Week 11 Viral Structure, Classification & Replication Study Questions

Front 1

Why is it not possible to grow viruses in artificial media?

Back 1

Obligate intracellular parasite

Front 2

List the main structures of an enveloped virus.

Back 2

Spikes (projections); Nucleic acid; Capsomeres (capsid subunits); Capsid (protein coat)

Front 3

What are the main functions of the structural proteins of a virus?

Back 3

• Make up viral structure
• Capsid made up of capsomeres - Capsomeres are made of long strands of polypeptide in ball like structure; Spikes protruding through lipid envelope, may have stabilizing membrane protein under lipid
• Facilitate entry into host cells
• Protect viral nucleic acid
• Core associated with nucleic acid (stabilization)

Front 4

What are the main types of viral capsid symmetries for pathogenic viruses?

Back 4

• Icosahedral symmetry (cubic): solid regular sides; 20 equal triangular sides, greatest number of capsomeres packed in a regular fashion; all DNA animal viruses except poxvirus and some RNA viruses
• Helical symmetry: spiral structure; capsomeres arranged in a stair case fashion; always contained within a lipoprotein envelope; glycoprotein spikes through lipid layer, connected to underlying protein by matrix (M) protein; ssRNA virus: influenza, parainfluenza and rabies
• Complex symmetry: viruses with large genomes (poxvirus); neither icosahedral or helical

Front 5

What is the main classification difference between Parvoviruses and Picornaviruses?

Back 5

Parvovirus is a class II: ssDNA virus (positive or “sense” strand)
Picornavirus is a class IV: positive ssRNA viruses (+ strand or sense) RNA

Front 6

Describe a Baltimore class 4 virus.

Back 6

Class 4 (ssRNA positive sense)
–Genome is used as mRNA directly
–Viral proteins translated first, then they direct replication of the viral genome

Front 7

List the main virus replication events.

Back 7

• Attachment: To host cell via specific receptor on cell membrane
• Penetration: Entry into host cell (internalization); “Uncoats” – shedding protein shell
• Replication of viral genome: This varies between viral types – production of viral mRNA; Production of early viral proteins
• Production of late viral proteins (structural)
• Assembly of the progeny virions
• Release of virions from cell (budding or lysis)

Front 8

What is the difference between “Lytic” and “Lysogenic” cycles?

Back 8

• Lytic (virulent): Release of viral particles via host cell lysis; Lysis and death of host cell
• Lysogenic (temperate): No lysis or death of host cell; Integration of viral genome onto the host chromosome (prophage, provirus); May enter lytic cycle

Front 9

A virus genome has partial dsDNA and ssDNA, and produces a reverse transcriptase. What is the Baltimore classification?

Back 9

Class 7 (partial dsDNA and ssDNA, reversivirues)
–Made fully dsDNA by host DNA polymerase
–mRNA transcripts made by host RNA polymerase
–Virus codes for “reverse transcriptase” which make partial DNA from RNA transcript for packaging

Front 10

What is the capsid symmetry of a Coronavirus?

Back 10

Helical symmetry

Front 11

Describe the mechanisms by which viruses cause disease.

Back 11

Viruses cause disease by two mechanisms:
1.Replication within the host cell leading to direct damage of the cell
2.Host defenses leads to cell damage as it attempt to clear the virus infected cells

Front 12

Describe the host factors that are important in viral infections.

Back 12

• Appropriate cell surface receptors: Determines if virus gets entry; Viruses generally have specific tropism
• Internal cellular environment suitability: Molecular machinery adequate for replication; Physical environment suitable; Respiratory viruses that replicate well at 330C limited to upper RT, those that replicate at 37°C but not at 33°C infect lower RT.

Front 13

What is “CPE” and how does it occur?

Back 13

•The effect of virus replication on the host cell
•Many viruses cause CPE in in host cells as well as cultured cell lines (used as a diagnostic tool)
•Different viruses give rise to different types of CPE: cell lysis, syncytia, inclusion bodies

Front 14

CPE - Cell Lysis

Back 14

•Production of virus early proteins cause shut down of host macromolecules
•Accumulation of large amounts of viral capsid proteins inhibit host cell and viral synthesis
First cells “round up” due to loss of host cell proteins (including adherence proteins)
Then complete lysis

Front 15

CPE - Syncytia

Back 15

•Cell fusion
•Certain viruses produce specified fusion proteins which mediate entry into cell
•These also cause plasma membrane of host cells to fuse
•Formation of giant multinucleated cells (Syncytia)

Front 16

CPE - Inclusion Bodies

Back 16

•Bodies that appear in cells as a result of viral infection (some bacteria e.g. Chlamydia)
•Aggregation of mature viral particles
•Altered staining patterns at sights of virus synthesis
•Degenerative changes due to infection
•Intracytoplasmic, intranuclear or both

Front 17

What is the main action of HIV that results in AIDS?

Back 17

Destroys T helper cells – CD4 cells (CD4 is receptor for HIV)

Front 18

List the events of a viral infection.

Back 18

1.Invade the host
2.Replicate in cells at sight of inoculation
3.Overcome/evade local defenses
4.Spread to other cells and other areas
5.Replicate again
6.Exit from host in large enough numbers to infect another host
•Some infections remain localized while others spread further (e.g. via blood stream)

Front 19

How can viruses evade the immune system?

Back 19

•Viruses poorly immunogenic
•Do not display enough antigen on cell surface
•Inactivate B cells, T cells, macrophages
•Interfere with expression or transportation of MHC proteins
•Excess antigen production to bind all neutralizing antibodies
•Mutations that change antigenic proteins of virus
•Infection of foetus before immune system developed

Front 20

What is the incubation time for measles?

Back 20

13 to 14 days (medium)

Front 21

What does “recruitment” mean in relation to prion disease?

Back 21

Abnormal protein contacts with normal protein will convert to abnormal conformation

Front 22

Describe the types of clinical manifestations resulting from viral infections.

Back 22

• Acute non-persistent infections: Most acute viral infections are self limiting and will resolve without intervention; Possible complications occur when CNS involved (encephalitis); Persistent infections; Infection not terminated by Immune response; Persistence of viral DNA in host cells; Only with DNA viruses or retroviruses; DNA may be integrated in host DNA or episomal
• Latent infections: Some latent infections never cause disease (sub clinical); During latent phase infections are sub clinical; Some are reactive causing episode of illness (HSV-1 in cold sores); Detection of virus may only be possible during episode of illness; Some latent infections lead to malignant disease

Front 23

Describe the basic structure of a Herpes virus.

Back 23

Isosahedral symmetry
Enveloped – phospholipid rich with viral glycoproteins for cell attachment

Front 24

What does VP16 do in Herpes virus infections?

Back 24

Viral gene expression is initiated by the virion protein VP16. VP16 does not bind DNA directly but forms a multiprotein complex on the viral immediate-early gene promoters with two cellular proteins: Oct-1 and host cell factor (HCF)
VP16 protein (in tegument) activates α phase
α genes, immediate early, regulators of gene expression – one phase activates the next (β and γ phases) and inhibits the previous phase.

Front 25

What are the differences between “chicken pox” and “shingles”?

Back 25

Both caused by the same virus, Varicella Zoster Virus.
Chickenpox is caused by the Varicella Zoster Virus which is an acute infection and it will remain dormant in host and when this latent infection erupts it will be shingles. Shingles is usually more localised affecting certain areas.

Front 26

What are the functions of the Haemagglutinin (H) and Neuraminidase (N) surface protein spikes on the influenza virus?

Back 26

•Surface peptides: Haemagglutinin H (15) and neuraminidase N (9)

•Binding to cell: Haemagglutinin on surface of virion; Binds sialic acid residues on mucus membranes (also on RBC – agglutination); Haemagglutinin also causes fusion and entry within endosomal vesicle

Neuraminidase (NA) involved in release of virions

Front 27

Where in the host cell does the influenza virus genome replicate?

Back 27

Class 5, ss(-) RNA segmented genome (8 segments), replicates in nucleus.

Front 28

What are “Antigenic Drift” and “Antigenic Shift”?

Back 28

•Antigenic Drift : minor changes due to host immune selection of mutants with slightly altered H & N (every 2-3 yrs). Types A and B.
•Antigenic Shift: major change in H & N due to recombination between human and animal types. Segmented genome increases chances of reassortment (interchange of gene segments of two viruses in one cell). Humans/birds/pigs. Type A.