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Virology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What is a Transformed Cell?

A

When a cell has new genetic material that changes its normal functions.

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2
Q

What are the 8 characteristics of a transformed cell?

A
  • immortal: can grow indefinitely
  • reduced requirement for serum growth factors
  • loss of capacity for growth arrest upon nutrient deprivation
  • growth to high saturation densities
  • loss of contact inhibition (can grow over monolayers)
  • altered morphology
  • anchorage independence
  • Tumorigenic
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3
Q

What is Acyclovir?

A

A highly effective anti=herpes simplex virus drug

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4
Q

What are the structures of acyclovir?

A

They are nucleoside analogs. Acyclic Sugar Group

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5
Q

How does acyclovir work?

A

Acyclovir compounds, ACV, is only phosphorylated by HSV thymidine kinase. Keeps adding additional phosphates which then get inserted into the virus genome by viral DNA pol. ACV does not have 3’ OH so replication is terminated.

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6
Q

What is immune memory?

A

The secondary response to a pathogen, after already seeing it, there is a stronger response in T cells and Antibodies. Immune system’s ability to recognize the return of a pathogen and respond quickly to it.

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7
Q

What is immune memory?

A

The secondary response to a pathogen, after already seeing it, there is a stronger response in T cells and Antibodies. Immune system’s ability to recognize the return of a pathogen and respond quickly to it.

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8
Q

Adenovirus

Strucutre, Genome, Attributes

A

Icosahedral T=25. Genome: dsDNA. Non enveloped. Cause cancer in hamsters, Viral T antigens are E1A and E1B which transforms cells. E1A necessary for E transcription units. Frees E2F. E2 is required for DNA synthesis and entry into L phase. IVa2 enhances L gene transcription.

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9
Q

What is Retinoblastoma, RB

A

Rb is a gene/protein that controls entry into the S phase (DNA replication) of the cell cycle. It is a tumor suppressor gene. Regulates restriction point of cell cycle.

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10
Q

What are T antigens?

A

They are virus encoded transcriptional regulators of both viral RNA and Host RNA. They are also responsible for transforming cells.

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11
Q

What do T antigens do?

A

Required for Replication

Activate viral transcription

Required for viral DNA synthesis

Only viral genes retained in tumor or transformed cells

can transform cultured cells alone

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12
Q

What are active vaccines?

A

A modified form of pathogen or a product derived from that pathogen that induces immunity. Provides long term protection.

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13
Q

Types of vaccines

A

Attenuated Vaccines

Inactivated vaccines

Frctionated Vaccines (subunits)

Cloning Vaccines

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14
Q

Transducing vs Non-Transducing Virus

A
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15
Q

When did viruses evolve and come to be?

A

Viruses came billions of years ago, predated cells. 450 million years ago were first estimated, herpesvirus arose 220 million years ago.

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16
Q

Why do viruses develop resistance to antivirals?

A

Viruses replicate efficiently to overcome constraints. Modest to high mutation frequencies.

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17
Q

Mechanism of drug resistance

A

Error prone RNA pol causes mutations and has no proofreading. DNA evolve more slowly than RNA viruses due to less diversity. RNA more prone to develop drug resistance.

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18
Q

Example of drug resistance

A

HSV develops drug resistance spontaneously. Causing some mutants not able to phsoporylate acv because of viral tk not working.. also sometimes they wont incorporate acv into DNA because DNA pol not working.

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19
Q

Examples of viruses that transform or cause cancer.

A

SV 40

Polyomaviruses

Papillomaviruses

Adenoviruses

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20
Q

How do viruses immortalize cells

A

They can deactivate tumor suppressor genes such as Rb and p53 that allow the normal cell cycle to continue indefinitely. SV40 LT sequesters p53. Adenovirus forms complex to ubiquitinated p53. Papillomavirus e6 binds to p53.

21
Q

Stage of Mitosis

A

PPMAT.

Prophase - Centromeres begin to align, nucleus begins to degrade, Chromosomes begin to condense

Prometaphase - Nucleus completes degradation, chromosomes start to attach to spindle.

Metaphase - Chromosomes align in division plate.

Anaphase - Chromsomes are split into sister chromatids by centromeres, cell furrow begins to stretch.

Telophase = Actin wraps around furrow further separating the 2 sister cells.

22
Q

What is a persistent infection?

A

Asymptomatic and Pathogenic. Aysmptomatic, virus continues for life but symptoms not apparent. Pathogenic, have long initial latent periods before fatal symptoms.

Occur when infection is not cleared by immune response. Viral genomes remain even if proteins are not in tact. No single mechanism.

Examples; EBV, HCV HBV, and Papillomavirus.

23
Q

What is a subunit vaccine?

A

Vaccine that breaks virus into components, immunizations occurs with purified components. Antigen is usually a capsid or membrane protein. HBV vaccine is example. Gardasil and Cervarix

24
Q

What is an attenuated vaccine

A

Live virus that is weakened. Infection induces mild or inapparent disease. Empiraccaly attenuated, grow the virus in nonhuman cells and wait for evolution to have the virus to specify for nonhuman type. Then innoculate weak viruses for humans to have an immune response.

25
Q

What is an inactivated vaccine

A

Virus infectivity is eliminated, but antigenicity is not compromised. Undergo chemical procedures to deactivate such as formalin. Polio vaccine is example.

26
Q

Normal Cell Cycle

A

G1 - Nomal metabolic Growth, prepping for DNA replication.

S - DNA replication and synthesis

G2- Second growth phase prepping for mitosis

M - Mitosis, then cytokinesis

27
Q

How can cells be transformed by viurses?

A

The infected cell does not die.

Transformed cells do not produce virions

It becomes immortal

28
Q

Effective Vaccines are:

A

Induce appropriate immune response; Th2 response wanted.

Antibodies are produced to provide protection from pathogens.

Safety: No disease, minimal side effects.

Induce protective immunity

Long-lasting protection.

Low cost, stable, and storage and delivery viable.

29
Q

What are the 4 general patterns for infection?

A

Acute, Latent, Persistent - Asymptomatic, Persistent- Pathogenic

30
Q

What are acute infections?

Example

A

Short duration, high viral titers, sometimes severe disease state. Rapid onset of viral reproduction.

Influenza, Poliovirus, Measles Virus, Norovirus, West Nile virus.

31
Q

What are latent infections?

A

Similar to acute, followed by periods of inactivation and reactivation. Everthing is infected by a chronic latent infection.

Herpes simplex virus

32
Q

Persistent - Asymptomatic

A

Virus production continues for life in the host, but symptoms are not apparent. Occur when virus is not cleared by immune system.

Adenovirus, ebv, JC virus

33
Q

Persistent - Pathogenic

A

Such as HIV. follow no symptoms for long latent period but then cause severe fatal symptoms.

HIV, SSPE

34
Q

Retrovirus history

A

Developed 450 mya

35
Q

Costs of drug discovery

A

R&D- 10-100m$

Preclinical : 10mil

Phase 1: 10 mil

Phase 2: 10-100mil

PHase 3: 100mil

36
Q

What is viral virulence

A

Capacity of a virus to cause diease in a host

37
Q

Virulence can be quantified

A

Viral titer, Appearnce of signs and symptoms, fever/weight loss, measure of pathology, mortality.

38
Q

Specific ways to measuring virulence

A

Measurement fo survival

Measurement of pathogenic lesions

LD50: Median Lethal Dose, number of infections particles will kill 50%

ID50: Median infectious dose. # of infections particles to infect 50% of challenged recepients.

39
Q

What are restriction points?

A

Points in the cell cycle that pauses if conditions are not correct.

p53 pauses before s phase.

Cyclins CDK.

40
Q

WHat is herd immunity?

A

When the spread of disease drops below a threshold. Population scale immunity. People are indirectly protected by vax individuals.

41
Q

Papillomaviridae.

A

HPV viruses. Oncogenic. First DNA virus identified. Causes warts. But Viral T antigens by E6 and E7 cause immortalization.

42
Q

What are 4 main drivers of viral evolution?

A

Large # of progeny

Large # of mutants

Quasi-Species effects

Selection

43
Q

Large # of progeny

A

Allows for rapid evolution as selective pressures are more sensitive in populations that have fast replication cycles.

44
Q

Large # of mutants

A

RNA viruses are more error-prone thus have more ability to produce mutant strains. With large progeny, mutations can appear quickly.

45
Q

Quasi Species effect

A

Viruses don’t exist as exact copies in a population but have similar replicons. Sometimes they have a consensus sequence. But most genomes may not have one.

46
Q

Selection

A

Survival of the fittest. Those that are able to successfully replicate, or develop beneficial mutations are more likely to have those mutations continue on.

47
Q

Specific Mechanisms for evolution

A

Genetic bottlenecks. Co-evolution between host and pathogen.

48
Q

What is metagenomics

A

Evaluation of all of the genomes in a community. All the genomes within the sample without the need to culture them. unbiased evaluation, and using bioinformatics to process data.

49
Q

Why do we use matagenomics?

A

To study phylogentics, gind taxonomic diversity, and discover new viruses within the environment.

Find out which viruses are abundant.

Virology (3 decks)

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