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Z MD1 Respiratory block > Viruses and their treatment > Flashcards

Viruses and their treatment Flashcards

1
Q

after the initial acute infection, the course of an infection is determined largely by

A

the immune response of the host –> clearance of persistence

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1
Q

what is antigenic variation

A

viruses can vary their surface antigens - allows the virus to escape neutralization by pre-existing antibody

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2
Q

what is the receptor for influenza viruses

A

carbohydrate - sialic acid

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2
Q

which virus causes croup

A

parainfluenza

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3
Q

what does post-translational cleavage of viral proteins involve

A

usually needs virus-coded proteases

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4
Q

how does HCV inhibit T cell priming by DC

A

blocks cytokine induced maturation of DC

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5
Q

how do viruses attach to cells

A

viral attachment protein binds specifically to a receptor (protein or carbohydrate) on the plasma membrane

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5
Q

which viruses infect the pharnx

A

adenovirus

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6
Q

why is tryptase Clara so important in influenza

A

HA must be cut for the influenza virus to be infectious - this enzyme is only in our RT –> stops it from infecting systemically

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7
Q

what is antigenic shift?

A

sudden appearance of an influenza A virus of a new HA (and sometimes a new NA) within the human population

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8
Q

how does budding of virons happen

A

patches of viral envelope glycoproteins accumulate in the plasma membrane. Capsid proteins and nucleic acid condense direcly adjacent to the cell membrane - the bulges out

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8
Q

barriers to infection in via the alimentary tract

A
  • sequestration in intestinal contents
  • mucus
  • acidity
  • intestinal alkalinity
  • proteolytic enzymes secreted by pancreas
  • lipolytic activity of bile
  • IgA
  • scavenging macrophages
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8
Q

what are the three outcomes when viruses infect a foetus

A
  • death and abortion by cytocidal viruses
  • developmental abnormalities by non-cytocidal viruses
  • immunological tolerance - but a carrier
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9
Q

2 ways viruses can penetrate cells

A
  • lipid viruses - can fuse with the host cell membrane and release virus nucleocapsid directly into the cytoplasm - entry via endocytosis
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9
Q

mechanisms of viral spread throughout the body

A
  • local spread on epithelial surfaces - subepithelial invasion and lymphatic spread - spread via bloodstream - viremia - neural spread
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10
Q

action of rotovirus

A

infect and destroy epithelial cells of the intestinal villi and M cells causing inflammation and diarrhoea. Also secretes NSP4 protein that increases fluid secretion even more

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11
Q

types of virus-induced changes in cells

A
  • transformation to tumour cells - lytic infection - chronic infection - latent infection
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12
Q

how does virus enter the cytoplasm once inside endosomes

A
  • triggered by low pH of these vesicles –> induces conformational change in the viral proteins that exposes a fusion region - cause lysis of the endosome
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12
Q

which viruses infect the URT

A

rhinovirus coronavirus adenovirus measles

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13
Q

assembly of non-enveloped animal viruses - 2 strategies

A
  • spontaneous assembly of capsid proteins around the nucleic acid genome - may require proteolytic cleavage to induce the final conformation in the capsid proteins of the viron
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13
Q

what are the mechanisms of viral-induced damage to tissues and organs

A
  • death of cells resulting directs from viral replication (cyotcidal virus) - death resulting from toxicity of viral products - initiation of apoptosis - loss of function
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13
Q

How does vaccinia virus inhibit T cell priming by DC

A
  • it encodes a homolog for the cytoplasmic tail of TLR4 that inhibits signal transduction to initiate maturation of the DC - blocks cytokine induced maturation of DC
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15
Q

where do DNA and RNA viruses usually replicate in the cell - what are the exception?

A

DNA - in the nucleus - exception poxvirus RNA - in the cytoplasm - exception influenza virus

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16
Q

where is translation of viral proteins done

A

by the ribosomes of host cell

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17
Q

what produces type 2 interferons

A

NK cells and T cells

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18
Q

What is a quasispecies

A

As a result of mutation, each virus that comes out of a person is slightly different to another infected person

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19
Q

what are viruses that infect the respiratory tract which spread systemically

A
  • mumps - measles - rubella virus - varicella-zoster
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20
Q

what produces type 1 interferons when infected by virus?

A
  • macrophages - DC cells - tissue cells
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20
Q

adaptive immune response to influenza virus

A
  • CD8+ cytotoxic T cells–> kill virus-infected cells - antibody - to HA and NA
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21
Q

what do interferons do to viruses?

A

inhibits translation of viral proteins by activating PKR - activated by dsRNA

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21
Q

how does the influenza virus give us immunity

A

induces antibodies (not cytotoxic T cells)

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22
Q

which viruses can be caught when coming through the birth canal

A

HSV varicella CMV coxsackie

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23
Q

how does RSV evade CD8 T cell recognition

A

decreases the Class 1 MHC gene transcription

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24
Q

which viruses evade the immune system by evading CD8 T cell recognition

A

HIV, HSV, CMV, adenovirus, RSV, EBV

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25
Q

release of non-enveloped animal viruses

A

only released when virions accumulated in such a number that the cell lyses

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25
Q

how does influenza bind to cells

A

HA binds to sialic acid-containing receptors on non-ciliated respiratory epithelium (alpha-2-6 linkage to galactose)

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25
Q

Example of viruses that bud out of the cell membrane and are secreted out of the cell membrane

A

Influenza - Budds out Coronavirus - secreted out

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26
Q

types of immunopathology caused by viral infection

A
  • antibody mediated pathology - T cell mediated pathology
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27
Q

typical influenza symptoms

A

fever/chills cough headache muscle aches fatigue loss of appetite

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28
Q

which viruses if infected during foetal life causes developmental abnormalities

A

rubella CMV

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29
Q

what is the difference between early and late proteins made by viruses

A

early proteins are usually non-structural late proteins are usually structural

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29
Q

what are the 2 main mechanisms for viruses evading the immune system?

A
  • not being recognised - interfering with the functioning of particular immune mechanisms
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30
Q

which viruses evade the immune system by inhibiting T cell priming by DC

A

vaccinia, HCV, HSV, measles, CMV

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30
Q

what is antigenic drift in influenza virus

A

mutations and selection of the HA and NA proteins –> pre formed antibodies dont recognise these

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31
Q

baltimore classes

A
  1. ds DNA 2. - or + ssDNA 3. ds RNA 4. + mRNA 5. - RNA 6. + RNA
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31
Q

what are the targets (and example of the virus) of inhibiting T cell priming by DC

A
  • block cytokine induced maturation of DC (vaccinia and HCV) - interfere with proteins on MHC and costimulatory molecules needed for T cell priming (measles and CMV) - blocks signal transduction from Toll-like Rs (HSV) on DCs - encode a homolog of the cytoplasmic tail of TLRs on DCs
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32
Q

what is the latent and eclipse periods of viral replication due to

A

when virus broken down into its particles and then amplication before genome assembled for release and spread

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33
Q

how does CMV protein evade CD8 T cell recognition

A

CMV protein binds to TAP transporter on luminal side and prevents peptide translocation to ER

33
Q

why are influenza pandemics rare?

A

because the virus has to come from birds - where the receptor is alpha-2-3 Gal. Therefore they receptor specificity of the virus has to change before it can affect us

34
Q

why doesnt rhinovirus spread throughout the RT

A

because it is unstable at higher temps of the LRT

35
Q

what type of viruses tend to survive in the alimentary tract

A

viruses with multiple capsids that are acid and bile resistant with no envelope

37
Q

what are cytopathic effects

A

morphological changes occurring in cells as a result of infection seen by light microscopy

38
Q

structure of influenza virus

A
  • enveloped virus (HA and NA) - has 8 segments of -ve sense ss RNA - Has M1 matrix protein - Has M2 ion channel
40
Q

routes of entry of viruses

A
  • conjunctiva - respiratory tract - alimentary tract - urogenital tract - parenteral inoculation - skin (via wound)
42
Q

what clinical sign is diagnostic of measles

A

Koplick spots - where the virus is initially replicating - where the lymphocytes are coming in to fight the infection (the spots are the lymphocytes)

44
Q

determinants of viral tropism

A
  • availability of receptors - optimal temperature for replication - stability in extremes of pH - ability to replicate in macrophages and lymphocytes - polarized release - presence of activating enzymes
45
Q

if tryptase Clara does not work on influenza, what happens

A

virus cannot escape the endosome

46
Q

flu spread by

A

droplet inhalation

48
Q

what is an example of cytopathic effects

A

inclusion bodies

48
Q

which viruses infect the alveoli

A

RSV parainfluenza 3 adenovirus

49
Q

currently, what does our influenza vaccine contain

A

H1N1, H3N2 and influenza B

50
Q

what is the receptor for rhinoviruses

A

protein - ICAM-1

51
Q

outcomes of viral infection

A
  • fatal - full recovery - recovery but permanent damage - persistent infection
52
Q

incubation and infectious periods of flu

A

incubation = 1-5 days infectious = 5-6 days

53
Q

what cells does the measles virus infect and what is its route through the body

A

local macrophages, lymphocytes and DC –> then draining lymph nodes –> then enter circulation and amplify in lymphoid tissue –> then returns to epithelial cells in lung and mouth

55
Q

first thing that virus has to do for replication

A

translation of nonstructural proteins ( including RNA-dependent, DNA polymerase) –> forms a polyprotein which autocleaves itself

55
Q

how can the flu lead to getting a secondary bacterial infection

A

viral replication can then go onto to replicate inside ciliated epithelium –> no elevator to stop normal commensals of the URT to move down into the LRT and colonise

56
Q

targets of vaccine-induced immunity to the influenza virus

A
  • antibody binds to HA - blocking attachment - antibody to NA - blocks efficient release
57
Q

what is the ancestral hosts of influenza type A

A

aquatic birds

59
Q

order of genome replication and protein synthesis in viral replication

A
  1. translation of nonstructural proteins 2. autocleavage and further cleavage of polyprotein 3. synthesis of minus strand 4. synthesis of new plus strands
60
Q

where does influenza multiply

A

in the epithelial cells of the upper and lower respiratory tract, but particularly large airways

61
Q

attachment of HIV virus

A

2 receptors - initial and then closer attachment - initial attachment via gp120 to CD4 protein on T cells –> conformational change in the glycoprotein - exposing the hydrophobic portion of GP41 protein and recruits chemokine receptors - binding of chemokine receptor to GP41

61
Q

Why are pigs so scary for influenza?

A

has mixed alpha-2-6 and alpha 2-3 linked SA receptors –> therefore can get coinfection with 2 viruses –> swapping of genes (reassortment) –> infectious to humans

62
Q

which viruses infect the bronchioles

A

RSV, parainfluenza 3

63
Q

How does fusion of the endosome with the influenza viral envelope occur

A

as the endosome becomes more acid - the HA changes conformation leading to fusion –> escape of the 8 viral RNPs

64
Q

Example of viruses that cause lysis of the cell

A

Enterovirus, reovirus

66
Q

the infectious process can be halted by:

A
  • antibody - blocks uptake and/or neutralises progeny virus - killing the infected cell by cytotoxic T cells, NK cells or Ab-mediated mechanisms - IFN - blocking the replication cycle by specific antiviral drugs
67
Q

current influenza viruses infecting humans

A

H1N1 H3N2

69
Q

which cells do viruses infect in the alimentary canal

A
  • enterocytes - M cells
70
Q

function of NK cells

A

spontaneous cytotoxicity towards a variety of tumour cells and virus-infected cells - major source of IFN-gamma

71
Q

action of HA and NA

A

HA - has 3 R binding pockets that bind and engage with sialic acid and gets into the cell NA - has 4 subunits that cuts off the sialic acid receptors from the cell surface

72
Q

viral genomes are continually changing as a result of

A
  • mutation - recombination - reassortment
73
Q

where does glycosylation of envelope glycoproteins occur

A

in the RER and Golgi vesicles –> results in their deposition in the cell plasma membrane

75
Q

how does HSV inhibit T cell priming by DC

A

it blocks signal transduction from TLR on DC

76
Q

6 steps of viral replication

A
  1. assembly 2. penetration 3. uncoating 4. amplification - genome replication, RNA synthesis and protein synthesis 5. assembly 6. release
78
Q

what is receptors of measles virus

A

CD150 and CD46

80
Q

what makes an avian influenza virus highly pathogenic

A

have different cleavage sites that can be cut by an enzyme found in all cells –> systemic spread

82
Q

How does HIV evade CD8 T cell recognition

A
  • by making Nef protein - inducing the endocytosis of Class 1 MHC molecules to remove presentation of antigen - antigenic variation of epitope presented by MHC - class 1 MHC gene transcription decreased
84
Q

how does antigenic variation arise

A

arise spontaneously through errors in RNA replication giving rise to point mutations in the genes

86
Q

what are viruses that infect the respiratory tract that stay localised

A
  • rhinovirus - Respiratory syncytial virus - influenza virus
87
Q

drug names of virals that act by blocking the action of NA of influenza

A

Relenza and Tamiflu

89
Q

what does the stage of uncoating entail

A

the release of the viral genome from its protective capsid to enable the nucleic acid to be transported within the cell and transcribed to form new progeny virus

90
Q

how do you get the symptoms of flu?

A

IL-1 –> fever IFN–> malaise, headache and muscle aches

91
Q

drug names of antivirals that act on the ion channel of influenza virus

A

amantadine and rimantadine

93
Q

3 ways viruses can escape the actions of interferons

A
  • produces small stretches of RNA that bind to PKR preventing interaction with dsRNA - virus-encoding protein binds to dsRNA preventing PKR activation - virus encoded homologue of eIF2 (translation factor) which competes for PKR inhibiting phsophorylation
94
Q

What is antibody mediated pathology of viral infections

A
  • Ab-dependent enhancement of infection - Antigen-Ab complexes - deposition causes damage
95
Q

who is particularly susceptible to H1N1 flu

A

pregnant women obese indigenous populations

96
Q

How does adenovirus evade CD8 T cell recognition

A
  • adenovirus protein binds MHC peptide complex and retains it in the ER - class 1 MHC gene transcription decreased
98
Q

how does HSV evade CD8 T cell recognition

A

HSV protein binds to cytosolic side of TAP transporter and prevents peptide translocation to ER

99
Q

how are there different subtypes of Type A influenza

A
  • differ in the form of HA and NA they encode (have similar internal proteins)
100
Q

functions of type 1 and 2 interferons against viruses

A
  • inhibits viral replication - activates NK cells (1) Activates macrophages (2) - enhances MHC class 1 expression targets
101
Q

how can viruses cause host damage

A
  • viral induced damage - consequence of the immune response: –> immnopathology, immunosuppression, autoimmunity
102
Q

how are enveloped viruses assembled and released - 2 strategies

A
  1. budding 2. utilise the secretory pathway
103
Q

targets of influenza antiviral drugs

A
  1. ion channel blockers - inhibits the function of the M2 ion channel, preventing endosome escape of RNPs 2. NA inhibitors
104
Q

which virus evade the immune system by affecting NK cell activity and how

A

human CMV - encodes an MHC class-1 like molecule that is expressed on surface of infected cell and delivers a negative signal to NK cell but cannot itself present peptides to CD8 T cells

105
Q

viruses that infect the GI system but then spread systemically

A

hep A poliovirus

106
Q

how does HIV penetrate the cell

A

the hydrophobic region of gp41, once exposed, can initiate fusion of the two membranes

107
Q

primary and secondary phases of viremia

A
  • primary - when virus first enters the blood (only a small amount of virus) - secondary - when it gets to target organ, the virus amplifies and then released into bloodstream again in large loads
108
Q

what is special about type A influenza

A

it also infects other species (type B and C don’t)

110
Q

barriers to infection in the respiratory tract

A

mucus, cilia, alveolar macrophages, temperature gradients, IgA

111
Q

How does antigenic shift cause pandemics?

A

complete lack of protective immunity –> rapid global spread

112
Q

definition of tropism

A

anatomical localization of infection

113
Q

humans with NK cell deficiency are highly susceptible to which viruses

A

varicella and CMV (herpes virus family)

114
Q

What are inclusion bodies

A

Represent accumulated viral proteins at he site of viral assembly

115
Q

how does EBV evade CD8 T cell recognition

A

it inhibits the proteosome

116
Q

activation mechanism of NK cells

A
  • activation receptor recognizes molecules on the cell surface that are there as a result of virus infection and will send a killing signal - the inhibitory receptor binds to MHC class 1 molecule on the tarted cell - if engaged will override the killing signal
117
Q

how does the measles and CMV inhibit T cell priming by DC

A

blocks T cell stimulation - by interfering with the proteins on MHC and costimulatory molecules needed for T cell priming

118
Q

how long does the flu normally last

A

~7 days - longer in those who have poor IS

119
Q

how are NK cells activated

A

in response to IL-12 or IFN-alpha/betta

Z MD1 Respiratory block (11 decks)

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