Flashcards in Lecture 12- Influenza Deck (24):
Ubiquitous in humans
common cause of illness and death
-causes epidemics and threats of pandemics
-large social/financial impact
Types of Influenza
-Influenza A, B and C
C not common
Structure of Influenza
single stranded RNA - sense virus. RNA is segmented, allows to unrelated RNA segments to SHARE genetic material.
-Envelope derived from host cells, studded with glycoproteins that allow in/out of cells
A bird virus
Humans are 'incidental'
-lots of subtypes based on different surface glycoproteins (haemagglutinin and neuraminidase)
-strains named by H & N type + place/year
A/H1/N1/Mexico City 2009
a human virus (only human-human)
- only 1 type of hemagglutinin and neuraminidase
-strains named after year & place of origin
Glycoprotein on influenza cell membrane
-allows for the binding/attachment to sialic acid, allowing entry into cell
Glycoprotein on influenza cell membrane.
- cleaves H from sialic acid, allowing exit from host cell. (otherwise it would get stuck), now virus is free to go infect other cells
Drugs against: only useful early on.
What strains of influenza are currently circulating
2 A strains
AH1N1: 'spainish flu', countless death, young died eldery protected (had immunity).
1 B strain
these are SEASONAL (flu season is winter)
Seasonal difference of influenza
little to none in summer. (nothing circulating)
Big peaks in winter
Recovery from influenza results in immunity... But then how do we get further infection & epidemics every year
immunity only lasts a few years. The flu virus doesn't 'proof read', virus mutates enough to be sufficiently different. "antigenic drift", slowly changing over time. ABs formed against H are ineffective if the virus changes enough. This mainly occurs with hemagglutinin.
Influenza A & B are ALWAY undergoing antigenic drift.
Frequency of Influenza attacks
kids:3-4 years (decreased memory)
Adults : 8 years
continuous minor changes in antigens. Leads to repeated infection with AH1N1, A H3N2 and influenza B
Pathology of Influenza
kills cells 'cytopathic' . Cells always regenerated
There is a very short incubation period (one day) before viral production peaks at day two. therefore fast infection/transmission in flu. How does the correlate with INF-a
INF-a released by lymphocytes and NK cells to try fight infection, peaks around day 1-2, when viral load is highest, and is the thing that causes the bulk of bad flu symptoms
Flu Virus transmission
-coughing, sneezing, talking
-requires close contact bc droplets dont' remain suspended in air
Contact spread (can remain viable on a smooth surface for 24hrs, not infectious once dried)
You can reduce the symptoms by half a day if you use certain drugs (oseltamivir) within the first 48hrs, why does this often not work
Because people rarely get to the doctor/ address their symptoms in this time.
-used for prevention, in hospital, rest homes etc.
Main why of reducing influenza virus. Why is this constantly changing?
Vaccine. changes due to antigenic drift.
How is a flu vaccine formed
circulating (H) gene we are worried about is combined with the non-virulent lab strain (H) gene, forming the
this is then cultivated in chick embryos, inactivated broken, split and washed so you don't get any virus RNA in the vaccine, just the Haemmaglutinin antigen
need protection against all 3 strains.
-only need little changes every year
-hard to cover all strains
In healthcare, who does vaccinations benefit?
Not only healthcare workers, but also their patients
-reduces death by 2/3
When theres an abrupt introduction of a new H or N gene. New A virus comes up.
-flu ! virus leaps from another species to humans and cause diseases = zoonotic flu = bird flu
Multiple different H genes out there, but most DON'T have the ability to..
Pandemic occurs when
an influenza strain emerges with surface proteins completely different from those on the influenza virus that have been circulating for recent decades.
No-one has AB to these, everyone susceptible to illness,.