Influenza Flashcards
Different types of influenza virus
Different types of influenza virus: Belongs to family orthomyxoviridae
* Influenza A
* Influenza B
* Influenza C
* Influenza D
Influenza A
Influenza B
Influenza A: consisting of 8 negative-sense single-stranded RNA molecules. The two surface glycoproteins found on the influenza A virus are, Hemagglutinin (HA) and Neuraminidase (NA)
Most cases of the flu
Infect animals and human
According to pathogenicity in chicken?
Influenza B: Also 8 negative-sense single-stranded RNA molecules
-Two proteins, NB and BM2, are unique to influenza B virus
-Only found in humans
-Classified into two antigenically distinct lineages, Yamagata and Victoria like viruses
Influenza C
Influenza D
Influenza C: Influenza C has a segmented genome consisting of 7 negative-sense single-stranded RNA molecules.
-Different from the other two viruses
-Nonsymptomatic
-Has as a little medical concern (reported in human and pigs)
Influenza D: One of the main differences is that Influenza D virus does not possess Hemagglutinin (H) and Neuraminidase (N) glycoproteins on its surface like Influenza A and B. Instead, it has a different glycoprotein called “HEF” (Hemagglutinin-Esterase-Fusion) that combines hemagglutinin and esterase functions into a single protein.
Infect pigs and cattle; no human infections
Antibodies have been found in persons exposed to cattle
II- Influenza Virus Replication
II- Influenza Virus Replication
Attacment and Entry to the cell: HA receptor-binding (The virus binds there) site.
Release of virus RNA: After the virus enters the infected cell by endocytosis, the M2 proton channel opens in response to the low pH of the endosome
vRNAs are then trafficked to the nucleus
The vRNA then enter the nucleus through nuclear pores
-Influenza genome is - sense segmented RNA. It must be converted firstly into a + RNA to serve as a template for the production of viral RNAs.
-The viral RNA dependent RNA polymerase (RdRp) initiates RNA synthesis
-The virus mRNA leaves the nucleus to the cytoplasm and translate to virus protein with the help of the host ribosome and ER
-The virus uses the host cell’s plasma membrane to form the viral particles that leave the cell.
Influenza A viruses and species barriers
Where the flu is from?
Influenza A viruses and species barriers
* The natural host of Influenza A virus is wild waterfowl
* Influenza A virus can transmit from wild waterfowl to domestic birds and further to other species
Barriers for Interspecies Transmission
Barriers for Interspecies Transmission
Chicken: Bind to α2,3-linked sialic acid (SA) receptors abundantly located in the lower respiratory tract of birds and the intestinal tract with respect to avian influenza viruses
Human: To α2,6-linked SA receptors which are predominant in thehuman upper respiratory tract with respect to human influenza viruses
Pig: To both linkages (α2,3 and α2,6-linked SA receptors) with respect to swine influenza viruses.
How Influenza Viruses Change?
How Influenza Viruses Change?
Two mechanisims:
Mutation – antigenic drift
Reassortment – antigenic shift
How Influenza Viruses Change?
Long version
How Influenza Viruses Change?
Antigenic drift
* Antigenic drift is mediated by stepwise mutations in the antigenic structure of the influenza virus as a result of natural selection pressure influenced by host immunity responses
* These mutations can accumulate continually over time and may result in antigenic variants.
* This may negatively affect the recognition by neutralizing antibodies created in response to a previous virus infection or vaccination
Antigenic Shift
* Antigenic shift is associated with major mutations in the virus through forming a new subtype since the segmented nature of the influenza viruses’ genome promotes genetic
reassortment
* Occur when a cell is simultaneously infected by two different strains of type A influenza.
Influenza in Humans
Influenza in Humans
- Cause: Influenza A (H1N1 and H3N2) Influenza B (Yamagata and Victoria)
- Acute, febrile respiratory illness affecting nose, throat, bronchial tubes and lungs with high levels of morbidity and mortality each winter.
- Symptoms:
– Fever
– Headache
– Muscle pain
– Cough
– Sore throat
– Body aches
– Decrease apetite
– Fatigue
– Chills - Vomiting (Less common, mostly in children)
What can make it more complicated?
What can make it more complicated?
Secondary bacterial infections
- Streptococcus pnemoniae
- Haemophilus influenzae
- Staphylococcus aureus
3 days - > 2 weeks after infection
Transmission of influenza A viruses
Transmission of influenza A viruses
- Incubation period:
1-3 days - Viral shedding
– Can start 1 day before the onset of symptom
– Peak shedding first 3 days of illness - Correlates with temperature
- Subsides after 5 days in adults, can be longer than 7 days in children
Transmission via respiratory secretions in droplet form.
Contact within contaminated surfaces is a secondary source of transmission.
Risk group
Risk group
-Infants and young children
-Elderly people
-Immunocompromised people
-Pregnant women
Reassortment
Reassortment among flu plays role when comes from different hosts and are reasons behind pandemics. Reassortment is a significant factor in the emergence of influenza pandemics.
Influenza A viruses in birds
Influenza A viruses in birds
Avian (For chicken and birds) influenza viruses
Pathogenicity and Symptoms
Pathogenicity and Symptoms
* Classification by OIE into two pathogenicity phenotype:
Low pathogenic AIV (LPAIV)
- Cause mild or asymptomic infection, such as:
- respiratory disorders
- ruffled feathers
- low weight gain
- decrease in egg production
High pathogenic AIV (HPAIV)
- Cause severe morbidity and mortality (More cases and dead cases), such as:
- cyanosis
- dyspnea
- edema
- diarrhea
- neurological disorders à up to 100% mortality
