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Microbiology E-Books > Introduction to Virology > Flashcards

Introduction to Virology Flashcards

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Biology 101 flashcards
1
Q

The infectious unit of the virus is called the

A

Virus particle or virion

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2
Q

Virions contain a nucleic acid genome surrounded by a protective shell or coat of protein. The complex of protein and nucleic acid forms the

A

Nucleocaspid

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3
Q

Surrounded by an envelope, a lipid bilayer derived from host-cell membrane in which virus-encoded glycoproteins are inserted

A

Nucleocaspids

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4
Q

Enveloped viruses are distinguished by their sensitivity to

-Disrupts the lipid bilayer and destroys infectivity

A

Ether

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5
Q

Proteins of the nucleocapsid and envelope are

A

Structural proteins

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6
Q

Protects the genome and forms the delivery system: it binds a virion to its host cell and enables the genome to enter it

A

Nucelocapsid (and envelope if present)

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7
Q

Virion enzymes, unlike the abundant structural proteins, are present in only a few copies and are not essential to the structural integrity of the virion. They are referred to as

A

Non-structural proteins

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8
Q

Isolated virions are metabolically inert. They do not synthesize proteins or nucleic acids. If they contain enzymes, there are no substrates. Virions of many viruses can be

A

Crystallized

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9
Q

The type of viral genome dictates the replication cycle: the infecting genome must produce both

A

mRNA and new genomes

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10
Q

Viruses replicate only in living cells. Because of their limited genetic capacity, they are totally dependent on their host cells. This is called

A

Obligate intracellular parasitism

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11
Q

The intimate molecular interaction between virus and host means that a virus may be able to replicate only in cells of a particular species. This is referred to as

A

Species, tissue, or cell tropism

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12
Q

Cells in which a virus an replicate are said to be

A

Permissive

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13
Q

In non-permissive cells, infection does not result in production of new infectious virus particles; such infections are

A

Abortive

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14
Q

Replication of a virus requires its

A

Disassembly

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15
Q

Because of their small genomes, viruses must produce nucleocapsids from one or a few types of

A

Protein

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16
Q

There are only two solutions to the problem of enclosing a genome with only a single type of structural subunit. The subunits must be arranged in either a

A

Helix, or icosahedron

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17
Q

The protein subunits of nucleocapsids are held together by

A

Non-covalent bonds

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18
Q

Consist of a single protein subunit which assembles in a spiral or helix to form an open tube. Nucleic acid may be wrapped around the interior face of the tube, or enclosed within the wall

A

Helical Nucleocaspids

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19
Q

At some positions six adjacent subunits meet at a point, rather than five. The two types of cluster are called

A

Pentons and Hexons

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20
Q

In some viruses subunits are sufficiently flexible to be used in both places. This is called

A

Quasi-equivalent pairing

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21
Q

A few of the largest viruses have nucleocapsids which, although geometrically regular, have no obvious symmetry. These are called

A

Complex nucleocaspids

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22
Q

Viruses are visualized in the EM by

A

Negative staining

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23
Q

After negative staining, virus coats often show regular arrays of

A

Protrusions (capsomeres)

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24
Q

Have single-stranded RNA genomes of negative polarity

A

Mono-negavirales

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25
Q

Intact skin is impermeable to

A

Viruses

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26
Q

Many viruses are transmitted via the

A

Respiratory route

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27
Q

The coat of a virus contains proteins which specifically bind to cell surface

A

Receptors

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28
Q

These receptors are not present to facilitate viral infection, but to carry out specific

A

Physiologic functions

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29
Q

Binds to CD21, a C3b receptor on B cells

A

Epstein-Barr virus

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30
Q

Binds to CD4 of helper T cells. Distribution of CD4 determines which cells it can infect

A

HIV

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31
Q

Enter cells by one of two routes: (1) direct fusion of the viral envelope with the plasma membrane, or (2) receptor-mediated endocytosis

A

Nucleocaspids

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32
Q

This process may be catalyzed by one or more

A

Fusion proteins

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33
Q

In viruses which use the second route, acidification of the endosome may be required to cause a conformational change, required for fusion, in the

A

Fusion protein

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34
Q

Exposure of the genome in a form competent for transcription/replication is called

A

Uncoating

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35
Q

For nuclear replication, the virus core or nucleocapsid must be transported into the

A

Nucleus

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36
Q

Transcription of viral genes, synthesis of viral proteins, and assembly of new virions occurs in which two phases?

A
  1. ) Early phase

2. ) Late phase

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37
Q

Where viral proteins are made which replicate the viral genome

-Some viruses also produce proteins which block synthesis of host-cell nucleic acids and/or proteins

A

Early phase

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38
Q

Where new structural proteins are made and new virions assembled

A

Late phase

39
Q

Have regulatory mechanisms which cause a switch from production of early to late proteins after genome replication has begun

A

Some viruses

40
Q

During the interval between disassembly of the infecting virion and assembly of the first progeny virions, an infected cell contains no

A

Infectious virions (called the eclipse period)

41
Q

Some virion genomes may contain suffered deletion/mutation of their genetic material, so that after infection no infectious progeny are produced. Such virions are

A

Defective

42
Q

Progeny virions of enveloped viruses assemble at, and are extruded from, cellular membranes. This is termed virus

A

Budding

43
Q

The replication cycle of Polio virus takes

A

6-8 hours

44
Q

Assembled and released by budding, at the plasma membrane or internal membranes

A

Enveloped Viruses

45
Q

Enveloped viruses are not infectious until they have acquired their

A

Envelope

46
Q

Virus infection may itself kill cells: new virions of some viruses can exit the host cell only by its

A

Lysis

47
Q

The immune response, both innate and acquired, may kill

A

Infected cells

48
Q

Cell death and the immune response produces inflammation, and this in itself may

A

Damage tissue

49
Q

Crucial to the early limitation of viral multiplication

A

Interferon system

50
Q

Interferons are cytokine made by cells in response to

A

Viral infection

51
Q

An important stimulus for interferon production is

A

Double-stranded RNA

52
Q

Binds to its receptors to kill infected cells before virus release, and to stimulate uninfected cells to produce antiviral defenses

A

Interferon

53
Q

Another defense against viruses is the apototic response of infected cells. Many viruses combat this by producing proteins which block

A

Apoptosis

54
Q

In order to clear the initial viral infection, we usually require production of

A

CTL

55
Q

Many viruses inhibit synthesis of MHC proteins or their export to the plasma membrane. These viruses are combated by

A

NK cells

56
Q

Other viruses establish infections, in which viral genomes persist in infected cells but few or no virus proteins are produced. These are called

A

Latent infections

57
Q

These >common cold= viruses are transmitted by the respiratory route and multiply in the epithelium of the nasal mucosa

A

Rhinovirus

58
Q

After rhinovirus infection, the asymptomatic incubation period lasts

A

2-4 days

59
Q

During the early symptomatic period large numbers of rhinovirus particles are present in

A

Nasal secretions

60
Q

Appears in serum and nasal secretions 7-21 days after rhinovirus infection, after virus numbers have already begun to fall

A

Neutralizing antibody

61
Q

The rhinovirus is classified as a

A

Local infection

62
Q

The varicella virus is classified as a

A

Disseminated infection

63
Q

Initial infection is by the respiratory route

A

Varicella Virus

64
Q

During the incubation period varicella virus multiplies in the respiratory epithelium and infects cells of regional

A

Lymph nodes

65
Q

Released virus is transported via the bloodstream (primary viremia) to cells of the

A

Reticuloendothelial system

66
Q

The end of the incubation period and the beginning of symptoms (10-21 days after inital infection) is marked by a

A

Secondary virema

67
Q

When the virus is transported back to the respiratory epithelium [patients are infectious during this stage], to skin, where it infects epithelial cells to produce the characteristic rash, and to dorsal root ganglia, where it becomes latent in sensory neurons

A

Secondary viremia

68
Q

Neutralizing antibody in plasma and secretions appears at about the same time as the

A

Rash

69
Q

Clearance of the infection depends critically on generation of

A

CTL

70
Q

The more rapid the CTL response the milder and less extensive is the

A

Rash

71
Q

Infectious virions can be detected by exposing a monolayer of susceptible cells to a sample of virus diluted until only a small number of virions are

A

Present

72
Q

When mammalian cells are used, the monolayer is overlaid with soft agar so that when infected cells release virions, they spread only

A

Locally

73
Q

The small number of initially-infected cells release new virus that infects and kills neighboring cells. After a few days, each focus of infection creates an area of cell death called a

A

Plaque

74
Q

Each plaque stems from a single

A

Virion

75
Q

Standard cell cultures are in small flat-sided bottles or petri dishes, or as monolayers on coverslips in small

A

Shell vials

76
Q

What are the two types of cells used for isolation of viruses?

A

Primary cultures and Cell lines

77
Q

Derived directly from samples of human tissue

A

Primary cultures

78
Q

Cells in primary culture are normal in nearly all respects but will not proliferate

A

Indefinitely

79
Q

They require stimulation by growth factors in serum and contact with extracellular matrix and are inhibited by contact with their neighbors

A

Primary cultures

80
Q

Have been adapted to long-term or continuous culture but may not be normal in all respects

A

Cell lines

81
Q

Infection may lead to cell death or characteristic changes in

A

Cell shape

82
Q

Contain proteins which allow viral envelopes to fuse with cellular plasma membranes

A

Viral envelopes

83
Q

When these proteins appear on the plasma membranes of infected cells, they can cause infected cells to fuse with neighboring uninfected cells, creating

A

Giant cells or syncytia

84
Q

Aggregates of virus particles or components visible under the light microscope after staining

A

Inclusion bodies

85
Q

Multiplies in the cytoplasm and its inclusion bodies (Negri bodies) are cytoplasmic

A

Rabies Virus

86
Q

Herpes viruses multiply in the nucleus and their inclusions are

A

Intra-nuclear

87
Q

Viral nucleic acid can be detected by

A

PCR or hybridization

88
Q

Results in production of virus-specific humoral and cell-mediated immune responses

A

Viral infection

89
Q

Methods include complement fixation, neutralization, ELISA, and hemagglutination inhibition (HI)

A

Viral serology

90
Q

Complement-fixing antibodies are often made to antigens common to a group of

A

Viruses

91
Q

Often highly specific to an individual virus

A

Neutralizing antibodies

92
Q

May rise and fall at different times after infection. This may be useful in establishing how long an infection has been going on

A

Antibody titer

93
Q

Because of immunological memory, use of virus-specific IgG to diagnose current infection requires comparison of titer between two samples, taken

A

10-14 days apart

94
Q

Because the first sample is often taken while the patient is acutely ill and the second while the patient has begun to recover, the samples are often referred to as

A

Acute and convalescent sera

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