Infectious Disease > Week 2: Virology > Flashcards

Week 2: Virology Flashcards

(93 cards)

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1
Q

What is a virus?

A

Intracellular obligate parasite

  • unable to replicate outside of a host cell
  • Unable to make own proteins
  • Depends on the cell machinery for replication and protein production
  • Are NOT living
  • must be able to infect a host to survive
  • Viral components are assembled - do not replicate by division
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2
Q

How do viruses enter cells?

A

Via host cell receptors

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3
Q

Viral genes expressed how?

A

using viral and/or host-encoded functions

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4
Q

What do viral proteins do?

A
  • modify host cell functions to ensure viral replication
  • Assemble into caspids that protect viral genomes
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5
Q

How do viruses propagate?

A

Viral proteins modify host cell functions to ensure viral replication and assemble into capsids that protect viral genomes and then the virus is released to infect new cells.

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6
Q

Range of viral infections?

A

Demonstrates viral tropism (viruses are found infected certain parts of the body because those tissues have receptors to allow viral entry)

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7
Q

Describe viral entry into the skin

A

require a breach of the physical integrity of the skin barrier and employs vectors

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8
Q

Describe viral entry into the conjunctiva and other mucous membranes

A

rather exposed site and relatively unprotected

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9
Q

Describe viral entry into the respiratory tract

A

possess sophisticated immune defense mechanisms which viruses must overcome

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10
Q

Describe viral entry into the Gastrointestinal Tract

A

gastric acid, bile salts, etc. provide a difficult environment so viruses would need to be adapted to infect and spread in this hostile environment

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11
Q

Describe viral entry into the genitourinary tract

A

relatively less hostile than the GI tract but is less frequently exposed to extraneous viruses

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12
Q

Factors affecting viral tissue tropism

A
  • Correct attachment protein to bind to a receptor on the cell surface to gain entry
  • Appropriate cellular machinery present within the host cell to allow the virus to replicate
    • Are dividing cells with high enough levels of dNTPs for viral DNA synthesis
  • A way to exit the host cell to spread the infection
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13
Q

Describe the steps of a typical viral infection

A
  • Primary replication
  • Systemic spread
  • Secondary replication
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14
Q

Describe the primary replication step of a viral infection

A
  • the place of primary replication where the virus replicated after gaining initial entry into the host cell
  • This frequently determines whether the infection will be localized at the site of entry or spread to become a systemic infection
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15
Q

Describe the systemic spread step of a viral infection

A

Apart from direct cell-to-cell contact, the virus may spread via the bloodstream and the CNS

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16
Q

Describe the Secondary Replication step of a viral infection

A

Secondary replication takes place at susceptible tissues/organs following systemic spread

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17
Q

Describe acute viral infection outcomes

A
  • Recovery with no residue effects (respiratory viruses)
  • Recovery wit residue effects (eg. acute viral encephalitis leading to neurological sequelae)
  • Death (Ebola virus)
  • Proceed to chronic infection
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18
Q

Describe chronic viral infection outcomes

A
  • Silent subclinical infection for life e.g. CMV, EBV
  • A long-silent period before disease e.g. HIV, SSPE, PML
  • Reactivation to cause acute disease e.g. herpes and shingles
  • Chronic disease with relapses and excerbations e.g. HBV, HCV
  • Cancers e.g. EBV, HTLV-1, HPV, HBV, HCV, HHV-8
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19
Q

Describe the possible viral pathogenesis time lines

A
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20
Q

Describe the virus-host interaction

A
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21
Q

Describe the ways the cells can respond to viral infections

A

cells can respond to viral infections in 3 ways

  • Failed infection (abortive infection)
    • non-permissive cell
  • Cell death (lytic infection)
    • prevent cellular growth
    • disrupt the structure and function of cells
  • Replication without cell death (persistent infection)
    • chronic - nonlytic viral synthesis
    • Latent - limited viral synthesis
    • Recurrent - periodic productivity
    • Transforming - immortalization of cell
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22
Q

What are prions?

A

Infectious proteins that causes a very slow infection happening a very long-time before the disease episode

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23
Q

Describe cellular pathogenesis of a persistent viral infection

A
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24
Q

How are cells damaged by a viral infection?

A
  • Direct cell damage and possibly death from a viral infection
  • Indirect cell damage as a result of a viral infection
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25
Describe direct cell damage and possibly death from a viral infection
* Diversion of a cell's energy * Shutoff of a cells macromolecular synthesis * Competition of viral promoters and transcriptional enhancers for cellular transcriptional factors such as RNA polymerases and inhibition of the interferon defense mechanisms
26
Describe indirect cell damage as a result of a viral infection
* integration of the viral genome * induction of mutations in the host genome * inflammation * host-immune response
27
Describe the viral life cycle
28
How are viruses classified?
29
Describe the difference between RNA and DNA viruses
30
What is viral symmetry?
Symmetry refers to the way in which capsomere units are arranged in viral capsid. Two kinds of symmetry are recognized in the viruses which corresponds to two primary shape ie. Rod and spherical shape of virus. Rod shaped virus have helical symmetry and spherical shaped virus have icosahedral symmetry
31
What types of viral symmetry are there?
**5 types** * Naked icosahedral * Naked helical * Enveloped icosahedral * Enveloped helical * Complex
32
Examples of Naked Icosahedral viruses
* Poliovirus * Adenovirus * Hepatitis A virus
33
Examples of Naked helical viruses
No known human viruses
34
Examples of Enveloped Icosahedral viruses
* herpes virus * yellow fever virus * Rubella virus
35
Examples of Enveloped Helical viruses
* Rabies virus * Influenza virus * Parainfluenza virus * Mumps virus * Measles virus
36
Examples of complex viruses
e.g. Poxvirus
37
Naked icosahedral viruses
Poliovirus Adenovirus Hepatitis A virus
38
Naked helical viruses
No known human viruses
39
Enveloped icosahedral viruses
Herpes virus Rubella virus Yellow fever viruses
40
Enveloped helical viruses
Rabies virus Influenza virus Parainfluenza virus Mumps virus Measles virus
41
Complex viruses
poxvirus
42
Capsid virus assembly
Individual proteins -\> larger units
43
Capsid viruses environmental stability
Environmentally stable
44
Enveloped viruses environmental stability
Environmentally liable
45
DS DNA viruses
Polyoma Papilloma Adeno Herpes Pox
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SS DNA viruses
Parvo
47
+RNA viruses
Picorna Noro Toga Flavi Corona
48
-RNA viruses
Rhabdo Paramyxo Orthomyxo Bunya Filo
49
DSRNA viruses
Reovirus
50
Retroviruses
Retrovirus
51
DNA virus replication
Viral DNA resembles host DNA Replication requires a DNA-dependent DNA polymerase
52
DNA virus early genes
Encode DNA-binding proteins
53
DNA virus Late genes
Encode structural proteins for assembly
54
DNA virus transcription location
Transcription occurs in the nucleus \*Except for Poxviruses\* which encode their own polymerase and transcription occurs in the cytoplasm
55
DS DNA viruses
Herpesviruses Adenoviruses Papovaviruses Poxviruses (Complex DNA virus)
56
SS DNA viruses
Parvovirus
57
Describe replication of simple DNA virus
DNA virus uses host cell machinery to replicate DNA replication occurs in the nucleus
58
Describe replication of Complex DNA virus: Poxvirus
Replication occurs in the cytoplasm Provide their own mRNA and DNA synthetic machinery
59
SS +RNA enveloped icosahedral viruses
Flaviviridae Togaviridae Retroviridae
60
SS +RNA enveloped helical viruses
Coronaviridae
61
SS +RNA nonenveloped icosahedral viruses
Picornaviridae Calciviridae
62
SS -RNA enveloped helical viruses
Orthomyxoviridae Paramyxoviridae Rhabdoviridae Filoviridae Bunyaviridae Arenaviridae
63
DS -RNA nonenveloped icosahedral viruses
Reoviridae
64
RNA viruses characteristics
* Must encode an RNA-dependent RNA-polymerase * Host cells have no mechanism of replicating RNA * RNA polymerases are error-prone * RNA is very liable and can be degraded by the cell * All RNA viruses must carry their own polymerase * \*Except (+) RNA viruses
65
Describe replication of simple RNA viruses
66
DS RNA viruses mechanism of replication
Reoviruses Birnaviruses The virion RNA is DS and so cannot function as mRNA Viruses package an RNA polymerase to make their mRNA after infection of the host cell
67
SS + RNA viruses
Picornaviruses Togaviruses Coronaviruses Flaviviruses
68
SS +RNA viruses transcription
In these viruses the genomic RNA functions as mRNA This mRNA can be translated immediately upon infection of the host cell using host cell machinery-\> it is infectious
69
SS -RNA viruses
Orthomyxoviruses Rhabdoviruses Paramyxovirus Filovirus Bunyavirus
70
SS -RNA viruses transcription
The virion RNA is negative sense -\> must be copied into the plus-sense mRNA before proteins can be made Packaged in the virion so that they can make mRNAs upon infecting the cell Transcription and replication occurs in the cytoplasm \*Except for influenza virus\*
71
SS -RNA viruses transcription location
Transcription and replication occurs in the cytoplasm \*Except for influenza virus\*
72
Retroviruses genome
Two identical (+)sense ssRNAs Neither directly transcribed nor translated Viral RNA-dependent DNA polymerase (reverse transcriptase) co-packaged with the viral genome Converts ssRNA into ds DNA Proviral cDNA integrated into the host genome Proviral genes transcribed by cellular RNA polymerase II Human pathogens: HIV-1, HIV-2, human T-cell leukemia virus (HTLV)-1 and HTLV-2
73
Describe Influenza virus genetics in action
* Surrounding the helical nucleocapsids is a lipid envelope with two viral glycoproteins: Hemagglutinin (H or HA) and neuraminidase (N or NA) * Genome consists of 8 individual segments of SS negative polarity RNA * Segments assemble at random into virions, some of which are infectious * Viral RNA polymerase is error-prone due to lack of proofreading activity so there is a high-mutation rate
74
How are influenza virus strains identified?
Strains are identified by the specific H and N antigen combination (eg H3N1)
75
Describe influenza virus RNA polymerase
polymerase is error-prone due to lack of proofreading activities, like most RNA viruses thus there is a high mutation rate
76
Epidemiology of influenza viruses
* May be endemic epidemic or pandemic * Epidemics result from antigenic changes in the SAME virus * Pandemics result from the emergence of a new influenza virus \*Only occurs in influenza A\*
77
Describe Antigenic drift
78
Effects of antigenic drift
Major changes in the viral antigens circulating the population
79
What are zoonotic viruses
* viruses that also infect animals * such as influenza A where birds and swine act as reservoirs
80
What is the key factor regarding antigenic shifts in influenza A
Zoonotic aspect of Influenza A
81
Factors regarding antigenic shifts in influenza A
* Zoonotic * Individual cells may multiply infected with viruses of different strains in birds, swine or humans * Segmented nature of the influenza genome * The end result is that random recombination of RNA segments from different strains of virus (including from different species)
82
Bacteria cell type
Prokaryotic
83
Virus cell type?
non-classified
84
Bacteria size of cell
typically 0.2-2.0 μm
85
Viruses size of cell
18-300 nm
86
Bacteria nucleic acid
Single circular chromosome (DNA)
87
Bacteria metabolism
* Heterophilic * Aerobic * Anaerobic
88
Bacteria reproduction
Most capable of independent reproduction
89
Bacteria method of cultivation
Visible growth on agar surface for most
90
Virus nucleic acid
* RNA or DNA * Single or double-stranded
91
Virus metabolism
Dependent on host machinery
92
Virus reproduction
Dependent on host machinery
93
Virus method of cultivation
* No visible growth on agar * requires host cells for propagation
Infectious Disease
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