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Exam 5 NYUMC > Influenza > Flashcards

Influenza Flashcards

1
Q

Characteristics of Influenza

A

sudden onset, fever, muscle and body aches, headache, pain in your eyes when moved, lack of appetite, dry cough, runny nose

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2
Q

The Influenza Virus is what type of virus?

A

orthomyxovirus

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3
Q

Orthomyxovirus of the flu- characteristics

A

enveloped, negative strand RNA with 8 different segments (prone to reassortment- which is important for the appearance of pandemic strains)

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4
Q

3 Different forms of Influenza Virus

A

IAV (most common and most commonly evolving; most significant in pandemics; can infect humans, pigs, birds, etc.)
IAB (humans only, generally milder)
IAC (least important, can infect humans but less common and less severe)

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5
Q

Components of viral influenza particle

A

10 proteins on 8 genomic RNA (2 M proteins and 2 NS proteins)

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6
Q

Components of viral influenza particle ENVELOPE

A

glycoproteins- hemagglutinin (HA) and neuraminidase (NA) (sialidase), along with small amounts of matrix 2 (M2) ion channel protein

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7
Q

Components of viral influenza particle NUCLEOTIDES

A

RNPs = 8 negative stranded RNA segments + nucleoportein and polymerase compex hetero-trimer PB2, PB1, PA

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8
Q

Components of viral influenza particle MATRIX

A

M1 protein which interacts with NA/HA and RNA/RNPs)

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9
Q

Components of viral influenza particle NONSTRUCTURAL REGULATORY

A

nuclear export protein NEP or nonstructural protein NS2; NS1 not within the virion, used inside host cell to block innate defenses

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10
Q

Trasmission method

A

aerosolized in droplets; droplets can survive for minutes to hours on hands

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11
Q

Basic Influenza Viral Replication Cycle

A
  1. virus binds to sialic acid moities on the cell surface receptor proteins 2. virus is endocytosed and fuses with vesicle membranes 3. acidifcation of the endosome allows for RNA/RNPs to be released into the cytoplasm and migrate to the nucleus 4. transcription of RNA segments to generate viral mRNAs that are translated by ribosomes in the cytoplasm for viral protein synthesis 5. creation of new genome segments cRNAs in the nucleus that go to cytoplasm 6. assembly of viral proteins at the plasma membrane 7. NA (sialidase) cleaves off the sialic acid allowing the particles to bud and exit
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12
Q

Pulmonary complications- how influenza virus causes them

A

Influenza virus targets and kills mucous secreting ciliated epithelia; uses neuraminidase to degrade and penetrate mucous layer making the upper respiratory tract vulnerable to pathogens; if it reaches lower respiratory tract, it can cause desquamation of bronchial and alveolar epithelia; also causes local inflammation with involvement of monocytes, lymphocytes, and neutrophils and submucosal edema, making the lungs overall more adherent to bacteria

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13
Q

Pulmonary complications- clinical manifestations

A

Cell damage and inflammation of upper and lower respiratory tracts
primary viral pneumonia
secondary bacterial pneumonia
croup (children)
cardiac failure (elderly)
watery diarrhea and conjunctivitis (avian)

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14
Q

3 Primary means of Self-Resolving Influenza Virus

A
  1. Innate defenses (interferons and cytokines)
  2. Cell-mediated response (T-cells, which is less serotype specific, but may provide protection against later infections)
  3. Neutralizing Antibodies (protection against future infection with same serotype; mostly specific to HA, some to NA)
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15
Q

Number of serotypes for HA and NA

A

16 HA, 9 NA = 144 combinations (but in reality there’s more)

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16
Q

Antigenic drift

A

replication errors causing individual nucleotide changes

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17
Q

Antigenic shift

A

reassortment of genomic fragments (whole gene changes)

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18
Q

Influenza A experiences ________

A

antigenic drift and shift

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19
Q

Influenza B experiences

A

only antigenic drift

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20
Q

Possible outcomes of different strains floating around in the population

A
  1. Seasonal flu
  2. Epidemic flu
  3. Pandemic flu
21
Q

Morbidity occurs with seasonal flu in….

A

children under 18 mo. and adults over 65

22
Q

With seasonal and epidemic flu

A

it follows a predictable pattern
there’s some immunity in the population
there is some mortality in the population
it is normally self-resolving
>200,000 hospitalizations per year
(epidemics is when it surpasses the normal seasonal baseline)
modest impact (school closing etc.)

23
Q

Pandemic influenza…

A

Has little in common with seasonal influenza
substantial increase in cases outside of flu season
substantial increase in mortality from let’s say .1% to 2.5%
global outbreaks of viruses of novel antigenic subtypes with limited resistance in the population.
up to 50% of the population can be infected in a pandemic year (efficient person-to-person spread)

24
Q

Genotypes of past strains

A

give clues as to the evolution of new strains:

in 2009 H1N1 there were segments of the strain’s genome that resembled H1N2 from the 1990’s

25
Q

Antiviral strategies

A
  1. clean practices/prevention
  2. uncoating M2 inhibitors
  3. neuraminidase inhibitors
  4. vaccines
26
Q

How M2 inhibitors work

A

When the virion attaches to siliac acid moities it is taken in by endocytosis and as the endosome moves towards the nucleus, it acidifies via proteins that pump H+ into the vesicle. When endosome reaches ph 5, virion undergoes conformatinal change that exposes fusion peptide which inserts into the endosomal membrane and allows it to fuse with the viral envelope. When this happens, the RNAs are released into the cytoplasm.

Virions of influenza virus have M1 that is underneath the viral envelope. Virion also has M2 which forms a channel to actively pump protons into the virion, which lowers the pH of the virion, releasing the virion from M1 and allowing them to move freely into the cytoplasm.

The M2 ion channel is the target of the antiviral ‘adamantanes’, drugs that block the channel and prevent it from pumping protons into the virion.

27
Q

Drugs that are M2 inhibitors

A

amantadine (symmetrel)
rimantadine (flumadine)

only active against IAV (not as effective against B because it doesn’t have M2)
widespread resistance since H3N2 and H1N1
limited use nowadays because of CNS side effects

28
Q

Main point of M2 inhibitors

A

block the viral genome from reaching the nucleus in a form where it can replicate

29
Q

How neuraminidase inhibitors work

A

(Tamiflu) Taken in as prodrugs, hydrolyzed in liver to form GS4071 which stops spreading of influenza if taken within 36 hours of onset of symptoms; slows down viral replication and gives the immune system time to deal with the virus
Zanamivir does the same but must be taken in as powder and inhaled in lungs
Peramivir must be injected.
Single amino acid change in N1 can cause resistance. (but this can be overcome with higher doses)

30
Q

Drugs that are neuraminidase inhibitors

A

oseltamivir (Tamiflu)
Zanamivir (Relenza)

effective against IAV and IBV

31
Q

Main point of neuraminidase inhibitors

A

they block the active site of neuraminidase and prevent the cleavage of sialic acid; by preventing the sialic acid removal from the receptors, these drugs prohibit viral budding

32
Q

Vaccines

A

Flu shot- killed flu virus administered by injection A+A+B+B+ quadrivalent
LIAV- also A+A+B+B+ quadrivalent, FluMist, approved for ages 5-49 for those without robust immune defenses

33
Q

If a person takes antivirals within 2 weeks of getting the nasal flu vaccine

A

they should get revacccinated

34
Q

LIAV has been genetically engineered

A

so that virus grows at 34.5 degrees, but not 37 degrees so it will replicate in the nasal mucosa, but not spread deeper

35
Q

CDC recommends flu vaccination for everyone 6 months or older…

A

universal flu shot vaccination; in reality we just need 85% and in reality less than 20% get the shot

36
Q

Benefits of flu vaccine

A

independent of resistance to M2 and NA inhibitors
limit person to person transmission
can prevent infection before symptoms begin

37
Q

Disadvantages of flu vaccine

A

limited efficacy in elderly and immunocompromised
involves informed guesswork and sometimes the predictions are wrong (difficult to predict which strains will actually circulate through population and there’s a narrow time window between first indications and prime flu season during which they need to make and distribute the vaccine)
not effective against all strains
GBS- fever, nerve damage, muscle weakness (may not 100% be vaccine-related)

38
Q

Challenges to universal flu vaccines

A

long lasting protection

high safety profile

39
Q

Universal flu vaccine requires

A

identification of invariant antigens

vaccine delivery methods that will give the right type of protection

40
Q

Vaccine approach 1-bnAbs

A

broadly neutralizing antibodies against the highly conserved stem region of HA; these are made during human or mouse infections but are less good at neutralizing the virus compared to antibodies against the variable head section. Overall, may block a fusion step necessary for cell entry.

41
Q

Vaccine approach 2- Ankara strain of vaccinia virus

A

poxvirus expressing flu M and NP proteins
elicits a T cell response and doesn’t have as much of a problem with resistance because it controls rather than eliminates the virus

42
Q

Why is the flu a continual threat?

A

Easily transmitted
Constant antigenic change
Abundant in animal reservoirs
Fewer drugs and increasing resistance
Pandemic strains are only identified once they have spread
Capable of leaps in antigenic profile and host tropism

43
Q

Diverse world of Respiratory Viruses

A

Influenza - 10-15%
Rhinoviruses-(40-50%)
Enteroviruses (EV68)
(Rhinoviruses and enteroviruses are picornaviruses)
Respiratory syncytial virus (RSV)
Human metapneumovirus (hMPV)
Parainfluenza
(RSV, hMPV, and parainfluenza are paramyxoviruses)
Adenovirus
Coronaviruses (15% of cases include SARS-CoV and MERS-CoV)

44
Q

Leading cause of LRT infections in infants and children

A

RSV- a negative strand RNA virus

45
Q

RSV often manifests as

A

broncholitis (inflammation and mucous blockage of the smallest bronchioles) and 40% of cases get otitis media (infection and inflammation of middle ear); it travels to LRT via cell to cell by transfer along cytoplasmic bridges (syncytia) (usually restricted to URT in older children and adults)

46
Q

Treatment for RSV

A

Treat symptoms (e.g. oxygen). Virus sensitive to ribavirin (Rebetol) and high risk cases treated with palivizumab (Synagis), a humanized monoclonal antibody against the RSV F protein

47
Q

SARS

A

positive strand RNA enveloped virus
parts of the 30,000 nt genome resembled parts of a bronchitis virus of turkey and chickens and parts of a coronavirus of cows and mice
Now, thought that bats are the natural reservoir transferred to humans via civet cats which are hunted

48
Q

SARS near-pandemic

A

10% mortality mainly in older patients; 70% viral pneumonia
Fever was the only unifying symptom
Rapidly spread from Guangdong Province, China to 37 countries

Exam 5 NYUMC (13 decks)

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