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Infection & Immunity > Anti Virals > Flashcards

Anti Virals Flashcards

1
Q

how do anti-virals work

A

they suppress the rate of replication of a virus so the host immune system can fight the infection

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2
Q

what is the structure of the herpes virus

A

spherical iscoahedron, double stranded linear DNA, enveloped, more than 35 proteins

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3
Q

what are the features of the herpes virus

A

encodes any enzymes, establish latent infections, lifelong persistence, significant cause of death in immunocompromised hosts, some can cause cancer

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4
Q

what are the three subfamilies of the herpes virus

A

alpha, beta, gamma

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5
Q

what distinguishes the herpes virus subfamilies

A

their genetic makeup

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6
Q

what strains of herpes are alpha subfamily

A

herpres simplex virus types 1 and 2, varicella-zoster virus

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7
Q

what strains of herpes are beta subfamily

A

cytomegalovirus, human herpesvirus 6 and 7

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8
Q

what strains of herpes are gamma subfamily

A

epstein-barr virus, human herpesvirus 8

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9
Q

what does HSV-1 cause

A

oropharyngeal sores in children

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10
Q

what does HSV-2 cause

A

herpes genitalia in young adults

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11
Q

what are the virulence factors of HSV-1 and HSV-2

A

gC bonds complement C3b (innate immune system)

gE is an Fc receptor for IgG (adaptive immune system)

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12
Q

how are HSV strains spread

A

by contact; the virus is shed in saliva, tears, genital and other secretions

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13
Q

what is the replication cycle of HSV-2

A
  1. host cell membrane fuses with viral envelope so nucleocapsid can enter the cytoplasm
  2. viral capsid is uncaoted and viral DNA of the genome enters the cell’s nucleus
  3. new viral DNA is synthesised by the nucleus
  4. mRNAs transported on cytoplasmic ribosomes into capsid and spike proteins
  5. capsid proteins enter the nucleus and combine with viral genomes to form new nucleocapsids
  6. viruses bud through the nuclear membrane but do not acquire their final envelope and spikes until reaching a Golgi cimpartment in the cytoplasm; exocytosis releases the new virons
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14
Q

what is aciclovir

A

structural analogue of guanosine that inhibits viral DNA synthesis

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15
Q

what formulations does aciclovir come in

A

topical, oral, IV

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16
Q

what viruses can aciclovir treat

A

HSV1 and 2, varicellar-zoster virus

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17
Q

what is the aciclovir mechanism of action

A

prodrug phosphorylated to aciclovir tri-phosphate (carried out by a viral thymidine kinase) with subsequent phosphorylation from host kinases
it is a chain terminator that gets incorporated into replicating viral DNA strand and blocking further replication; its incorporated by viral DNA polymerase

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18
Q

treatment for HSV-2

A

aciclovir 400mg tds for 7-10 days
valaciclovir 1000mg bd for 7-10 days
famciclovir 250mg tds for 7-10 days

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19
Q

what is valaciclovir

A

L-valyl ester drodrug of aciclovir

only available orally but has high oral bioavailability due to ester

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20
Q

what are the adverse effects of valaciclovir

A

headache, nausea, weakness, dizziness, confusion

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21
Q

what is famiciclovir

A

cyclic guanine analogue, converted to penciclovir in the liver and intestines
only available orally

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22
Q

what formulation is penciclovir used in

A

topical only, due to poor bioavailability

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23
Q

what are some adverse effects of famiciclovir

A

headache, GI

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24
Q

what is the structure of the varicellar-zoster virus

A

double stranded DNA, enveloped virus, long and short genome fragments, only one antigenic serotype

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25
Q

what age group does VZV infect

A

4-10 year olds

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26
Q

how does VZV gain entry to the target site

A

through the respiratory tract and then spreads to the lymphoid system, it incubates for 14 days then arrives at the skin

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27
Q

where does VZV remain latent

A

in the cerebral or posterior root ganglia

can be dormant for decades

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28
Q

what happens when VZV reactivates in ganglion

A

tracks down the sensory nerve to the area of the skin supplied by the nerve, producing a vericella form rash in the distribution of a dermatome

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29
Q

what does the varicellar virus cause

A

chickenpox

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30
Q

what is the incubation period of varicellar

A

14-21 days

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31
Q

how does varicellar present

A

fever and widespread vesicular rash

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32
Q

what is herpes zoster

A

shingles

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33
Q

what age group are commonly affected by herpes zoster

A

50+ years

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34
Q

how does herpes zoster occur

A

latent virus reactivates in a sensory ganglion and tracks down the sensory nerve to the appropriate segment
characteristic eruption of vesicles in the dermatome which is often accompanied by intensive pain lasting for months

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35
Q

how is varicellar virus managed

A

self-limiting disease

aciclovir can accelerate resolution time

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36
Q

what drugs can be used for the treatment of herpes zoster

A

aciclovir, valaciclovir and famiciclovir

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37
Q

what are the replication stages for HIV infection

A
  1. adsorption - virus attaches to host cell by specific binding of spikes to cell receptors
  2. penetration - the virus is engulfed into a vesicle by endocytosis
  3. uncoating - envelope of the virus is removed and RNA is freed into the cytoplasm
  4. synthesis - replication and protein production - cell synthesises RNA molecules, capsomers and spikes of viruses
  5. assembly - viral spike proteins are inserted into the cell ,e,brane for the viral envelope; nucleocapsid is formed from RNA and capsomers
  6. release - enveloped viruses bud off, carrying away an envelope with the spikes, ready to infect another cell
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38
Q

what is the structure of HIV

A

icosahedral, enveloped retrovirus, ssRNA virus

contains two copies f RNA, enzymes and envelope proteins

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39
Q

what is a retrovirus

A

transcribes RNA to DNA

40
Q

what enzymes does the HIV virus contain

A

reverse transcriptase, integrase, protease

41
Q

what envelope proteins does the HIV virus contain

A

gp120, gp41 (protein binding)

42
Q

how does HIV replicate

A

HIV gp120 protein mainly binds to CD4 receptors, but other receptors are involved in infection (called co-receptors)
CD4 defines the cell type that HIV will infect

43
Q

what are the main co-receptors in HIV replication

A

CCR-5

CXCR4

44
Q

which receptor will HIV use

A

very few HIV strains can use both receptors

most people have HIV that uses either CCR-5 or CXCR4

45
Q

steps of HIV replication -

what enzyme copies viral DNA within the cell

A

reverse transcriptase

46
Q

what is the site of action of AZT

A

reverse transcriptase (synthesis of viral DNA in the cell)

47
Q

how does the HIV infiltrate the cell

A

via co-receptors, which internalise the contents

48
Q

steps of HIV replication -

what is the role of integrase functions

A

to incorporate DNA into host cell genome (integrated provirus)
they are not used in unintegrated proviruses as DNA just circularises
they circularise viral DNA and form a preincorporation complex which moves into the nucleus; integrated protein inserts viral DNA into cell nucleus DNA - this is a permanent change in the cell

49
Q

what is the site of action for integrase inhibitors

A

the DNA incorporation into host cells by integrase enzymes

50
Q

why is HIV called a retroavirus

A

it uses reverse transcriptase which converts RNA back to DNA

51
Q

what happens in HIV replication after host cells are activated

A

viral DNA is transcribed, yielding mRNA and viral genome RNA

52
Q

what happens to viral RNA during HIV replication

A

they are translated, yielding viral enzymes (including protease) and structural proteins

53
Q

what happens to viral membrane proteins during HIV replication

A

they are transported to host cell membrane

54
Q

what happens during the final stage of HIV replication

A

final viral assembly and budding take place

55
Q

what is the role of protease in HIV replication

A

it ‘chops’ long polypeptide chain that are inactive to allow them to be active as smaller proteins (chains of viral genetic info)

56
Q

what drugs target HIV replication

A

NRTIs - nucleoside/nucleotide reverse transcriptase inhibitors
NNRTIs - non-nucleoside reverse transcriptase inhibitors
PIs - protease inhibitors
fusion inhibitors
integrase inhibitors
CCRS antagonists (entry inhibitors)

57
Q

what is Fuzeon

A

fusion inhibitor
blocks entry of HIV into cells (CD4 or T cells)
mimics components of Gp41 and displaces them, preventing normal fusion
it causes change in cell shape

58
Q

what is the mechanism of HIV fusion

A
  1. HIV approaches host CD4+ T-cell (its viral membrane contains trimeric glycoprotein spikes with each spike containing gp41 and gp120 subunits)
  2. fusion begins with the binding of gp120 to CD4 and chemokine receptors on the cell membrane
  3. binding induces conformational change in gp120, exposing gp41
  4. fusion is mediated by gp41, which contains two heptad repeat domains, HR1 and HR2
  5. ‘zipping’ - gp41 is exposed, the hydrophobic terminus of gp41 embeds itself into the cell membrane. the HR2 domain coils into grooves exposed on trimeric HR1 domain of gp41. this destabalises both cell and viral membranes punching a hole into both membranes which allows the HIV capsid to pass through the cell membrane
59
Q

what shape if HR1 used in HIV fusion

A

spiral/coil

60
Q

what shape is HR2 used in HIV fusion

A

disordered, floppy chain

61
Q

what is the relationship between HR1 and HR2 in HIV fusion

A

HR2 coils down HR1 which strains and breaks membranes; allowing fusion of HIV with the T-cell

62
Q

what is the mechanism of Fuzeon

A

peptide mimic of HR2 region of gp41, so it binds to the HR1 region
zipping cannot take place so the infection is blocked
it competitively binds to the HR1 before HR2 can ‘zip’, preventing membrane stress

63
Q

what action do CCR5 entry inhibitors have

A

they block the attachment of HIV to the CCR5 receptor, halting HIV replication
CXCR4 receptors will be unaffected, so replication can continue

64
Q

how do integrase inhibitors work

A

targets integrase enzymes that incorporate viral DNA into host cells
breaks DNA by breaking bond between sugar and phosphate which requires metal ions; drug competes for metal ions

65
Q

how do nucleoside/nucleotide RT inhibitors work

A

based on the structure of nucleotides/nucleosides and lack a hydroxyl group
NTRIs act as chain terminators or inhibitors at the substrate binding site of reverse transcriptase

66
Q

how do non-nucleoside RT inhibitors work

A

inhibit viral DNA replication by binding at the allosteric non-binding site of RT, causing a confrontational change of the active site

67
Q

how do protease inhibitors work

A

proteases process GAG and POL polyproteins into mature HIV components. PI drugs contain a hydroxyethylene bond instead of a peptide bond, which makes PIs non-scissile substrate analogues for HIV protease
drugs mimic shape to bond and prevent breaking/cleaving of bonds so are competitive inhibitors

68
Q

what does HAART stand for

A

highky active anti-retroviral therapy

69
Q

what is the common combination of HAART drugs used

A

3 anti-retrovirals from at least two different classes (2NRTIs and 1NNRTI, PIs or II)
reduces resistance

70
Q

what can be a side effect of HAART

A

liver disease due to toxicity

71
Q

what is a nucleocapsid

A

capsid and nucleic acid of a virus

72
Q

what is a naked virus

A

without an envelope, only the nucleocapsid

73
Q

how are DNA viruses release from host cells

A

budded off the nucleus

74
Q

how are RNA viruses released from host cells

A

they multiply and are then released from the cytoplasm

75
Q

what are the two main modes of penetration used by viruses

A

endocytosis and fusion

76
Q

what form of penetration do naked viruses use

A

endocytosis

77
Q

what method of penetration do encapsulated viruses use

A

fusion

78
Q

what is viral pathogenesis

A

the process where a viral infection leads to disease

disease is abnormal and of no advantage to the virus

79
Q

what are the outcomes of acute viral infection

A

no residue effects, recovery with residue effects like neurological issues, death, chronic infection

80
Q

what are the outcomes of chronic infection

A

silent subclinical infection for life, long period before disease, reactivation to cause acute disease, chronic disease with relapses and exacerbations, cancers

81
Q

what factors determine viral pathogenesis

A

cellular pathogenesis, entry into host, course of infection, cell/tissue tropism, cell/tissue damage. host immune response, virus clearance or persistance

82
Q

what are some methods of transmission for viruses

A

respiratory transmission, faecal-oral transmission, blood-bourne transmission, sexual transmission, animal or insect vectors

83
Q

what are the sites of viral entry

A

skin, conjunctiva or mucous membranes, respiratory tract, gastrointestinal tract

84
Q

what is primary replication

A

where the virus replicates after gaining entry into the host

this determines whether infection is localised or spread

85
Q

what is systemic spread

A

spreading of a virus via bloodstream or CNS

86
Q

what is secondary replication

A

infection taking place at susceptible organs/tissues following systemic spread

87
Q

what is cell tropism

A

viral affinity for specific body tissues

88
Q

what determines cell tropism

A

cell receptors for virus, cell transcription factors that recognise viral promoters and enhancer sequences, ability of cell to support virus replication, physical barriers, temp/pH/O2, digestive enzymes may inactivate some viruses

89
Q

what are the effects of picornaviruses

A

cause cell lysis and death when they replicate, leading to fever and increased mucous secretion
like rhinovirus or poliovirus

90
Q

what are the primary events in the innate immune response

A

induction of type 1 interferons

activation of NK cells

91
Q

what happens during induction of type 1 interferons

A

double stranded RNA of the virus induces the expression of the interferons by the infected cell
the bound interferons will activate the JAK/STAT pathway responsible for the synthesis of several genes (one encodes 2-5A synthetase that activates ribonuclease)

92
Q

what role do interferons and natural killer cells have

A

IFN-alpha and IFN-beta binding induces a specific protein kinase called RNA-dependent protein kinase
the binding to NK cells induces lytic activity which is effective in killing virally infected cells and enhanced by IL-12

93
Q

what is the function of antibodies

A

if produced to the viral receptor, can block infection and prevent binding to host cells
some can cause lysis of enveloped virions
some agglutinate viral particles and function as opsonising agent

94
Q

what are the two main components of cell-mediated antiviral defence

A

CD8+T cells

CD4+T cells

95
Q

how do viruses respond to host-immune responses

A

they encode proteins that interfere at various levels
some evade IFN-alpha/beta action, some inhibit antigen presentation, some evade complement-mediated destruction, some cause immunosuppression-direct viral infection of lymphocytes or macrophages, some constantly change their antigens

Infection & Immunity (22 decks)

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