1. Influenza
Michelle Lin

2. Classic Flu Symptoms Infection Incubation (1-2 days)
Symptoms (1-2 weeks)
So after a person is infected with the infleuza virus, there is an incubation period of about 1-2 days and then the classic symptoms of Headache, muscle aches, FEVER F, cough, fatigue, weakness, sore throat, nasal congestion, nausea/vomiting emerge
Influenza usually a mild illness and self limiting with a full recovery in 2 wks or less without medical intervention
Betts, Robert, Stanley Chapman, and Robert Penn. A Practical Approach to Infectious Diseases. 5. Philadelphia: Lippincott Williams and Wilkins, Print.
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3. Who is at Risk?
However, the influenza virus can damage the lining of the respiratory tract allowing other bacterial infections and complications such as pneumonia, bronchitis, and pericarditis to take place
People at risk for developing these complications are the elderly, infants and young children, pregnant women, and people with underlying chornic conditions such as COPD
Death rate of 0.1% for seasonal flu
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On average annually in the US: 5% to 20% of the population gets the flu, over 200,000 people are hospitalized from flu complications, and about 23,600 people die from flu-related causes.
Highest attack rates in the young, but biggest public health impact on the elderly
Children  poor respiratory etiquette
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Van-Tam, Jonathon, and Chloe Sellwood. Introduction to Pandemic Influenza. Oxfordshire, UK: CABI, Print.

4. Modes of Flu Transmission
3 Basic Modes:
Direct
Airborne
Indirect
Influenza is spread is 3 main ways:
Direct transmission is when an infected person sneezes mucus directly into the eyes, nose, or mouth of another person
Airborne transmission is through inhaling the aerosols produced by the infected person coughing, sneezing, or spitting
Indirect transmission is through contacting contaminated surfaces
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Annual influenza epidemics in humans affect 5–15% of the population, causing an estimated half million
deaths worldwide per year
Van-Tam, Jonathon, and Chloe Sellwood. Introduction to Pandemic Influenza. Oxfordshire, UK: CABI, Print.
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5. The Taxonomy of Influenza Virus
Orthomyxoviridae family
Genera (Types) – A, B, C
Antigenic differences
So the influenza virus is part of the orthomyxoviridae family of RNA viruses
There are 3 diff genera of influenza virus ---- Types A, B, C that have antigenic differences in there nucleocapsid and matrix proteins
Type A 65% of cases
Type B 35% of cases
Type C does not cause classic influenza illness
I will focus the rest of my presentation on Type A since the majority of human influenza cases are caused by this specific type
Type A’s natural hosts are aquatic birds from which they are occasionally transmitted to other species such as pigs, seals, humans, mammals
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Influenzavirus A, Influenzavirus B, Influenzavirus C, Isavirus and Thogotovirus.
The type A viruses are the most virulent human pathogens among the three influenza types and cause the most severe disease
Influenzavirus A infects humans, other mammals, and birds, and causes all flu pandemics
Influenzavirus B infects humans and seals
Influenzavirus C infects humans and pigs
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print
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6. Structure of Influenza Virus
Spherical
Enveloped
Matrix protein
Membrane
proteins
Nucleocapsid
8 -ssRNAs
This is an overview of the viral structure
The virus is a spherical enveloped virus with an underlying shell of matrix protein (M1) and segmented RNA genome encapsulated in nucleocapsid protein and membrane proteins (Hemagluttanin, Neuraminidase, and M2 protein)
Now I’ll go into depth about each major component
EXTRA:
Hemagglutinin spikes (HA) – viral entry
Neuraminidase spikes (NA) – viral exit
The non-structural NS1 protein
RNA-dependent RNA polymerase – talk more about, - strand, how it replicates, and how it packages --- buds or lyse
M2 Protein (only in Type A)
The lipid membrane is derived from the plasma membrane of the infected cell during the budding process
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print
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7. The viral genome is composed of segmented negative-sense RNA
Influenza A virus RNA segments and the proteins they encode
RNA segment (no. of nucleotides)
Gene product (no. of amino acids)
Molecules per virion
1 (2341)
Polymerase PB2 (759)
30–60
2 (2341)
Polymerase PB1 (757)
3 (2233)
Polymerase PA (716)
4 (1778)
Haemagglutinin (566)
500
5 (1565)
Nucleoprotein (498)
1000
6 (1413)
Neuraminidase (454)
100
7 (1027)
Matrix protein M1 (252)
3000
Matrix protein M2 (97)
20–60
8 (890)
Non-structural proteins
NS1 (230) –
NS2 (121)
130–200
So the genome consists of 8 segmented negative sense single stranded RNAs each encoding 1 or 2 viral proteins. --- Reassortment of the segments genome contribute to genetic variability
Each RNA segment is coiled into a hairpin structure and associated with a RNA dependent RNA polymerase complex composed of 3 different proteins (PB1, PB2, and PA) and each segment is independently encapsulated by viral nucleoprotein (NP)
Together an RNA segment, polymerase complex, and nucleoprotein form a single ribonucleoprotein (RNP)
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The viral polymerase complex is a heterotrimer composed of 3 proteins ---- PB1, PB2, and PA
PB1 carries the polymerase and endonuclease activities
**A short region of duplex vRNA (formed between the 5′ and 3′ ends) constitutes the binding site for the heterotrimeric RNA-dependent RNA polymerase**
PB2 binds to 5’ methylated cap structure on host cell pre-mRNAs before they are cleaved to provide primers for viral mRNA synthesis
Function of PA is unclear
The nucleoprotein is required for viral RNA synthesis ---- binds to ssRNA in a non-sequence specific manner and associated with PB1, PB2, and M1
The transcriptionally active form of the genome is the viral ribonucleoproteins (RNPs)
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print
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8. RNA-dependent RNA Polymerase synthesizes RNA from RNA3’ 5’
Influenza virus uses RNA-dependent RNA polymerase to transcribe mRNA from viral RNA and replicate complementary RNA from viral RNA through 2 different mechanisms
To transcribe mRNA from vRNA, the Rdrp polymerase complex bound to vRNA snatches and cleaves a portion of host pre-mRNA (known as cap snatching) and uses the 3’ end as a primer to start transcribing from the 3’ end of the viral RNA
Towards the 5’ end of vRNA Rdrp stutters on a sequence of uracils and the mRNA transcript has a poly-A-tail at the 3’ end
The mRNA is then transported to the cytoplasm to direct the synthesis of viral proteins.
B/c the mRNA has a host derived cap at the 5’ end and truncated 3’ end with a poly A tail, it cannot be used as a template to synthesize more negative sense RNA
So theres another process to replicate a full length cRNA from negative sense viral RNA
This FL cRNA can then be used as a templates to synthesize more copies of –vRNA that’s later packaged into virions
The exact mechanism by which this occurs is unclear but involves both host and viral factors.
Much less cRNA is synthesized than mRNA
5-10% of total +sense RNA is cDNA
This is because much more viral proteins are needed to assemble a whole virus
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Once the (-) strand influenza viral RNAs enter the nucleus, they serve as templates for the synthesis of + sense capped and polyadenylated mRNAs and +sense uncapped FL complementary RNA through 2 different mechanisms both carried out by RNA dependent RNA polymerase
mRNA transcription is primed by capped RNA segments snatched from host cell pre-mRNAs by the viral polymerase, whereas cRNA/vRNA
synthesis is primer-independent
*mRNA synthesis:
Unlike most –RNA viruses, transcription of the influenza genome takes place in the nucleus of infected cells
Synthesis of Capped and polyadenylated mRNA is primed by capped oligonucleotides of around nucleotides which are scavenged from host cell pre-mRNAs by an endonuclease activity contained within DNA dependent RNA polymerase (PB1)
Influenza mRNAs contain host-cell derived sequences at their 5’ ends
Transcription terminates nt before the 5’ end of the vRNA and the mRNA is polyadenylated
STEPS:
PB1 of the Polymerase complex binds to the 5’ end of a vRNA segment  conformational change in polymerase  activates cap-binding activity of PB2 and allows the polymerase to bind host cell mRNA
The 3’ end of vRNA template enters the complex through combination of protein-Rna interactions and base pairing b/t the 5’ and 3’ sequences  stimulates endonuclease activity and the 5’ host cap structure of host pre-mRNA is cleaved by PB1, the 3’ end of the cleaved mRNA is then used as a primer for transcription intitiation by PB1
The mRNA chain is elongated by addition of ribonucleotides directed by vRNA template
PB2 dissociates from the cap structure after the first nucleotides have been added
Processive synthesis of mRNA terminates at a stretch of 5-7 uridine residues about 17nt from the 5’end of the vRNA template
RNA is polyadenylated by the viral polymerase stuttering at this site – reiterative copying of the U(5-7) track
**Key features: polymerase assembles on 5’ end of vRNA  cap binding is activated  polymerase then binds to 3’ end of vRNA and this results in endonuclease activation
*Mechanism of Replication – synthesis of cRNA (unprimed): 5-10 % cRNA out of total +RNA
Possibiliyu – take 1 ATP to prime
Unclear but need both host and viral factors
The process of genome replication is not as well characterized as that of mRNA synthesis
Complementary RNA acts as the replicative intermediate for synthesis of further –RNA
Uncapped full length complementary + RNA
Synthesis of CRNA involves unprimed intiation and readthrough of the polyadenylation signal to produle FL copoes of the vRNA template
These RNAs are packaged into RNPs
Generation of FL +sense copies (cRNAs) of the genomic RNA segments, which are then used as templates for amplification of vRNA
Much less cDNA is synthesized during the infectious cycle than mRNA
FL transcripts of virus genome (cRNAs) are dependent on viral protein synthesis
Viral mRNAs cannot serve as replicative intermediates bc:
They possess host derived seqs as their 5’ ends as a result of cap snatching and they are truncated at the 3’ end where polyadenylation occurs
The replication of vRNA generates uncapped complete cRNA copies that are not polyadenylated
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These molecules are then transported back to the cytoplasm, where they direct the synthesis of viral proteins.
However, the mRNAs are not complete copies of the viral (-) strand RNAs – they are missing sequences from both the 5′- and 3′-ends.
Therefore, to produce more viral (-) strand RNAs that are needed to assemble new virions, a full length (+) strand is produced, which in turn is copied to a full-length (-) strand RNA. The (-) strand RNAs are then used to assemble new virions. 
During replication cycle, 2 types of +sense RNA are synthesized from the RNPs:
This cycle is carried out by the viral RNA-dependent RNA polymerase (heterotrimeric complex)
The capped RNA primers required for the initiation of influenza virus mRNA synthesis are produced by the viral polymerase itself, which consists of three proteins PB1, PB2 and PA. Production of primers is activated only when the 5'- and 3'-terminal sequences of virion RNA (vRNA) bind sequentially to the polymerase, indicating that vRNA molecules function not only as templates for mRNA synthesis but also as essential cofactors which activate catalytic functions
Paradoxically, although the interaction ofthe 3′ and 5′ ends of the template to createa panhandle structure is essential for
both mRNA and cRNA/vRNA synthesis,the steric hindrance of this secondarystructure is incompatible with transcription of a full-length cRNA copy
. Based on the RNA-binding capacity of NP, some have proposed that the protein promotes cRNA/vRNA synthesis by altering pan handle structure
In addition, biochemical studies have suggestedthat NP can associate directly with thepolymerase, possibly preventing its capsnatching activity and promoting unprimed transcription
Li, Mei-Ling, Bertha Ramirez, and Robert Krug. "RNA-dependent activation of primer RNA production by influenza virus polymerase: different regions of the same protein subunit constitute the two required RNA-binding sites." EMBO Journal. 17 (1988): Web. 6 Mar <
Kawaoka, Yoshihiro. Influenza Virology: Current Topics. Norfolk: Caister Academic Press, Print.
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9. Hemagglutinin (HA) assists in viral entry
Hemagglutinin is a spike shaped protein that recognizes and binds to sialic acid at the terminus of glycoproteins on the surface of host cells.
After the virus binds to the host cell, the whole virus is internalized into a host endosome which begins to acidify eliciting a conformational change in hemagluttinin which exposes a fusion peptide that inserts into the endosomal membrane mediates fusion so that the the virus is released from the endosome into the cytoplasm of the host
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The HA is a trimer of identical subunits which contains the receptor binding activity at the tip of the molecule , and the membrane fusion activity which is activated by the low pH in the endosome during entry into the cell
he three-dimensional structure of the influenza haemagglutinin (HA). The HA monomer (left) and trimer (right) are shown. In the monomer, the globular HA1 subunit is shown in dark blue, the HA2 subunit in light blue, with the “fusion peptide” in red. The receptor-binding site of HA1 is located at the tip of the molecule.
The HA spike protrudes approximately 13.5 nm from the viral surface. 11, 12 HA1 and HA2 appear in the structure of the spike as distinct subunits. HA1, the globular domain at the distal end of the spike, is responsible for binding of the virus to its cellular sialic acid receptor, the receptor-binding pocket being located close to the very tip of the molecule
HA2 forms the fibrous stem of the viral spike. The N-terminus of HA2 contains a conserved stretch of 20, mostly hydrophobic, amino acid residues. This sequence is generally referred to as the “fusion peptide”; it triggers the membrane fusion process between the viral envelope and the host cell membrane
The low pH in the late endosome triggers the conformational change in the HA which causes the virus membrane to fuse with the endosome membrane to release the nucleocapsid of the virus into the cytoplasm
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print
"Molecule of the Month: Hemagglutinin." RCSB PDB Molecule of the Month. 2012: n. page. Web. 6 Mar < education_discussion/molecule_of_the_month/download/Hemagglutinin.pdf>.
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10. M2 is a membrane ion channel protein
M2 Membrane Channel
The endosome containing the virus is acidified through host proton pumps
But In order for the interior of the virus to become acidic, it needs M2 - a membrane ion channel protein to pump the H+ in the endosome into the virus
The acidification of the interior of the virus causes the ribonucleoproteins to dissociate from the M1 protein so that when the virus is released from the endosome into the cytoplasm, free ribonucleoproteins are able to enter the host nucleus through nuclear pores.
Note that M2 membrane ion channel are in type A but not B influenza viruses
EXTRA:
M2 is involved in the infection process by modulating the pH within virions, weakening the interaction between the viral ribonucleoproteins (RNPs) and the M1 protein
M2 channel allows acidification of the interior of the virus while it passes through the acidic endosome, which is though to be needed for the release of RNP particles into the cytoplasm after the membrane fusion step
H+ flow through the M2 channel in the virus membrane promotes a low pH- induced dissociation of the M1 protein from the RNP which is necessary to allow entry of the RNP into the nucleus and iniate replication
Acidification of endocytic vesicles is required for dissociation of the M1 protein from the RNPs, only then are the RNPs imported into the nucleus via nuclear pores
Thisprotein forms a bridge that crosses the membrane of the virus, barely protrudingfrom the surface
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Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print

11. Neuraminidase (NA) assists in viral exit
Neuraminidase catalyzes the cleavage of sialic acid from the glycoproteins on the host cell surface so that newly formed virions can bud from the cell surface and go on to infect other host cells
Without neuraminidase, virions would just self-aggregrate on the host cell surface and not be able to disperse
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The neuraminidase is a tetramer of identical subunits which contains the receptor destroying activity necessary for release of newly formed virus from the surface of the infected cell
Promotes release of progeny virions that are formed by budding from the cell surface
Neurtaminidases catalyze the cleavage of glycosidic linkages adjacent to N-acetyl-neuramic acid
Viral enzyme is destroying its own receptor
Fxns to remove sialic acid to prevent self aggregration and promote dispersion
he second envelope glycoprotein NA has enzymatic activity, cleaving sialic acid residues from glycoproteins or glycolipids. 9 Since sialic acid functions as a receptor for attachment of influenza virions, the neuraminidase activity of NA, cleaving such receptors, 14 mediates the release of newly formed virus particles from the surface of infected cells
Neuraminidase is also known as sialidase because it breaks the linkages between sialic acid and cellular glycoproteins and glycolipids found in cell walls. 
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print
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12. Life Cycle of Influenza Virus
This is a summary of the viral life cycle tying in all the viral components together
Upon infection, the Virus enters the respiratory tract
Hemagluttanin spikes bind to sialic-acid at the ciliated epithelial cell surfaces , and the virus is taken in through endocytosis
M2 mediates dissociation of RNP from M1 while the virus is in the endosome, then the action of Hemagluttanin fusion peptide triggers the release of the virus into the cytoplasm and then RNP enters the nucleus
Once in nucleus, the Virus uses its own RNA dependent RNA polymerase to make more –ssRNA that will be packaged into virions and mRNA that goes to the cytoplasm to be translated into viral proteins
the viral membrane proteins (HA, NA, and M2) assemble on the host cellular membrane and the other viral proteins and -ssRNA assemble just under the cellular membrane
Through budding process, viruses are ready to be set free, Neuraminidase cleaves the sialic acid to release the virions so they can infect other cells
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Van-Tam, Jonathon, and Chloe Sellwood. Introduction to Pandemic Influenza. Oxfordshire, UK: CABI, Print

13. Anti-Influenza Drugs Block a Step in the Replication Cycle
Antiviral drugs work by blocking a step in the replication cycle of the influenza virus and should only be used in complicated cases of influenza
The most common drugs M2 inhibitors like Amantadine and Rimantadine and Neuraminidase inhibitors such as Zanamivir and Oseltamivir
M2 inhibitors clog the M2 ion channel so that RNP cannot dissociate from M1 and enter the nucleus while neuraminidase inhibitors bind to highly conserved sites on neuraminidase to prevent the release of newly formed virus particles
Resistant strains develop in 30% of cases treated with M2 inhibitors alone and develop in <3% of cases treated with neuraminidase inhibitors alone
When M2 inhibitors and Neuraminidase inhibitors are used together they create enhanced antiviral effects and decrease the likelihood of resistant strains emerging
EXTRA:
Amantadine and Rimantadine are M2 inhibitors --- these drugs are only effective in influenza type A because influenza type B does not have M2 protein
These M2 inhibitors clog the ion channel formed by the M2 protein that spans the viral membrane and prevents M2 ion channel from pumping protons into the virion while its in the endosome, so that M1 protein cannot dissociate from RNP and RNP cant enter nucleus via nuclear pores
M2 inhibitors associated w/ rapid emergence of drug resistance strains, about 30% of treatment courses result in the development of resistant strains
Resistance is conferred by point mutations in the M2 gene resulting in changes in amino acids in the transmembrane domain of the M2 ion channel
Zanamivir and Oseltamivir are neuraminidase inhibitors that are effective in treated both type A and B of influenza
These drugs bind to highly conserved sites on neuraminidase interfere with the release of newly made viruses from infected cells
It is important to note that these drugs do not kill the virus but merely slow viral replication down to a level where the immune system can more easily destroy it.
Neuraminidase inhibitors are associated with a lower rate of drug resistance strains (<3%) when compared to M2 inhibitors
Resistance is conferred by point mutations in either the Hemagluttanin or Neuraminidase genes causing reduced binding efficiency b/t Hemagluttanin and its host cell receptor or reduced binding efficiency b/t Neuraminidase and its inhibitor.
Generally, neuraminidase mutations lead to a functionally defective enzyme, which reduces the fitness of the virus and causes decreased pathogenicity
These drugs should not be administered simultaneously for treatment and prophylaxis in different patients within the same institution because of the risk of development of drug resistance.[5] The M2 protein inhibitor-resistant variants emerge rapidly when these drugs are administered for treatment; approximately 30% of treated children or adults start shedding resistant variants 2-5 days after the beginning of treatment
When antiviral drugs used for prophylaxis, they are only effective for as long as theyre is being taken—there is no lasting protection once the pills have run out.
The biggest problem with prophylaxis, especially if it is haphazard, is that it may encourage the development of resistant strains
Prophylaxis 2 situations:
seasonal prophylaxis -- antiviral agents is administered throughout the influenza season
reductions of 70-90% of lab confirmed influenza cases
consider in high risk pts in whom vaccination is not possible or contraindication, for immunodeficient individuals who do not respond to vaccinatoin, or for uncaccinated indivudals who care for high risk pts
postexposure prophylaxis – drug is given for a relatively shorter period of time following a known exposure to an infleunza infecter person
Development of a protective immune response following influenza vaccine can take as long as 2 wks, so short term prophylazis should be used in high risk pts who are not vaccinated until after influenza activity has begun
Short term prophylaxis of famiy members
resistant influenza A viruses have emerged rapidly and transmitted when amantadine and rimantadine were used both for treatment of cases and prophylaxis of contacts
Prophylaxis post outbreak in chronic care institutions
if possible should separate treated pts from pts receiving prophylaxis
selection and spread of resistance
 Taking the drugs in the wrong dose or for too short a time can lead to the development of new, drug-resistant strains
Betts, Robert, Stanley Chapman, and Robert Penn. A Practical Approach to Infectious Diseases. 5. Philadelphia: Lippincott Williams and Wilkins, Print.
Van-Tam, Jonathon, and Chloe Sellwood. Introduction to Pandemic Influenza. Oxfordshire, UK: CABI, Print
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14. Antigenic Drift and Shift Contribute to the Genetic Variability of Influenza virus
Influenza virus is has high genetic variability due to antigenic drift and shift.
Antigenic drift are subtle changes in HA and NA within a strain due the the errors made by RdRp since it lacks proofreading fxn. This is responsible for our seasonal epidemics in the winter
Antigenic shift are huge changes in HA and NA resulting from 2 or more different strains infecting the same host cell and the recombination of segmented RNAs. This is responsible for the development of emerging novel strains that can cause pandemics.
Ex. Swine flu pandemic in 2009, bird and human virus combined in pig and then became virulent in humans
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When the host is infected by 2 strains of different subtypes, recombination can occur among the each strains 8 segmented RNAs
Potential of generating 2^8 or 256 combinations
Can lead to major changes in HA or NA from acquiring RNA segments from another strain
A host infected with influenza virus develops antibodies against that virus; as the virus changes, the "first" antibody no longer recognizes the "newer" virus and infection can occur because the host does not recognize the new flu virus as a problem until the infection is well under way. 
Van-Tam, Jonathon, and Chloe Sellwood. Introduction to Pandemic Influenza. Oxfordshire, UK: CABI, Print
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15. Annual Vaccines are Used to Prevent Influenza
Inactivated vs. Live-attenuated
New each season
One way to prevent influenza is through vaccination each flu season.
Each year , researchers collect virus samples from around the world to identify the influenza viruses that are the most likely to cause illness during the upcoming flu season, these strains are incorporated into a injectable inactived vaccine composed of killed virus and into a nasal spray live attenuated vaccine composed of weakened virus
Vaccinations are especially recommended for the groups at risk for influenza related complications and people working in healthcare facilities
Vaccines work by inducing our bodies to produce antibodies against viruses, but because the influenza virus can mutate rapidly, antibodies made towards prevalent pathogenic strains one flu season will not be effective towards the strains next flu season
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Target groups for influenza vaccination – groups at increased risk for influenza-related complications (elderly, ppl who have chronic disorders of the pulmonar or cardio sys, pregnant woman), people who can transmit influenza to those at high risk (ppl working in healthcare facilities)
Immunity to influenza is principally related to antibody to HA and the appearance of a new virus subtype with a different HA means that immunity acquired from past influenza infection confers no protection against the new virus subtype
Each year, experts from FDA, WHO, U.S. Centers for Disease Control and Prevention (CDC) and other institutions study virus samples collected from around the world to identify the influenza viruses that are the most likely to cause illness during the upcoming flu season so that people can be protected against them through vaccination.
Influenza reaches peak prevalence in winter, and because the Northern and Southern Hemispheres have winter at different times of the year, there are actually two different flu seasons each year. This is why the World Health Organization (assisted by theNational Influenza Centers) makes recommendations for two different vaccine formulations every year; one for the Northern, and one for the Southern Hemisphere.[88]
Inactivated vaccine – virus is killed – vaccine is more stable and safer than live vaccines although they induce a weaker immune response
Inactivated influenza vaccines % effective in the prevention of influenza illness when there is a good antigenic match b/t vaccine and epidemic viruses
inactived influenza vaccines consist of inactivated whole virus, dirupted virus, or purified H and N subunit vaccines
trivalent formation – 3 diff strains
single dose sufficient for most individuals, but 2 doses of vaccine are required in those who have not been primed by previous infection or vaccination with similar antigen type (children under 9, event of antigenic shift)
Live attenuated vaccine (Flu mist, nasal spray)– weakened form of virus that can’t cause disease, induce strong immune response, could mutate and regain ability to cause disease
currently recommended for all healthy persons at least two years old and under 50 years of age wishing to protect themselves from influenza and its complications, or to avoid spreading the flu to members of certain vulnerable groups
trivalent
"Vaccine Selection for the and Influenza Seasons." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 23 Feb Web. 6 Mar <
Nicholson, Karl., Robert Webster, et al. Textbook of Influenza. Oxford: Blackwell Science Ltd, Print.
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