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BS127: AIDs > Lectures 15-22 > Flashcards

Lectures 15-22 Flashcards

1
Q

What is a virus?

A

A small, infectious agent.

It has a protein coat (capsid).

Needs a host to replicate.

Contains either RNA or DNA.

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2
Q

What is the difference between Viral and Bacterial replication?

A

Bacteria replicate through binary fission.

Virus’ replicate through assembly of pre-formed components, then the eclipse phase and finally an exponential phase.

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3
Q

What is present in the structure of a virus?

A

Nucleic acid.

Capsid.

Envelope.

Spike proteins and viral attachment proteins.

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4
Q

What are non-structural proteins used for in virus’?

A

Viral Replication.

Pathogenesis.

Transformation.

Modulation of hot defences.

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5
Q

What is not encoded in viral genomes?

A

no genes encoding the complete protein synthesis machinery.

no genes encoding for proteins involved in cell wall production or membrane biosynthesis.

No centromeres or telomeres found in the standard host chromosome.

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6
Q

Describe the capsid in a virus.

A

The protein shell that surrounds the viral genome.

Composed of protein molecules arranged in a repetitive and precise manner.

The capsomere is the subunit.

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7
Q

What is the difference in arrangement of round and rod virus’?

A

Round virus’ are arranged in an icosahedral symmetry.

Rod virus’ are arranged in helical symmetry.

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8
Q

How is metastability achieved?
(Stable Structure)

A

Through symmetrical arrangement of protein subunits, providing maximum contact.

Each subunit has identical bonding contacts. Repeated interactions provides symmetry.

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9
Q

How is metastability achieved?
(Unstable Structure)

A

The contact is not covalent.

Can be dissociated once the genome is released.

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10
Q

What are VLPs?

A

Capsid proteins assemble into virus-like particles.

From the outside they look like virus’, but they lack nucleic acid.

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11
Q

What is the definition of a subunit?

A

A single folded polypeptide chain.

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12
Q

What is the definition of a structural subunit?

A

A unit from which the capsid is built.

Usually 3 proteins bound together, then repeated to form the structure.

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13
Q

What is an icosahedron? Why is this shape relevant to Virus’?

A

20 Faces

30 Edges

12 vertices

This structure permits the greatest number of capsomeres to be packed.

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14
Q

How are the length and width of a virus determined?

A

The length is determined by nucleic acid length.

The width of a virus is determined by size and packaging of protein subunits.

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15
Q

Describe the structure of the viral envelope.

A

A phospholipid bilayer membrane derived from the host cell.

Envelope made by budding nucleocapsid.

Nucleocapsid has icosahedral or helical symmetry.

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16
Q

What is classification based on Diseases?

What are the disadvantages?

A

Grouping virus’ based on what they affect.

Focuses on some virus’ and ignores others.
A single virus may cause more than one disease.
Virus’ can infect more than one host.

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17
Q

What is classification based on Host?

What are the disadvantages?

A

Grouping virus’ based on the host it infects/species.

Restricted host range.
Small range of hosts.

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18
Q

What is classification based on morphology and nucleic acid?

A

Either RNA or DNA.
ss or ds.
Linear, circular, single molecule or segmented.

Capsid symmetry either icosahedral, helical or complex.

Presence or absence of lipid envelope.

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19
Q

What are the characteristics for ICTV?

A

Host range.
Morphological features.
Nucleic acid nature.
Additional features.

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20
Q

What is the Baltimore classification system?

A

7 viral genome types:

dsDNA
ssDNA+
gapped dsDNA
dsRNA
ssRNA+
ssRNA-
ssRNA -> ssDNA-

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21
Q

What are viroids?

A

Agents of disease in plants.

Has single circular ssRNA.

No protein components.

Rod-shaped or dumbbell-shaped

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22
Q

What are Prions?

A

Agents of disease that are characterised by neurological degeneration.

Slow replication in the host.

Abnormal forms of cellular proteins.

Induce changes in the shape of their normal homologues.

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23
Q

What is the basic process of viral replication?

A

Attachment.

Penetration.

Uncoating (capsid removal).

Biosynthesis.

Assembly (makes viral particle).

Release.

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24
Q

How is Recognition carried out?

A

Glycoproteins on the envelope bind to specific receptors.

Capsid enters the cell. Digestion of capsid releases genome.

Genome acts as template for synthesis of complementary RNA strands via RNA polymerase.

New copies of viral genome RNA are made. Also function as mRNA which is turned into glycoproteins and capsid proteins.

Vesicles transport envelope glycoproteins to the plasma membrane.

A capsid assembles around each capsid. New virus forms.

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25
Q

What is viral tropism?

A

The specificity of a virus to a specific host.

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26
Q

The process of entry by enveloped virus’.

A

Attachment to receptors.
Endocytosis.

Endosome becomes acidified, lowering pH.

Low pH triggers conformational change in envelope glycoproteins.
Fusion peptide is exposed, glycoproteins insert into membrane.

Envelope fuses with membrane, releases genome into cytoplasm.

Genome released from capsid, enters nucleus, new virions made.

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27
Q

What are ways in which a non-enveloped cell can penetrate?

A

Receptor-mediated endocytosis. Attach to receptors, triggers uptake, pH-dependent conformational change enables genome release into cytoplasm.

Straight-up penetration.

Injection via bacteriophages.

Cell-to-cell contact.

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28
Q

How does a dsDNA virus replicate?

A

1) DNA polymerase for straight replication.

2) Transcription with RNA polymerase. Translation.

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29
Q

How does a ssDNA virus replicate?

A

1) Host DNA polymerase.

2) Host cell DNA polymerase, ssDNA -> dsDNA.

RNA polymerase.

Translation.

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30
Q

What is RdRp?

A

Replication of virus’ is via RNA-dependent RNA polymerase.

Cells do not have RdRp.

RNA virus genomes encode RdRp.

RdRp produce RNA genomes and mRNA from RNA templates.

31
Q

How does gapped dsDNA replicate?

A

Begins w/ recognition and binding of initiator proteins to the origin of replication.

dsDNA unwound by helicase enzymes.

ss gap is primed with short RNA primer, provides a free -3’OH group for DNA polymerase to start making a new strand.

DNA polymerase adds nucleotides to the -3’OH end of the primer.

Once first strand is made, second polymerase binds to nicked strand and uses first strand as template.

Nick is sealed using DNA ligase. A phosphodiester bond is formed between the -3’OH of first strand and -5’OH of second strand.

32
Q

How does a +ssRNA virus replicate?

A

+ssRNA viruses enter host, uncoat their genome, RNA into cytoplasm.

RNA is template for protein synthesis by host ribosomes. Replicase proteins made first, used to replicate RNA.

Replicase form a complex with RNA. (RdRp) catalyzes -RNA using +RNA genome as a template.

-RNA is template for new +ssRNA genome.

Genome is replicated, viral proteins made by ribosomes at same time, including structural proteins.

New RNA and proteins form a virion, released to infect new cells.

33
Q

how does a -ssRNA virus replicate?

A

Initially needs to replicate into another RNA which is +.

Then follows same path as + ssRNA.

34
Q

how does does a dsRNA virus replicate?

A

The virus enters host, capsid removed to release dsRNA genome.

Viral dsRNA used as template for new dsRNA using RdRp. RdRp makes errors, leads to viral varients.

New dsRNA is template for viral mRNA by RdRp. This mRNA is translated into viral proteins.

RNA strands assemble to make virus particles.

35
Q

How does a +ssRNA retrovirus replicate?

A

Virus enters host, capsid removed, viral RNA genome released.

RNA genome reverse transcribed into dsDNA intermediate by reverse transcriptase. Goes to host nucleus and integrated as provirus.

Provirus transcribed by RNA Pol II, making viral mRNA, which is spliced to remove introns and make mature mRNA.

Viral mRNA translated into proteins by ribosomes.

36
Q

What is the difference between in vivo and in vitro

A

In vitro refers to experiments or observations that are conducted outside of a living organism in an artificial environment, such as a test tube, cell culture dish, or other laboratory apparatus.

In vivo, on the other hand, refers to experiments or observations that are conducted within a living organism, whether it be a plant, animal, or human.

37
Q

How are virus’ cultivated in cell vultures?

A

A primary cell culture is prepared from tissues.

Cells extracted from tissues to release single cells.

Suspended in a liquid culture medium in petri dish, cells stop dividing due to contact inhibiton.

Cells transferred to fresh growth medium.

38
Q

What are Cyto Pathic Effects?

A

Distinct and observable abnormalities/changes in the cells due to viral infection.

39
Q

What is Hemadsorption?

A

Cells infected with certain virus’ acquire the ability to bind to and absorb red blood cells.

R.B.C + Virus = hemagglutination.

40
Q

Cell Culture Caveats

A

Relatively slow.
Low sensitivity.
Susceptible to bacterial infection.
Success depends on viability of virus.

41
Q

Describe ELISA.

A

Coating: A specific antigen or antibody is attached to the bottom of a well in a microplate.

Blocking: Any remaining exposed surfaces on the plate are blocked to prevent non-specific binding.

Incubation: The sample containing the target protein or antibody is added to the well, and allowed to incubate for a set period of time.

Washing: The plate is washed to remove any unbound material.

Detection: A secondary antibody that is specific to the target protein or antibody is added to the well, along with an enzyme that can produce a color or fluorescent signal.

Development: A substrate is added to the well that reacts with the enzyme to produce a visible signal.

Quantification: The amount of signal produced is measured using a spectrophotometer or other instrument, and compared to a standard curve to determine the concentration of the target molecule in the sample.

42
Q

What is Immunofluorescence? (IMF)

A

In immunofluorescence, a primary antibody that recognizes and binds to the target molecule of interest is applied to the sample. This primary antibody is typically labeled with a fluorescent molecule, which allows the location and distribution of the target molecule to be visualized using a fluorescence microscope.

When the fluorescently labeled primary antibody binds to the target molecule in the sample, it produces a bright, glowing signal that can be observed and captured using the microscope. The signal is specific to the target molecule and can be used to visualize its distribution, localization, and expression in the sample.

43
Q

How do you quantify Virus’?

A

Number of viral particles.

Amount of viral proteins.

Number of nucleic acid copies.

Number of infectious particles.

Infectivity assays.

44
Q

Plaque Assays.

A

Virus is added to monolayer of cultured cells.

Agar added on top to prevent dilution.

Incubated.

Infect different plates for each dilution. Stain with crystal violet.

45
Q

What is a pathogenicity assay?

A

It is the ability to lysis.

TCID.50 assay = looking for culture that caused CPE in half of the tissue cells.

AID.50 assay = dilution that causes disease in half of the tissue cells.

LID.50 assay = dilution that causes death in half of the tissue cells.

46
Q

Virus Single-Step Growth Curve.

A

Inoculation

Eclipse

Burst

Burst Size

47
Q

What are the different portals of entry for virus’?

A

Susceptible Cells: has specific receptors recognised by VAPs.

Resistant Cells: no receptors.

Permissive cells: has proteins necessary for replication.

Non-Permissive cells: does not support viral replication.

48
Q

What is viremia and uraemia?

A

The presence of virus’ in the blood and urine.

49
Q

What is pathogenesis?

A

The ability of a virus to cause disease.

50
Q

What is the mechanism of viral injury and disease?

A

Transformation,

Direct Viral Cytotoxicity,

Virus-induced Immune Suppression,

Virus-induced Immune Pathogenesis.

51
Q

HIV noteworthy features:

A

Enveloped

Two surface glycoproteins

gp120
gp41

x2 ssDNA + strands.

52
Q

How does HIV replicate?

A

Interaction between gp120 and CD4 receptor.

Virus enters, nucleic acid released from capsid.

Synthesis of viral proteins.

Nucleic acid replication.

Assembly.

53
Q

What is the Acute Phase in HIV?

A

Activation of CD4+ T cells in lymphoid tissues.

Death of many cells, reduction in number of CD4+ T cells.

Levels usually return to normal, the CD4 cells created as quick as they are destroyed.

54
Q

What is the Chronic Phase in HIV?

A

Virus spreads to infect Helper T cells, macrophages and dendritic cells in peripheral lymphoid tissues.

Loss of CD4+ T cells is replenished from progenitors.

Patients asymptomatic or have minor infections.

55
Q

What is the Aids phase in HIV?

A

Lymph nodes and spleen are sites of continuous replication.

Number of CD4+ T cells declines over time.

CD4+ T cells < 200 cells/mm^3.

56
Q

Clinical Features of HIV:

A

CD4+ T cells needed for cell-mediated and humoral immune responses.

Loss of lymphocytes is the main reason why patients with AIDS become susceptible.

57
Q

Cytopathic effects of viral infection:

A

gb41 and gp120 production increases permeability of plasma membrane.

Influx of lethal amounts of calcium, induces apoptosis.

Osmotic lysis of cell caused by influx of water.

58
Q

Killing of infected cells by specific cytotoxic T cells.

A

Cytotoxic T cell recognises infected cell, becomes activated and produces molecules that allow it to bind and kill the infected cell.

Perforin creates pores in the membrane of infected cell, allowing granzymes to enter and trigger apoptosis.

59
Q

Decrease in T cell responses to antigens and weak humoral immune responses.

A

HIV targets and infects CD4+ T cells. Leads to weakening of immune system as T cells play a role in coordinating the immune response.

Weaker immune response leads to increase in opportunistic infections.

HIV also impairs the function of B cells, leading to weak humoral immune response.

60
Q

Viral Toxin Proteins (NSP4):

A

NSP4 is a viral enterotoxin that is produced by rotavirus, a common cause of gastroenteritis in infants and young children.

The main role of NSP4 is to induce secretion of fluid and electrolytes from intestinal cells, leading to diarrhea. NSP4 is a multifunctional protein that is able to affect several cellular processes, including calcium signaling, protein trafficking, and gene expression.

One of the ways in which NSP4 induces diarrhea is by activating a specific type of cell receptor, known as the 5-HT3 receptor. This receptor is found on the surface of intestinal cells and, when activated by NSP4, triggers a signaling cascade that leads to the secretion of fluid and electrolytes into the intestine.

NSP4 can also disrupt the normal functioning of intestinal cells by altering calcium signaling pathways and disrupting protein trafficking, which can further contribute to the development of diarrhea.

61
Q

Host Genes that determine the susceptibility to viral infections (CCR5):

A

CCR5 gene: The CCR5 gene encodes a protein that is involved in the immune response to viral infections, particularly HIV. A variant of the CCR5 gene, known as the delta-32 mutation, confers resistance to HIV infection by preventing the virus from entering host cells.

62
Q

Determinants of virulence:

A

Very Young:
Immature Immune Response.

Old:
Less elastic alveoli,
Weaker respiratory muscles,
Diminished cough reflex,
Reduced rate of production of new immune cells.

63
Q

What is a vaccine?

A

A biological product used safely to induce an immune response that confers protection against infection.

64
Q

What is a live attenuated vaccine?

A

Contains the whole virus that has been weakened to produce an immune response similar to that seen during infection.

Strong and long lasting immune response.

65
Q

What is a killed/inactivated virus?

A

Contains the whole virus which has been killed so that it cannot replicate.

Not a strong and long lasting immune response.

66
Q

What is a subunit vaccine?

A

Do not contain the whole virus, they have one or more specific components/antigens from the surface of the virus.

Not a strong and long lasting immune response.

67
Q

What is a nucleic acid/genetic vaccine?

A

Provide genetic instructions that encode for viral antigens that are specific to the host cell.

Genes are expressed by host cells to produce viral antigens.

68
Q

What are Antiviral Drugs?

A

Vaccines that prevent viral diseases.

They have limited or no therapeutic effect if someone is already infected.

69
Q

Why do we have a limited number of antiviral drugs?

A

A drug must be potent, to completely inhibit viral replication.

Expensive and long process.

Many infections are short-lived. Need to be given drug early which is hard to do.

70
Q

What does Maraviroc do?

A

Blocks the chemokine receptor CCR5.

It is a binding inhibitor. Essentially prevents binding to other protiens.

71
Q

What does Amantadine and Rimantadine do?

A

Inhibit entry and NA release. Block the M2 ion channel.

They are entry inhibitors.

72
Q

Why has Hydroxychloroquine failed?

A

Drug for malaria.

HCQ inhibits replication by disrupting endosomal acidification.

IDK why it failed.

73
Q

What do anti-HIV drugs do?

A

Control viral replication by inhibiting at different phases.

BS127: AIDs (3 decks)

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