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PH1123 Microbiology > Viruses > Flashcards

Viruses Flashcards

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1
Q

what is a virion?

A

a delivery system that surrounds a payload

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2
Q

what is the payload of the virion constitute?

A

structural components used by the virus to survive in the environment (viral genome + enzymes for initial viral replication)

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3
Q

what is a capsid?

A

a single or double layer protein shell that surrounds the nucleic acid of a virus

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4
Q

what is a nucleocapsid?

A

when the capsid surrounds the nucleic acid

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5
Q

what are the subunits that form the capsid called?

A

capsomers

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6
Q

how are the viral capsid proteins arranged?

A

icosahedral:-

  • 20 triangular faces, 12 vertices
  • spherical
  • nucleic acid inside the spherical core

Helical:-

  • proteins bound in a regular periodic fashion along nucleic acid
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7
Q

what is the difference between enveloped and non-enveloped viruses?

A

enveloped viruses possess an envelope that surrounds the nucleocapsid whereas the non-enveloped don’t

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8
Q

what does the viral envelope contain?

A
  1. virus specific proteins (matrix proteins)
  2. lipids
  3. carbohydrates
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9
Q

where is the matrix protein located?

A

it lines the inner surface of the viral envelope and is in contact with the nucleocapsid

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10
Q

what is the function of matrix proteins?

A
  • stabilize the interaction between viral glycoproteins and the lipid envelope
  • direct the viral genome to intracellular sites of assembly
  • help in virus budding
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11
Q

briefly, what are the general steps in virus replication?

A
  1. attachment & penetration
  2. macromolecular synthesis
  3. assembly of progeny virions and release from host cells
  4. dealing with defective viruses
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12
Q

define adsorption

A

attachment of the virus to the host cell surface as a result of random collision between the virions and the target cell

(first step of viral infection of a susceptible cell)

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13
Q

how are viruses able to attach to cell surfaces?

A

viruses have attachment proteins to facilitate adsorption, for example hemaglutinin in influenza

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14
Q

describe the mode of attachment of enveloped and nonenveloped viruses

A

Enveloped viruses: have more than one attachment protein on their surface

Nonenveloped viruses: they have surface exposed regions of capsid proteins to mediate virus attachment

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15
Q

how are some viruses able to attack different cell types?

A

some viruses use multiple receptors as points of attachment which allows them to invade various cell types

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16
Q

what happens after adsorption?

A

payloaad is translocated across the plasma membrane of the host cell

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17
Q

how do enveloped and non-enveloped viruses gain entry to the inside of the cell?

A

-Enveloped viruses gain entry directly by fusing their envelop with the plasma membrane

-Non enveloped viruses: virus is taken by endocytosis and fuses with endosomal membrane inside the cell

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18
Q

continue the blanks

  • non enveloped viruses bind at receptors that aggregate at the ________ & then endocytosed within clathrin-coated vesicles before delivery to endosomes
A

clathrin-coated pits

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19
Q

what is uncoating?

A

process in which the capsid is removed to make the viral genome accessible to cellular transcription and translation mahinery

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20
Q

TRUE OR FALSE

for many viruses, penetration and uncoating occur together

A

TRUE

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21
Q

How are capsids removed for nonenveloped viruses during replication?

A

by host cell enzymes

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22
Q

how are reoviruses capsids removed?

A

reoviruses have proteases in late endosomes, and lysosomes that remove the outer capsid proteins producing a subvirion particle

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23
Q

what is the function of a subvirion particle?

A

it penetrates endosomal membranes leading to activation of virus transcription in the cytoplasm

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24
Q

what is macromolecular synthesis in viral replication?

A

translation of viral mRNA into virus specific proteins

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25
Q

what enzyme is used to produce viral RNA?

A

Virus-encoded RNA-dependent RNA polymerase

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26
Q

how is positive sense RNA produced during macromolecular synthesis?

A

virus encoded RNA dependent RNA polymerase synthesizes a negative sense RNA that serves as a template for the synthesis of positive sense RNA that is then packaged into progeny virion

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27
Q

TRUE OR FALSE

viral RNA acts as mRNA, translated by cellular ribosomes to produce viral proteins

A

TRUUUE

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28
Q

how is mRNA translated in poliovirus?

A

mRNA is translated to a single large polyprotein that is cleaved by virus encoded proteases to release individual viral proteins

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29
Q

How is negative sense RNA synthesized in macromolecular synthesis of viral replication?

A

During replication of the viral genome, RdRp synthesizes a positive-sense antigenome that it uses as a template to create genomic negative-sense RNA

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30
Q

why must double stranded RNA viruses copy their RNA strands to single positive sense RNA?

A

because the double stranded character of RNA cannot function directly as mRNA, thus it must be copied to single positive sense RNA for it to act as mRNA

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31
Q

which enzyme is used to generate a negative strand of the double stranded RNA to synthesize a single stranded positive sense RNA?

A
  • virus encoded RNA dependent RNA polymerase
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32
Q

explain the process of RNA replication through DNA intermediates

A

positive sense RNA serves as a template for the enzyme (RNA dependent DNA polymerase), whereby DNA is then integrated into host chromosomal DNA and transcription is carried by host cell DNA dependent RNA polymerase

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33
Q

what virus is an example of viral replication that occurs through DNA intermediates?

A

Retroviruses (HIV)

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34
Q

How do DNA viruses, like herpesvirus, make mRNA?

A

by using strategies similar to those of the host cell’s, they are tightly regulated and result in synthesis of early and late mRNA transcripts

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35
Q

what is the difference between early and late mRNA transcripts?

A

early transcripts: encode regulatory proteins and proteins required for DNA replication

Late transcripts: encode structural proteins of the virion

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36
Q

why is it that poxvirus is unable to use host RNA polymerases during replication?

A

because the initial steps of transcription and translation occur in the host cell cytoplasm, and RNA polymerases are located in the nucleus

however, poxvirus carry its own DNA-dependent RNA polymerase to initiate transcription

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37
Q

what happens after the process of macromolecular synthesis?

A

intact virions are assembeled and released from host cells

nucleocapsid formation (viable virions)

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38
Q

what events lead to viral cell death/disruption

A
  1. inhibition of host macromolecular synthesis
  2. disorganization of host cell cytoskeleton
  3. alteration of host cell membrane structure
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39
Q

how are enveloped and non-enveloped viruses released?

A

non enveloped: upon cell death

enveloped: from infected cell by budding

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40
Q

how do viruses kill cells?

A

by apoptosis characterized by cell shrinkage, membrane blebbing, condensation of nucleur chromatin, and cleavage of cell DNA

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41
Q

What is a defective virus?

A

A virus particle that contains insufficient nucleic acid to provide for production of all essential viral components

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42
Q

what is an example of a defective virus?

A

Hepatitis delta, for hepatitis delta to manifest, one must also be infected by Hepatitis B, which allows the replication of hepatitis delta

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43
Q

how are defective viruses diagnosed?

A
  • by antigen search
  • culture in the presence of a helper virus
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44
Q

define a helper virus

A

virus that allows an otherwise-deficient coinfecting virus to replicate

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45
Q

what are the characteristics of herpes virus?

A
  • double stranded DNA genome
  • icosahedral nucleocapsid
  • enveloped
  • life-long latent infections
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46
Q

what are herpesvirus subfamilies?

A
  • alpha (HSV1/HSV2/VZV)
  • beta (cytomegalovirus/HSV-6/HSV-7)
  • gamma (Epstein barr/HSC-8)
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47
Q

How are HSV-1 & HSV-2 transmitted?

A

HSV1 → oral-oral / oral-genital

HSV2 → oral-oral / oral-genital / genital-genital

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48
Q

How is VZV transmitted?

A

Respiratory route via aerosols/vesicular fluid

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49
Q

why is it that asymptomatic HSV infected patients can still transmit the infection?

A

because shedding from epithelial surfaces can occur even if lesions aren’t noticeable

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50
Q

TRUE OR FALSE

HSV is almost always asymptomatic, VZV is almost always symptomatic

A

TRUE

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51
Q

what organs does herpes virus infect?

A

mainly mucous membranes (genitals,mouth, respiratory tract,anus,eyes)

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52
Q

what is the first line of defense against herpes?

A

skin

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53
Q

how come herpes affects mucos membrane but not skin?

A

the thick keratin layer of the superficial epidermis prevents access of HSV to its receptors, and because mucous membranes present a more formidable barrier that is readily affected

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54
Q

how does herpes virus infect cells?

A
  1. attaches to susceptible cell
  2. glycoproteins projecting from viral envelope inteact with surface receptors
  3. glycoproteins interact with heparan sultate chain on the proteoglycan and bind to it
  4. virus will be close to molecules that facilitate its entry
  5. binding triggers fusion of viral envelope with either cell membrane or plasma membrane
  6. viral nucleocapsid is released into the cytoplasm
  7. viral genome released into nucleus
  8. replication occurs inside the cell in temporal fashion (proteins→genome→progeny virions)
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55
Q

what is a herpesvirus latent infection?

A

viral genome circularizes in the nucleus as an episome with minimal gene transcription

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56
Q

when do you refer to an infection as productive infection?

A

when virus replication occurs, immediate early genes are transcribed with transcription factors in the virion tegument

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57
Q

what is a virion tegument?

A

space between nucleocapsid surface and envelope

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58
Q

what are the proteins encoded by immediate early genes?

A
  1. early genes: required to replicate viral DNA
  2. Late genes: encode proteins that assemble and comprise progeny virions + glycoproteins inserted into cell membrane
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59
Q

what immune responses occur in herpes virus?

A

neutrophils

NK cells

Cytokines

Interferons

t lymphocytes

60
Q

why is it that the immune system is unable to get rid of herpesvirus 1 & 2?

A

because cells of latent infections do not stimulate the immune system, thus it does not attack it

61
Q

who is considered a risk patient for HSV?

A

neonatal HSV, which could be lethal due to greater innate susceptibility and immunological immaturity

62
Q

what tissue does HSV infect?

A

epithelial, causing vesicular lesions that rupture to a shallow gray/white ulcers on en erythmatous base

63
Q

why are HSV infected epithelial tissues able to fully regenerate?

A

because viral replication and spread are contained by innate and cell mediated response

64
Q

what causes symptoms of itching, tingling, burning, and pain in HSV infected patients?

A

because of the damage and inflammation to nerves during acute phase of infection

65
Q

what triggers reactivation of HSV?

A
  • immune impairment
  • emotional stress
  • menstruation
  • sunburn
66
Q

how is herpes treated?

A

nucleoside analog drugs such as acyclover

67
Q

what is the mechanism of action of a nucleoside analogue (e.g. acyclover)?

A

it is phosphorylated by herpes enzymes and incorporated into viral DNA as a chain terminating nucleotide since it is a guanosine analog

68
Q

what is a prodrug?

A

drug substance that is inactive in the intended pharmacological actions and it must to be converted into the pharmacologically active agent by metabolic or physico-chemical transformation.

69
Q

what are prodrugs of acyclover?

A

valacyclover

lialacyclover

70
Q

what is one key pharmacological feature of prodrugs?

A

they have improved oral bioavailability

71
Q

TRUE OR FALSE

long term treatment with acyclover prevents hsv recurrences and flare ups

A

TRUE

72
Q

what genes are required for retroviral replication?

A
  1. gag (core proteins)
  2. pol (RNA dependent RNA polymerase/integrase)
  3. env (gp120/gp41)
  4. pro (proteases)
73
Q

what is the function of proteases in retroviruses?

A

cleave gag and pol to their active forms

74
Q

what are the means of transmission of HIV?

A
  • sexual intercourse
  • vertical transmission (birth)
  • IV drugs (through needles)
75
Q

who is a risk patient for HIV?

A

Hemophilia, because they receive blood donations from thousands of donors and it’s from factors VIII & IX

76
Q

what roles do genes have in HIV infection?

A

presence of CCR5 receptor is important for HIV infection, if it is defected, infection with HIV will progress very slowly to aids

77
Q

why is it that the 2 RNA molecules resemble eukaryotic mRNA in retroviruses?

A

because they contain a cap structure at the 5’ end and a polysequence at the 3’ end

78
Q

what is the main target of HIV?

A
  1. Helper t-lymphocytes (CD4)
  2. monocytes
79
Q

what are the steps of HIV infection?

A
  • binding
  • fusion
  • DNA synthesis
  • integration
  • latency & transmission
  • progeny virion synthesis
80
Q

how does HIV bind to CD4?

A

HIV binds to CD4 via gp120 which reacts with CCR5 or CCR4 making attachment easier on the cell surface.

81
Q

what happens after gp120 binding to CCR5/CCR4?

A

a conformational change, bringing hydrophobic domain of the protein in apposition with cell membrane.

82
Q

which enzyme facilitates the release of the viral core into the cytoplasm?

A

reverse transcriptase

83
Q

what does integrase do in viral replication?

A

catalyzesthe transport of DNA to the nucleus by joining LTR and host cell DNA

84
Q

what is a provirus?

A

viral genetic material in integrated state, which is analagous to cellular gene (passed to daughter cells at division)

85
Q

what does LTR do?

A

directs RNA synthetic machinery

86
Q

explain transactivation

A

when the expression of HIV macromolecules is subject to regulation by viral gene products that operate at soluble elements

87
Q

what are the viral genes that contain transactivating factors?

A

Tat

Rev

88
Q

what is the function of transactivating factors?

A

increase the expression of viral RNA proteins

89
Q

what does tat do?

A

accelerate transcription of viral RNA by host RNA

90
Q

what does rev do?

A

enhances transport of viral RNA from nucleus to cytoplasm

91
Q

Bonus fact

when infected with a provirus, infectious process may be halted, and then reinitiated explosively due to high level of transactivation

A

read that again

92
Q

what are the genes that facilitate evasion of virus specific immune responses

A

nef: downregulated cell surface expression of MHC-1
vif: facilitate destruction of ABOBEC 3G
vpu: downregulated tethrin

93
Q

how does HIV persist in the body despite immune response?

A

because virus gene products are invisible to immune cells, they change their antigenic specificity and replicate in lymphoid follicles

94
Q

which HIV gene products direct immune response?

A

gag +pol → show stability from one isolate to another

env: mutations that lead to variation in its products (gp120/gp140)

95
Q

true or false

some antibodies can neutralize viruses

A

true

96
Q

what are the properties of the viral envelope?

A
  • extensive polysaccharide coating, limits immunogenecity
  • hypervariable regions, permit virus to present new antigenic variation to host
97
Q

which gene gives the virus the ability to change its antigens?

A

gp120

98
Q

how does gp120 provide antigenic variation?

A

by hiding conserved sequences, thus protecting them from the neutralizing antibodies by carbohydrates and hypervariable region

99
Q

what is the function of RNA transcriptase?

A

uses RNA to as a template similar to that of the human’s to produce DNA. (Reverse transcription)

such viruses are capable of causing cancer

100
Q

what is the mechanism of action of non-nucleoside reverse transcriptase inhibitors?

A

prevent HIV from replicating by blocking the reverse transcriptase enzyme.

101
Q

what is acute HIV infection

A

Acute HIV infection is the earliest stage of HIV infection, and it generally develops within 2 to 4 weeks after infection with HIV

102
Q

what is the immune response against acute HIV

A

cytokines - chemokines

103
Q

what happens after a few week after HIV infection?

A
  • virus specific cytotoxic t cells appear in peripheral blood and lymphoid tissue
  • neutralizing antibodies are detected in plasma
104
Q

what is the primary cell target of HIV?

A

99% CD4

1% monocytes & resting CD4 Tcells

105
Q

what leads to progressive immunodeficiency (aids) in HIV?

A

the loss of CD4 & t cell population. with a count of 50cells/ mm3

normal count is = 1000 cells/mm3

HIV count is = 200 cells/mm3

106
Q

what does a high virus load in plasma indicate (105 copies)

A

HIV disease progression to AIDS within a few years

107
Q

define lymphopenia

A

decreased number of t cells

108
Q

how does HIV cause immunodeficiency?

A

by causing t cells to malfunction, leaving the body unable to produce antigens, therefore the patient becomes immunodeficient

109
Q

what is the main cause of death in AIDS patients?

A

pneumonia jiroveci and mycobacterium tuberculosis

110
Q

how is HIV/AIDS diagnosed?

A

cell culture

PCR assay

serologic test

111
Q

why is it that during the diagnostic testing of HIV, absence of antibodies does not exclude HIV infection?

A

because some patients lose their antibody detection due to the long time they have been infected with the virus

112
Q

what is the initial test for HIV?

A

ELISA (twice) because it has a possibility of false-positive

113
Q

what classes of drugs are used for HIV?

A

nucleoside reverse transcriptase inhibitors

didoxynucleotides

nonnucleoside reverse transcriptase inhibitors

protease inhibitors

114
Q

what is the mechanism of action of NRTI

A

When RT is creating new DNA, it inserts a molecule of zidovudine rather than a nucleoside this terminates DNA chain and no more can be appended to it

115
Q

what is the mechanism of action of NNRTIs

A

NNRTIs attach to the reverse transcriptase and affect the activity of the enzyme by restricting its mobility and making it unable to function

116
Q

what is the mechanism of action of protease inhibitors?

A

HIV protease inhibitors binds to enzyme active site, thus HIV virus unable to process proteins

117
Q

what is the mechanism of action of neuraminidase inhibitors?

A

inhibition of the activity of the viral neuraminidase, preventing the release of virions

118
Q

what are the 3 enteroviruses?

A

polioviruses

echoviruses

coxsackieviruses

119
Q

where is poliovirus found?

A

feces 💩

120
Q

what what causes poliomyelitis?

A

polioviruses found in feces, due to contaminated water or through fecal-oral route

121
Q

where do polioviruses replicate?

A

oropharyngeal and intestinal mucosa

122
Q

do polioviruses enter the blood stream?

A

yes, causing viremia within 7 days of infection with a poliovirus

123
Q

what is a rare complication of polioviruses?

A

1% invade CNS causing paralysis 11-13 days after infection

124
Q

why certain sites don’t allow replication of poliovirus even though all cells have CD155?

A

due to tropism, influenced by host immune response, and cell is protected by interferons that put tissue in antiviral state

125
Q

what are the properties of the coronavirus?

A
  • enveloped
  • positive sense RNA virus
  • responsible for 30% of common colds
  • undergoes rapid genetic change
126
Q

what is SARS?

A

Severe acute respiratory syndrome (SARS) is a viral respiratory disease caused by a SARS-associated coronavirus.

127
Q

what is SARS COV derived from?

A

Bats

128
Q

what is the function of RNA dependent RNA polymerase in coronaviruses?

A

can jump between RNA templates resulting in RNA-RNA recombination

129
Q

what is the function of RNA exonuclease in coronaviruses?

A

mediate RNA proofreading and regulate replication fidelity

130
Q

how are coronaviruses able to adapt to various new hosts?

A

coronaviruses have RNA dependent RNA polymerase which can jump betweenn RNA template resulting in RNA-RNA recombination,

and they have RNA exonuclease which mediates RNA proofreading and regulate replication fidelity

131
Q

what is antigenic drift and antigenic shift?

A

antigenic drift: accumulating changes in hemagglutinin and neuraminidase

antigenic shift: novel hemagglutinin and neuraminidase by exchange of genes with another virus

132
Q

define reassortment

A

process of exchange of genes with another virus

133
Q

what is the structure of influenza virus

A

RNA segments encapsidated by viral nucleoprotein + 3 virus encoded polymerase proteins (PA/PB1/PB2) and M proteins, surrounded by host derived lipid membrane

134
Q

how many proteins does the RNA of influenza encode, and in how many segments?

A

8 segments, 12 proteins

135
Q

what is the peak season for influenza encounter?

A

october-april

december-march

136
Q

how does influenza gain entry to the body?

A

via aerosols and direct contact, through the upper and lower respiratory tract

137
Q

what cells are the first to be infected with influenza?

A

nonciliated epithelial cells

138
Q

what is the incubation time of influenza?

A

2-3 days

139
Q

what receptor is the preferred target for influenza?

A

terminal siacilic acid with 2-6 linkage to galactose

140
Q

what is influenza infection manifestation dependent on?

A

neutralizing antibodies and immune interferons

141
Q

what drugs can be used to treat influenza?

A

neuraminidase inhibitors, prevent the removal of cell surface sialic acid, thus inhibiting spread of virus to uninfected cells

142
Q

what is the mechanism of action of amantadine?

A

inhibit uncoating and genome release into the cytoplasm, directing release back to the nucleus. this allows the formation of viral nucleoproteins and budding of new particles from cytoplasm, and then neuraminidase removes sialic acid receptors from the virus particle and cell surface leaving them unable to adhere to cell surface and each other

143
Q

what are the complications of influenza?

A

primary viral pneumonia

bacterial pneumonia

otitis media

in children: reye syndrome (brain swelling/fatty degeneration)

144
Q

how is influenza diagnosed?

A

mainly based on symptoms, or nose/throat swab for sputum

culture with chicken eggs

RT-PCR immunoassay

hemagglutinin inhibition test for previous infections

145
Q

what is the most effective treatment of influenza?

A

prophylactic treatment via vaccines

146
Q

what types of vaccines are there for influenza?

A

inactivated: formaldehyde-treated preparation, given intramuscularly, efficacy 60-90%, doesnt cause symptoms

live,attenuated, cold adapted: nasal spray, local mucosal response, longer lasting immunity, reactive against variants

147
Q

why is it important that patients of coronary disease get vaccinated for influenza?

A

to lessen the chance of myocardial infarction complication

PH1123 Microbiology (9 decks)

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