Influenza Flashcards
(48 cards)
1
Q
Payload of a virus
A
- contains the genome and enzymes necessary to initiate the first step in virus replication
2
Q
Influenza overview
A
- Flu is an acute viral infection of the respiratory tract (nose, mouth, throat, bronchial tubes and lungs)
- Highly infectious illness which spreads rapidly in closed communities
- Even people with mild or no symptoms can infect others
- Most cases in the UK occur during an 8 to 10 week period during the winter
3
Q
what type of viruses are influenza viruses
A
orthomyxoviruses
4
Q
orthomyxoviruses
A
- Spherical
- Enveloped
- Segmented, negative strand RNA genome
5
Q
influenza genes
A
negative strand RNA genome
8 genes encoding 11 proteins, including 11 proteins including 3 RNA polymerases (high error rates)
6
Q
what are the two surface antigens
A
Haemagglutinin and Neuraminidase
7
Q
Haemagglutinin (H)- 18 types
A
Binds to the cell of the infected person
8
Q
Neuraminidase (N)
A
9
Q
types of influenza
A
Influenza A virus
Influenza B virus
Influenza C virus
10
Q
Influenza A viruses
A
- Causes outbreaks most years and are the usual cause of epidemics and pandemics
- Live and multiply in many different animals and may spread between them
11
Q
Influenza A: Natural host range
A
- Birds particularly wildfowls
- Swine
- Equine
- Marine mammals
12
Q
Influenza A: Epidemiology
A
Antigenic shift and drift
13
Q
Influenza B viruses
A
Tends to cause less severe disease and smaller outbreaks
14
Q
Influenza B: natural host
A
Predominantly found in humans
15
Q
influenza B: burden of disease
A
mainly children
16
Q
influenza B: epidemiology
A
- Antigenic drift only
- 2 lineages cocirculate
17
Q
Influenzas C
A
Mild disease without seasonality
18
Q
Influenza C: Natural host range
A
- Humans
- Swine
19
Q
Influenza C: epidemiology
A
- Antigen drift only
- Multiple variants
20
Q
replication of the influenza virus
A
21
Q
Transmission of the influenza virus
A
Influenza viruses are transmitted from person to person via the respiratory route (coughing, sneezing, inhaling)
22
Q
Three potential modes of transmission
A
- Small particle aerosols (<10um mass diameter)- remain suspended in air for many hours
- Larger particles or droplets will typically fall to the grounding within 3m of the infected persons- direct contact
- Viral particles could land on surfaces where influenzas viruses remain infectious- infect others through indirect contact
23
Q
Barriers to entry via the respiratory route
A
- Respiratory epithelial cells are covered by a thick glycocalyx and tracheobronchial mucus that can trap particles
- Ciliated resp epithelial cells continually sweep mucus up from the lower resp tract into the upper respiratory tract where it is swallowed
- In the lung- immunologic defences
- Include secretory igA
- NK cells
- macrophages
24
Q
So how does the virus enter cells?
A
Haemaglutinin binds to Neu5Ac (NANA) residues – sialic acid on a glycoprotein/glycolipid which acts as a receptor for influenza virus
entry via receptor mediated endocytosis
25
26
**So how does the virus leave the cell?**
**Neuraminidase** comes along and cleaves sialic acidà then able to leave the cell and infect cell
27
MSK symptoms of influenza
* Myalgia- muscle ache
* fatigues
28
neurological symptoms of influenza
* Fever
* Confusion
* Serious: meningitis- rare
29
respiratory symptoms
* Dry cough
* Sore throat
* Nasal congestion
* Serious: otitis media and croup
30
GI symptoms
* Nausea
* Vomiting
* Diarrhoea
31
overview of symptoms fo influenza
32
diagnostic test?
Mostly done on history and not formal test (bar those in hospital)
* Antigen detection- rapid diagnostic test
* RT-PCR
33
treatment
* antivirals
* neurominidase inhibitors
34
antivirals
* **Antivirals (used less now)**
* E.g. rimantadine and amantadine
* Which inhibit viral uncoating after uptake probably through M2 **protein influenzas A**
35
**Neuraminidase inhibitors**
* Oseltamivir (Tamiflu), Zanamivir (relenza)
* Inhibits viral release from infected cells and cause aggregation of viral particles
36
prevention
* Formalin-inactivated vaccine (quadrivalent/ trivalent) by injection of influenza A and B
* Live, attenuated, cold-adapted vaccine (quadrivalent) by nasal spray influenza A and B (children)
37
**Time course of influenza A virus infection**
* Incubation period of 1-5 days (average 2-3 days)
* Sudden onset of fever, chills, headache, muscle/joint paint, extreme fatigue, dry clough sore throat and stuffy nose
38
**Risk factors for complications of influenza**
* **Child under 6 months**
* **Older people**
* **Those with underlying health conditions such as resp, cardiac diseases and long term neurological conditions or immune suppression**
* **Pregnant women**
* **Morbid obesity (BMI \>40)**
39
**Genetic changes in the influenzas virus**
* Viral RNA polymerases have a high error rate
* High error rate and lack of proofreading ability ability leads to mutations
* Genetic variation and resistance
* Surface antigens haemagglutinin and neuraminidase
* antigenic drigt and shift
40
**Antigenic drift**
involves **point mutation** in the hemagglutinin and/or neuraminidase genes- encoding envelope glycoproteins, thus r**educing the binding affinity of antibodies** raised against previous strains. This is why individuals can become reinfected with influenza and why the content of seasonal vaccines must be altered annually.
41
**Antigenic shift**
is the genetic reassortment of genome segments between animal and human strains leading to the expression of novel hemagglutinin subtypes- essentially creating new virus’ to which pre-existing immunity exists e.g. Spanish flu.
Dramatic changes in antigenic properties of the H and/or N proteins
* Occurs infrequently – maybe every 10 or 20 year
* **Only influenza type A show antigenic shift**
42
explain antigenic shift
1. influenza type A viruses in many animals, including horses, pigs, and wild migrating waterfowl.
2. reassortment can occur between influenza A viruses that infect different animal and avian species, e.g., pigs can be infected by human- and avian-specific influenza viruses
3. In environments where pigs, birds and humans coexist, it is possible for a pig to be simultaneously infected with multiple influenza subtypes.
4. “Reassortants” can, therefore, be produced within one host animal (the pig), in which the mRNAs encoding the H and N antigens have been reassorted into unique combinations.
5. The reassortant virus then has the potential to spread among humans, birds, and pigs.
43
**Consequence of antigenic shift**
* New subtype of influenza virus
* May not have been seen in circulation in population for many year
* Immune systems of many indiivduals have no defence against this new subtype
44
epidemic
Prevalent among a people or a community at a special time, and produced by some special causes not generally present in the affected locality
45
pandemic
epidemic over a very large area; affecting a large proportion of a population – often the world
46
**Occurrence of major outbreaks of type A influenza**
4 pandemics in past 100 years:
* 1918 H1N1, from seasonal human and avian (bird) flu
* 1957 H2N2, from human and avian reassortment
* 1968 H3N2 human and avian components
* 2009 novel H1N1 contains genes from a combination of human, swine, and avian reassortment.
47
key characteristic of a pandemic e.g. the spanish flu
waves
48
**How does the flu actually kill people**
**Symptoms= the body’s immune response to viral invasion**
* Antibodies triggered and immune cells move to site of infection
* Release of cytokines leading to local inflammation
**HOWEVER..**
* The immune system may ‘overreact’- T cells attack and destroy the tissues in which the virus is replicating- particularly the lungs
* There is an opportunistic secondary infection i.e. bacterial (streptococcus or staphylococcus species)- usually in the lungs
