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411- VIROLOGY > LESSON 1: INTRODUCTION > Flashcards

LESSON 1: INTRODUCTION Flashcards

1
Q

General description of a virus:

A
  • Obligatory intracellular infectious
    agents,
    -size from 20 to 400 nanometer (nm)
  • Filterable agents
    -Nocellular organization and do not have organelles
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2
Q

are thesmallest viruses (20nm)

A

picornaviruses

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2
Q

The picornaviruses (e.g.)

A

Foot and Mouth-Disease virus

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3
Q

are the largest viruses
(300nm)

A

poxviruses

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3
Q

Viruses cannot be seen by light microscope because of their small size except

A

poxviruses

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4
Q

Contain only one type of nucleic acid

A

DNA or RNA

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5
Q

Viruses multiply by a complex process involving

A

protein synthesis and nucleic
acid production

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6
Q

Viruses are unaffected by

A

antibiotics

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7
Q

Threecategories:

A

-DNA viruses,
-RNA viruses and
-Viruses that utilize both DNA
and RNA for replication

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8
Q

the viruses that infect bacteria

A

Bacteriophages or phages

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9
Q

an infectious extracellular virus particle consists of nucleic acid (DNA or RNA) that is covered by a protein coat called capsid

A

Virion

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10
Q

a shell of subunits of proteins called capsomere that encloses the
genome of vertebrate viruses

A

Capsid

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11
Q

capsid functions

A

protection
attachment
antigens

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12
Q

are the two types of capsid symmetry
described in viruses (Fig. 3). But large viruses with large genome have
complicated symmetry which is neither icosahedral nor helical such as poxviruse

A

Icosahedral and helical symmetries

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13
Q

the term used to refer to the combined nucleic acid and capsid
which can either be naked or covered with a membrane termed an envelope

A

Nucleocapsid

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13
Q

:the proteins that make up the subunit of capsid.

A

Structural proteins

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13
Q

The viral
genome also codes for important enzymes
- required for viral replication but are not incorporated in the virion

A

non-structural proteins

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13
Q

are generally assembled in the host cell prior to incorporation of the viral nucleic acid.

A

Icosahedral capsids

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14
Q

are formed by the insertion of protein units between each turn of
the nucleic acid helix, incorporating the RNA in the tubular package. The length
of the helix is determined by the length of the RNA molecule

A

Helical capsids

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14
Q

a lipid bilayer and associated glycoproteins that cover a nucleocapsid

A

Envelope

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14
Q

is acquired when the nucleocapsid buds through a cellular membrane,
endoplasmic reticulum, the Golgi apparatus or the nuclear membrane.

A

Envelope

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14
Q

are usually susceptible to detergent and are rendered non
infectious following damage to the envelope

A

Enveloped viruses

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14
Q

the proteins encoded by viral nucleic acid for binding to
receptors on host cells, membrane fusion, uncoating of the virion and destruction
of receptors on host cells

A

Glycoproteins

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14
Q

are knob-like projections from the envelope formed from
the oligomers of glycoproteins.

A

Peplomersor spike

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14
Q

Present in certain viruses including

A

coronaviruses, retroviruses, orthomyxoviruses, rhabdoviruses and
paramyxoviruses, and used to bind to cell receptors or may have enzymatic
activity

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15
Q

a layer of protein present between the nucleocapsid and the
envelope in some enveloped viruses that provides additional rigidity to the virion.

A

Matrix protein

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15
Q

papovavirus

A

papilloma

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15
Q

vacuolating

A

polyoma

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15
Q

pico/small–rna–virus

A

picornavirus

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15
Q

Coronaviruses

A

(halo or corona/crown of spikes),

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15
Q

Togavirus

A

(Toga/cloak),

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16
Q

Fourorders containing viruses of animals are so far recognized:

A

Mononegavirale
Herpesvirales
Picornavirales:
Nidovirales

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16
Q

Rhabdovirus

A

(Rhabdo/Rod-shaped)

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17
Q

Calicivirus

A

(Calix/cup-shaped depression

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18
Q

have common attributes
including a single stranded, non-segmented, negative sense
RNA genome, similar replication strategies.

A

order Mononegavirale

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18
Q

e is made up the families Paramyxoviridae,
Rhabdoviridae, Bornaviridae and Filoviridae.

A
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19
Q

comprising the families Herpesviridae, Alloherpesviridae and Malacoherpesviridae

A

Herpesvirales

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20
Q

comprising the families Picornaviridae, Iflaviridae,
Dicistroviridae, Marnaviridae and Secoviridae;

A

Picornavirales

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21
Q

are infectious particles, which can transmit a disease, composed mainly
of a protein without any detectable nucleic acid.

A

Prions

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21
Q

comprising the families Coronaviridae, Arteriviridae and
Ronivirida

A

Nidovirales

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22
Q

apparently have no virion
structure or genomes and evoke no immune response in the infected host.

A

Prions

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23
Q

These are extremely resistant to inactivation by

A

heat, disinfectants, and radiation.

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24
Q

The prions are causative agents of slow viral infections, such as

A

Subacute spongiform encephalopathy

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24
Q

more resistant than bacteria to chemical disinfectants such as

A

phenol

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25
Q

After long incubation period of years, they produce
a progressive disease that causes damage to the central nervous system,
leading to

A

subacute spongiform encephalopathy

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26
Q

Active virucidal agents include

A

formaldehyde and betapropiolactone

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27
Q

most active antiviral disinfectants.

A

hydrogen peroxide
potassium permanganate,
hypochlorite, and
organic iodine compounds

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27
Q

Theviruses usually remain viable in a pH range of — but are sensitive to
extremes of acidity and alkalinity

A

5–9

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28
Q

Most of the viruses with few exceptions are highly heat labile.
They are inactivated within seconds at

A

-within seconds at 56°C, within
-minutes at 37°C, and
-within days at 4°C

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29
Q

Radiations: the viruses are readily inactivated by

A

sunlight, ultraviolet (UV)
radiations, and ionizing radiations.

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29
Q

Lipidsolvents:
are active against enveloped
viruses but are not active against non-enveloped, naked viruses.

A

chloroform, and detergents

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30
Q

The replicative cycle of a virus may range from

A

6 to 40 hours

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31
Q

The replicative cycle of a virus may range from 6 to 40 hours. Within hours of
infection, an occurs

A

eclipse phase

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32
Q

After this eclipse phase, it is followed by the
—- as new viral particles are formed and released from the cell
wherein the number of viral particles increases exponentially

A

productive stage

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32
Q

Steps in virus replication

A
  1. attachment
    2.entry
  2. uncoating
    4.biosyntesis
  3. maturation or assembly of virus
  4. release daughter virion
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33
Q

the initial stage of virus replication
whereby the infecting virus loses its physical identity and most or all of its infectivity

A

eclipse

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34
Q

: Initial virus–cell interaction is a random event, which relates
to the number of virus particles present and the availability of appropriate receptor
molecules.

A
  1. Attachment:
35
Q

Virus–cell
interaction determines both the host range and the tissue tropism of viral species.

A
36
Q

Virus receptors on cells could be

A

glycoproteins or glycolipids; proteoglycans,
glycoconjugates with terminal sialic acid residues, integrins and the IgG superfamily
of transmembrane proteins

37
Q

is the process of separation of viral nucleic acid from its protein
core for transcription to take place.

A

Uncoating

37
Q

Mechanism of entry:

A

A. Endocytosis:
B. Fusion
C. Direct introduction of viral genome into the cytoplasm (injection) t

37
Q

ollowing attachment, the virus gains access to the host cell internal
environment where replication takes place

A
  1. Entry
37
Q

However, in certain viruses, transcription may
proceed without complete release of the viral genome (ex:

A

reoviruses

38
Q

In enveloped
viruses, in which the nucleocapsid is discharged directly into the cytoplasm,
transcription can usually proceed without complete uncoating

A
39
Q

. In non-enveloped
viruses, uncoating involves conformational changes,, proteolytic enzyme activity ,
progressive loss of structural proteins and weakening of intermolecular interactions.

A
40
Q

Uncoating may occur on the

A

cell membrane
cytoplasm, or nucleus

41
Q

while some viruses uses their
own enzymes.
Most RNA viruses generate its own enzyme (——) to
trancribe and replicate mRNA

A

polymerase

42
Q

The synthesis of viral
proteins by host cells, which is the central event in replication of viruses, requires the
production of

A

Biosynthesis or Replication of nucleic acid.

viral mRNA

43
Q

Some viruses (most DNA viruses) makes use of the host
cells enzymes (transcriptases) to synthesize mRNA,

A
44
Q

DNA viruses replicate their DNA in the
nucleus of the host cell by using viral

A

enzymes

45
Q

However, they synthesize their
capsid and other proteins in the cytoplasm by using host cell enzymes

A

cytoplasm

46
Q

Most
of the DNA viruses

A

herpesvirus, papovavirus, adenovirus, and hepadnavirus

47
Q

is an exception,
because all of its components are synthesized in the cytoplasm

A

Poxvirus

48
Q

The RNA viruses replicate in the cytoplasm except

A

orthomyxoviruses and Borna disease virus w

49
Q

of each segment
is transcribed to produce individual mRNA molecules

A

negative-sense strand

50
Q

Transcription occurs in the cytoplasm under the
direction of a

A

viral transcriptase

51
Q

single stranded RNA viruses can act directly as
mRNAfollowing infection

A

positive-sense

52
Q

The assembly of the protein capsid is the
first step in viral maturation. The mechanisms for the assembly and release of
enveloped and non-enveloped viruses are distinct.

A

Maturation/Assembly of virus:

53
Q

The envelope
develops around the capsid by a process

A

The envelope
develops around the capsid by a process

54
Q

are present intracellularly as fully
developed viruses, but in case of enveloped viruses, only the nucleocapsid is
complete

A

nonenveloped viruses

55
Q

nucleocapsid is surrounded by an envelope, which
is derived from the host cell membrane during the process of budding

A
56
Q

Release from the cell can occur either b

A

exocytosis or by cytolysis.

57
Q

are released
into the surrounding environment and may affect new host cells

A

Progeny virions

57
Q

Abnormal replicative cycles may occur in four ways:

A
  1. Incomplete viruses
  2. Pseudovirions:
  3. Abortive infections:
  4. Defective viruses:
57
Q

defect during assembly of viral components, some of
the daughter virions that are produced may not be infective.

A

Incomplete viruses

58
Q

Example: an influenza
virus that shows a

A

high hemagglutination titer but with a low infectivity

59
Q

are the viruses that occasionally enclose host cell
nucleic acid instead of viral nucleic acid, therefore, are non infective and lack the
capability to replicate

A

Pseudovirions

60
Q

In this type of infection, the virus components may be
synthesized but the maturation is defective maybe due to infection of the wrong host
cells by the virus

A

. Abortive infections

61
Q

These are viruses that produce fully mature virions only in the
presence of helper viruses which supplement the genetic deficiency in the defective
viruses

A

Defective viruses

61
Q

Ex: Hepatitis D virus (defective virus) replicate only in the presence of

A

hepatitis B virus (helper viruses)

62
Q

Spontaneous and random errors in the copying of viral nucleic acid,
termed mutations, can occur during the replication of viruses.

A

Mutation

63
Q

genomic structure by two principal methods—

A

—mutations and
recombination.

64
Q

It is the most important
mechanism by which a virus can be genetically modified which results in production
of new viral strains showing properties different from parental or wild-type virus such
as

A

inactivation of viruses,
altered antigenicity and pathogenicity of the virus, and
nduce drug resistance in viruses.

65
Q

Mutation may be induced by mutagens like

A

X-rays,
UV irradiation or
chemical agents, or may even occur spontaneously

66
Q

resulting from single nucleotide substitutions, are the most common type
of mutation.

A

Point mutations,

66
Q

. Less common types of mutation result from the

A

deletion or insertion of
one or more nucleotides

66
Q

a new area of antiviral research wherein those RNA viruses with
inherently high mutation rates are administered with mutagenic agents to drive viral
extinction through violation of the error threshold and error catastrophe

A

Lethal mutagenesis

67
Q

is the extinction of an organism as a result of excessive
mutations.

A

Error catastrophe

67
Q

a virus mutant which can replicate only under defined
permissive conditions.

A

Conditional-lethal mutants
:

68
Q

can multiply most
efficiently at temperature ranges different from parental virus.

A

temperature-sensitive mutants

69
Q

s are used extensively for the study of viral genetics and are also
evaluated for possible use in live viral vaccines.

A

temperature
sensitive mutants

70
Q

viruses that replicate in the presence of antibody.
Because of altered antigenic surface determinants, the mutants are unaffected by
neutralizing antibodies induced by the —

A

wild-type virus

70
Q

variant strains showing differences in the tissue type and
species of target cells affected by viruses.

A

Host-range mutants:

70
Q

viruses that replicate in the presence of antibody.
Because of altered antigenic surface determinants, the mutants are unaffected by
neutralizing antibodies induced by the wild-type virus.

A

Antibody escape mutants
:

71
Q

rendering a virus towards low viral load and low viral fitness by
subjecting it to a combination of mutagenic agents and antiviral compounds.

A

Viral suppression

72
Q

a virus with decreased infectious titer despite a high
number of viral particles. This mutant promote the establishment and maintain
persistent infections.

A

Defective-interfering mutants
:

73
Q

—variant strains that cause less serious infections in humans
and animals.

A

Attenuated mutants

74
Q

the exchange or transfer of genetic material between different
but closely related viruses infecting the same cell simultaneously, or between virus
and host cell.

A

Recombination

75
Q

occurs between two closely related DNA or RNA
viruses.

A

Intramolecular recombination
:

75
Q

a recombination between positive-sense single
stranded RNA viruses and occurs through a template switching mechanism; RNA
polymerase switches between template strands during synthesis of the
complementary negative-sense strand

A

Copy-choice (template switching)
:

75
Q

The alteration of genetic information may result from

A

intramolecular
recombination,
copy-choice recombination, reassortment or
genetic reactivation.

75
Q

has led to the formation of western equine encephalitis virus, another togavirus.

A

recombination of Sindbis and eastern equine encephalitis virus

75
Q

:
is another process of genetic recombination.

A

Reassortment

76
Q

segmented
influenza virus A and B

A

(8 segments),

77
Q

Reoviridae

A

(10–12 segments)

78
Q

Bunyaviridae

A

(3 segments), a

79
Q

Arenaviridae and
Birnaviridae

A

(2 segments)

80
Q

An exchange of segments occurs between these viruses,
resulting in production of new

A

hybrid strains.

80
Q

infectious progeny are produced from parental viruses, of which one or
both are non-infectious, following mixed infection of a ce

A

Reactivation recombination

81
Q

when infectious progeny are produced from related viruses inactivated by lethal
mutations at different loci in their genomes

A

Multiplicity reactivation:

82
Q

occurs when an inactivated virus becomes capable of replicating after acquiring
genetic material from an infective virus

A

Cross-reactivation or genome rescue

83
Q

is widely used for virus propagation; inoculation of chick
embryos and experimental animals is employed for the isolation and production of
particular viruses.

A

Tissue culture

84
Q

Tissue culture: growth and maintenance of living tissue

A

in vitro

84
Q

a tissue fragment is used to isolate viruses from animals
with persistent infection.

A

A. Explant cultures

85
Q

the tissues are digested into individual cells by mechanical
cutting followed by digestion with enzymes such as

A

trypsin

85
Q

is required for the isolation and identification of
viruses involved in disease, for the titration of viruses for vaccine production and for
the provision of stocks for research purposes.

A

Propagation

86
Q

Three types of cell
culture:

A

a) Primary cell culture
b) Semi-continuous
c) Continuous cell cell culture

86
Q

derived directly from tissues and contain many cell
types such as epithelial cells, fibroblasts, keratinocytes, melanocytes,
endothelial cells, muscle cells, hematopoietic cells, mesenchymal
stem cells, etc

A

Primary cell culture:

87
Q

diploid cell lines retain
their characteristic diploid chromosomal constitution and can support
the growth of a wide range of viruses.

A

Semi-continuous:

87
Q

or immortal cell lines are derived from
either normal or neoplastic tissue and can be passaged indefinitely.

A

c) Continuous cell cell culture:

87
Q

Such cell lines can be obtained commercially from organizations like

A

American Type Culture Collection (ATCC).

88
Q

American Type Culture Collection (ATCC). Examples

A

HeLa cells, or
Madin Darby bovine kidney (MDBK)

89
Q

How to detect viral growth in cell cultures

A
  1. Using light microscopy, microscopic changes or cytopathic effect (CPE)
  2. Serological tests using flourescein-labelled antibody
90
Q

to be
observed in virus-infected cells are change in shape, cell detachment, fusion leading
to syncytium formation, the presence of inclusion bodies and cell death.

A

cytopathic effect (CPE)

90
Q

induce cell lysis and cellular transformation in cell culture

A

Burster (lytic) virus

91
Q

Two types of virus according to CPE production:

A

a) Burster (lytic) virus:
b) Creeper virus

92
Q

these induce formation of multinucleated giant cells.

A

b) Creeper virus:

92
Q

though no longer extensively used, this remains
the preferred method for isolation of influenza A viruses and for many avian
viruses.

A

Inoculation on embryos

92
Q

Modes of inoculation:

A

via the allantoic cavity,
the amniotic cavity or the
yolk sac,
chorioallantoic membrane (CAM), or intravascularly.

93
Q

Routes for inoculation of viruses into embryonated eggs.

A

1, Into allantoic
cavity;
2, into amniotic cavity;
3, into yolk sac;
4, on to chorioallantoic membrane.

93
Q

However, for several virus families, animal
inoculation either on laboratory animals or natural hosts remains the preferred
procedure for the following studies:

A

(a) detection of arthropod-borne viruses and
for rabies virus,
(b) inoculation of the natural host species as requirement for the
isolation of some viruses,
(c) challenge experiments in the natural host species
to evaluate vaccines,
(d) the production of antisera,
(e) investigation of the
pathogenetic mechanisms relating to viral infections and the subsequent immune
response of the host

411- VIROLOGY (6 decks)

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