9-10: Influenza Flashcards
symptoms associated with influenza infection
many non-specific symptoms
- fever, headache, dry cough, sore throat, runny/stuffy nose, muscle aches
diagnosis is difficult
influenza A circulation
wild/domesticated birds
then infects humans with new species/subtypes that are permanent
subtype
new species/subtypes of a virus
- divided into genetic clades or groups
each subtype has many strains/variants
influenza A and B circulation
in humans
influenza A: antigenic shift
“mixing” of genes from influenza viruses
caused pandemics from antigenic shift in animal reservoir and then widespread human infections
influenza B: antigenic drift
accumulation of a series of minor genetic mutations
drift is generally linear
well-adapted since its only in humans
influenza A structure
classic RNA virus
- envelope + envelope proteins
hemagglutinin (H) and neurominidase (N)
- main proteins/antigens on the surface of the virus
- 16 major variants of H, 9 major variants of N
- each major variant with hundreds more subtle variants
influenza life cycle
RNA goes and multiples, making new virions which bud and are released
classic and simple
- only infects epithelial cells
- cause most disease in lungs but can spread to the whole body
naming of human viruses
type/location/isolate number/year (subtype)
naming of viruses with a non-human host
type/host/location/isolate number/year (subtype)
strain/isolate number
specific virus obtained from a host
specific to an individual animal/human
three types of influenza causing disease in humans
seasonal
- always one annually
pandemic
zoonotic
usually a zoonotic influenza can become a pandemic which evolves to be seasonal
seasonal influenza
typically occur during winter in temperate climates
in tropical regions, occurs throughout the year
- closer you are to the equator, the more likely you are to have two peaks
flu peaks in Feb for the northern hemisphere
influenza endemic year-round
some infections all the time but epidemic with seasonal influenza every winter
hypotheses to why flu is seasonal
people spend more time indoors in close contact
host factors increase susceptibility/transmission
virus persists longer/transmits better in cold dry weather
immune response to seasonal influenza A
immune system makes antibodies to the specific version of H and N present on the virus
- main antigen targets
- unique and not common so it is not a PAMP
next flu season, variant viruses have subtle changes to H and N so they evade pre-existing antibodies
immune weapons to seasonal influenza A
neutralising antibodies
- IgG and IgA
cytotoxic T cells (CTLs)
both of the above kill infected cells
however, seasonal virus mutates to evade antibodies and CTLs
- need infection or vaccination every few years
antigenic drift in seasonal flu viruses
mutations and changes in H/N antigens
- higher mutation rate with influenza than other viruses
antigenic drift occurs within an influenza subtype and an influenza type
- leads to annual/seasonal flu
antigenic drift vs. antigenic shift
drift
- same subtype
- point mutations
-causes seasonal flu
shift
- genetic reassortment/exchange of gene segments (two different viruses infecting the same cell allowing genetic reassortment of subunits)
- new subtype
- causes pandemic and can be zoonotic
cycles of influenza epidemics/pandemics
caused by antigenic drift/shift
1918 flu
caused by influenza A H1N1
> 500 million infections, 20-50 million deaths
- 2.5% case fatality rate
mortality mostly due to secondary bacteria linfections
1919 flu also caused by H1N1 but fewer deaths because everyone had protection (herd immunity)
unusual features
1. three waves of infections (sign of a pandemic/new flu rather than seasonal)
2. high mortality rate killing 18-45 and males disproportionately
H5N1
2003
virulent in domestic birds
- changed the world of agriculture
doesn’t spread easily to humans but causes severe disease
- 53% mortality (highest so far)
was going to be the new pandemic
new H1N1
2009
first new pandemic influenza infection in 42 years
displacement of old H3N2 and old H1N1
combination of Eurasian and NA swine viruses
- H1N2 that was already a triple reassortment in pigs, Eurasian swine H1N1 from 1918 swine flu
- 6 gene segments from triple reassortment H1N2 and 2 from swine H1N1
not nearly as virulent so lower fatality rate even though it was a brand new pathogen (0.05%)
H9N2
2015
no human-human transmission
endemic in domestic birds
H5N6
2014
domestic bird outbreaks in winter
very high fatality rate (43%)
no human-human transmission
H7N9
2016
no human-human transmission
triple genetic reassortment of three avian flu viruses H7N3, H7N9, H9N2
virus found in respiratory tracts and not just digestive tract
