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Block 2 Microbiology > Basic Virology > Flashcards

Basic Virology Flashcards

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Biology 101 flashcards
1
Q

What is a virus?

A
  • Obligate IC parasites that replicated by self assembly of individual components rather than by binary fission
  • Cannot make energy or proteins independent of host cell
  • Contain genome of limited size that is either DNA or RNA, not both
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2
Q

What are the physical and biochemical characteristics used to classify viruses?

A
  • Size
  • Morphology (shape and presence/absence of envelope)
  • Type of genome
  • Mechanism of replication
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3
Q

What are capsids? Name their 3 forms.

A
  • Rigid structures that withstand environmental conditions
  • Result of self-assembly of virally-encoded capsomeres
  • Helical, icosahedral or spherical, complex: shape dictated by capsomeres that self-assemble, not by shape of genome
  • Genome + capsid = nucleocapsid = virion for “naked” viruses
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4
Q

What are the characteristics of enveloped viruses?

A
  • Lipid envelope derived from cellular membranes
  • Virally-encoded glycoproteins inserted into membrane and serve as virus attachment/membrane fusion proteins
  • Nucleocapsid + membrane = virion for enveloped viruses
  • B/c envelope is mostly lipid, enveloped viruses are less stable than naked viruses -> 1) more susceptible to drying, 2) sensitive to detergents and alcohols, 3) can’t survive in GI tract
  • Spread in large droplets, secretions, organ transplants, and blood transfusions
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5
Q

What are the 8 major steps in viral replication?

A
  1. Attachment
  2. Penetration: endocytosis, membrane fusion
  3. Uncoating
  4. Early transcription and synthesis of nonstructural proteins (A: RNA viruses via virally-encoded RNA-dependent RNA polymerase; B: DNA viruses via host RNA polymerase, except poxvirus)
  5. Genome replication (A: RNA viruses cytoplasmic; B: DNA viruses nuclear, except poxvirus)
  6. Late transcription and synthesis of structural proteins
  7. Assembly of virus particles (A: RNA virus cytoplasmic; B: DNA viruses nuclear, except poxvirus and hepadnaviruses)
  8. Release of viral particles: cell lysis, budding (enveloped viruses)
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6
Q

What are the 6 elements of viral cytopathogenesis?

A
  1. Inhibition of cellular protein synthesis
  2. Inhibition and degradation of cellular DNA
  3. Alteration of cell membrane structure
  4. Disruption of cytoskeleton
  5. Formation of inclusion bodies
  6. Toxicity of virion components
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7
Q

Describe +RNA virus genome replication.

A

+RNA genome serves as mRNA and is immediately translated by cellular ribosomes:

  1. Translated as polyprotein that must be cleaved into individual proteins (including RNA-dependent RNA polymerase)
  2. RNA-dependent RNA polymerase transcribes -RNA strands from the +RNA genome
  3. -RNA strands used as templates to make many copies of +RNA genome
  4. +RNA copies used as mRNA to make structural proteins, and are encapsidated to make nucleocapsids
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8
Q

Describe -RNA virus genome replication.

A
  • RNA genome cannot be used as mRNA; must be used as template to transcribe +RNA (mRNA) strand
    1. To transcribe -RNA genome, incoming virus particle carries RNA-dependent RNA polymerase
    2. Resulting +RNA strand translated into proteins (incl. more RNA-dependent RNA polymerase), and used as template for add’l -RNA genomes
    3. newly produced -RNA genomes encapsidated to produce nucleocapsids
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9
Q

Describe retrovirus genome replication.

A

Retrovirus particles carry RNA-dependent DNA polymerase (reverse transcriptase):

  1. +RNA genome reverse transcribed into dsDNA, and integrated into host genome
  2. Retrovirus proteins and +RNA genome produced by host enzymes
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10
Q

Describe DNA virus genome replication.

A

DNA virus (except poxvirus) genomes are transcribed by host DNA-dependent RNA polymerases:

  1. Many viruses have host shut-off mechanism that degrades host mRNAs
  2. Many viruses use specific transcription factors that redirect host polymerases to viral genes and away from cellular genes
  3. Viral genome replication dependent on virally-encoded DNA-dependent DNA polymerases for larger viruses, but smaller viruses use host DNA polymerase
  4. Newly produced DNA genomes are encapsidated to produce nucleocapsids
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11
Q

What is MOI?

A

Multiplicity of Infection: ratio of the number of infectious particles to number of target cells to be infected

  1. MOI = 1 will only infect about 60% of cells in monolayer
  2. MOI b/t 5 and 10 needed to ensure all cells are infected
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12
Q

What is a plaque assay?

A

Measure the number of infectious virions in a given volume of lysate:

  1. Generally measured as plaque-forming units (pfu) per mL of lysate = titer
  2. Biological assay of infectivity
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13
Q

What is a lysate?

A

The suspension of virions in culture medium that results from unrestricted growth of virus on cell monolayer. Not all virus particles produced in lysate are infectious:

  1. Physical assays exist to measure # of virus particles
  2. Particle-to-pfu ratio measures # of physical particles compared to # of infectious virions
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14
Q

What is a plaque?

A

Hole in confluent monolayer of cells resulting from viruses lysing infected cells

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15
Q

What are the 2 periods of the single-cycle growth curve?

A
  1. Eclipse period: post-penetration phase phase until virus can be detected IC (corresponds to uncoating, early transcription, and genome replication steps -> ends at virus assembly)
  2. Latent period: post-penetration phase until virus can be detected EC, including the eclipse period (corresponds to uncoating, early transcription, genome replication, virus assembly, and release)
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16
Q

Why do viral mutations occur at a relatively high frequency (2)?

A
  1. In part, due to the large # of genome copies produced in every infected cell
  2. Also due to polymerase errors, especially for RNA viruses
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17
Q

What is complementation?

A

An exchange of proteins:

  1. If genome with lethal mutation in gene X arises along with wild-type genome in same cell, wild-type copy of gene X can provide function for mutant genome
  2. Mutant genome packaged in capsid and able to infect second cell upon release
  3. Mutant not able to replicate in second cell, b/c genome still contains lethal mutation in gene X
18
Q

What are the three processes virus genomes can undergo in a single cell?

A
  1. Complementation
  2. Recombination
  3. Reassortment
19
Q

What is recombination?

A

Exchange of genetic material on same segment of genome:

  1. Genome with lethal mutation in gene X arises along with wild-type genome in same cell, then mutation removed by recombination with wild-type genome
  2. Virus not able to replicate in second cell because it now contains a wild-type genome
  3. Recombination frequent with DNA viruses
  4. True recombination doesn’t occur with RNA viruses, but they can exchange genetic material in similar manner
20
Q

What is reassortment?

A

Exchange of genetic material on different segments of genome:

  1. If two segmented viruses infect same cell, they can exchange some of their segments at time of virus assembly
  2. Novel strain of virus composed of segments from both parents can be released from infected cell
  3. Important mechanism in devo of new influenza strains
21
Q

What is syncytia formation?

A

Enveloped viruses that fuse infected cell with uninfected cells to directly spread to surrounding cells

22
Q

What is the most common route of viral infection?

A

Inhalation. Can also enter through breaks in skin or mucosa.

23
Q

How do initial replication and localized spread of viruses occur?

A
  • Initial replication: in cells that express viral receptors and contain appropriate cellular factors for replication
  • Localized spread via:
    1. Release of virus from infected cell and subsequent infection of surrounding cells
    2. Syncytia formation (enveloped viruses)
24
Q

What is viremia?

A

Presence of virions in blood

25
Q

How does secondary spread happen?

A
  • May spread from original site of infection by gaining access to bloodstream or lymphatic system
  • Can gain access to CNS by circumventing BBB, through cerebrospinal fluid, or by direct uptake in peripheral NN
26
Q

What is the incubation period?

A

Postinfection period prior to onset of symptoms:

  1. 1-2 days is a short incubation period and is characteristic of viruses that do not require secondary spread for symptomology
  2. 12-14 days is usually minimum for viruses requiring secondary spread
  3. Some viruses have extended incubation periods of months, or years (HIV)
  4. W/most diseases, patients can be infectious during incubation period, unknowingly spreading virus
27
Q

What is the acute phase of infection?

A

The symptomatic phase:

  1. Many viral infections are mild or asymptomatic
  2. Most viral infections completely resolve following acute phase (virus completely eliminated from body)
28
Q

What are the 3 forms of persistent infection?

A
  1. Chronic (productive): virus produced at low levels, but may not continue to cause disease symptoms (i.e., Hep B)
  2. Latent: virus genome remains in cells indefinitely, but virus particles not produced, except during reactivation (i.e., herpes)
  3. Transforming: intact or partial virus genome integrates into cellular DNA or is otherwise maintained in cell and immortalizes cell, altering its growth properties (i.e., oncogenic viruses)
    A: RNA viruses - retroviruses, Hep C
    B: DNA viruses - Hep B, papilloma virus, polyoma virus, adenovirus type 2, EBV, human herpesvirus-8, pox
29
Q

What is the first defense to viral infection?

A
  • Nonspecific immune response, including NK cells and interferon
  • Three forms of IFN (alpha, beta, and gamma), but all secreted cytokines that regulate immune and inflammatory responses
30
Q

How are alpha and beta IFN induced? What are the most common PAMPs?

A
  • PRRs like TLRs and cytoplasmic PRRs recognize viral PAMPs

- Main PAMP is dsRNA; others include unmethylated DNA and 5’ modified ssRNA

31
Q

How do secreted IFNs prevent viral replication?

A

Bind to surrounding, uninfected cells and induce pathways that prevent viral replication:

  1. Protein kinase (PKR) pathway: inactivates translation initiation factor eIF-2, inhibiting viral protein translation
  2. 2-5A system: activates RNAse L, which cleaves viral RNA, destroying RNA genomes or inhibiting viral transcription
  3. Mx pathway proteins: GTPases that inhibit RNA polymerase activity
32
Q

What is the major cellular response to primary viral infections?

A

CD8+ cytotoxic T cells: infected cells targeted for lysis via antigen presentation (antigen-specific responses arise several days post-infection)

33
Q

How are antibodies involved in inhibition of viral infection?

A

Can neutralize virus binding or facilitate lysis of enveloped viruses with complement

34
Q

Are children defective in Ab production more susceptible to viral infection?

A

No- indicating the importance of cellular immunity compared to humoral immunity in viral infections

35
Q

List four examples of viral immune defense mechanisms.

A
  1. Antigen variation to escape humoral immune response
  2. Inhibition of antigen presentation to escape cellular response
  3. Cytokine homologs that down-regulate or block cellular response
  4. Latent infection in neurons where is no MHC I
36
Q

List 5 examples of viral immunopathogenesis.

A
  1. Flu-like symptoms caused by IFN and lymphokines
  2. Inflammation caused by T cells, macrophages, and PMNs
  3. Immune complex disease caused by Ab and complement
  4. Hemorrhagic disease caused by T cells, Ab, and complement
  5. Immunosuppression
37
Q

When are vaccines not practical?

A
  1. If large number of viral strains (serotypes) that cause disease (e.g., over 100 strains of common cold)
  2. If virus undergoes much antigenic variation due to high mutation rates in dominant antigenic structure
38
Q

What are the advantages (2) and disadvantages (3) of attenuated, live vaccine strains?

A

Advantages:
1. Cheap to produce
2. Long-lasting, strong response (IgG, IgA, T cell)
Disadvantages:
1. Can be labile in transport
2. Cannot be given to immunocompromised pts
3. Can revert to virulence in rare cases

NOTE: cause subclinical infections

39
Q

What are the advantages (3) and disadvantages (2) of killed virus vaccines?

A 
Advantages: 
1. Very stable 
2. Rare side effects 
3. Cannot revert to virulence 
Disadvantages: 
1. More expensive to repair 
2. Shorter term immunity mostly limited to IgG

NOTE: cannot cause illness

40
Q

What are subunit (recombinant DNA) vaccines? List advantages (2) and disadvantages (1).

A

Composed of single viral proteins are expressed in yeast using recombinant DNA technology (Hep B and HPV).

Advantages: 1) cannot cause disease, 2) not derived from blood (another Hep B vaccine is)

Disadvantage: requires multiple injections

41
Q

List some frequently used FDA-approved vaccines.

A

Polio, Hep B and A, flu, varicella-zoster (chickenpox), and measles, mumps, rubella

42
Q

What are immune globulin antivirals? When are they used?

A

Passive immunization: used in both pre- and post-exposure prophylaxis

Block 2 Microbiology (4 decks)

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