservoirs in nature, is always present in environment
● Incubation period: 1-4 days. Causes antibody response to envelope proteins haemagglutinin (H) and
neuraminidase (N). Type of H + N determine infection severity
● H = binds to sialic acid (α2,3 or α2,6). HA1 - initial binding, HA2 - membrane fusion.
● NA = ensures effective release of progeny virus from infected cells. Cleaves HA-SA interactions. Targeted by
antiviral drugs.
● M1 = Matrix protein that forms a protective layer just under the viral envelope. Most abundant protein
● M2 = Envelope protein. Acts as an ion channel so pH in viral cytoplasm can be adjusted allowing viral and
endosomal membrane fusion and release of viral nucleic acids
● NP = Surrounds the viral genome segments so protecting them from damage. Interacts with viral and cellular
proteins to ensure effective viral gene expression.
● Human subtypes H1N1, H3N2, H1N2. Each animal has its own subtypes it can be infected with/transmit
Entry
● H binds to sialic acid on host cell. Sialic acid found on end termini of galactose. Type of galactose +
sialic acid binding (eg. α2,6 or α2,3) allows different types of H+N subtypes to bind (eg. human, avian).
This is receptor specificity
● Binding allows envelope of virus and host cell membrane to fuse. Endocytosis occurs and
virion contents released into cytoplasm → replication
Replication
● Capsid assembly → envelope protein synthesis and glycosylation in Golgi → packaged RNA
segments are enveloped by host membrane → mature virions bud out of cell membrane
● N cleaves sialic acid receptor to release progeny virus
Epidemics
● Disease incidence and RNA isolates are monitored
● If 2 virus subtypes infect same cell, reassortment can occur which gives increase viral fitness and harder to
treat and evades immune system
● A more segmented genome leads to seasonal epidemic
● Antigenic changes ie drift (mutations in epitopes) or shift (recombination forms new H subtype) can cause
pandemics. No immunity in population so spreads easily
● During major pandemics, eg 1918 Spanish flu, secondary infections are common and often confused as cause
of death
○ Is possible a novel virus with effective transmission and high pathogenicity could occur again
● Influenza will always be present. Best way to deal with it is to prepare for pandemics with surveillance
● H5N1 mutations prone to acquisition of more mutations allowing more effective transmission through ability
to easily replicate and be spread as aerosol virus
● Difficult to make vaccines for avian flu because experiments involve working with activated forms
