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Medical Microbiology > Week 13 - Virology > Flashcards

Week 13 - Virology Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

General Properties of Viruses

A 
Obligate intracellular parasite
- replicate within host cell only 
- unable to grow on synthetic media
Host specific
Size 10-300 nm
Genetic material either DNA or RNA
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2
Q

Viral Proteins

A 
Structural
- make up viral structure
- capsid made up of capsomeres
- facilitate entry into host cells
- protect viral nucleic acid
Non-structural 
- coded for in viral genome
- not part of virion however can be packaged in virion
- contains enzymes needed for replication
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3
Q

Icosahedral and Helical Viral Symmetry

A

Icosahedral (cubic)
- solid regular sides
- 20 equal triangular sides
- greatest number of capsomeres packed in regular fashion
- all DNA animal viruses except poxvirus
Helical
- spiral structure
- capsomeres arranged in stair case fashion
- always contained within lipoprotein envelope
- glycoprotein spikes through lipid layer connected to underlying protein by matrix protein
- ssRNA viruses: influenzae, rabies

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4
Q

Baltimore Scheme Classification of Viruses

A

Class 1 - dsDNA
Class 2 - ssDNA
Class 3 - ds segmented RNA
Class 4 - ssRNA, positive
sense
Class 5 - ssRNA, negative
sense
Class 6 - ss RNA positive sense with ds DNA
intermediate before replication (retroviruses)
Class 7 - ds DNA with positive sense, part ss DNA,
with ss RNA intermediate (reversiviruses)

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5
Q

Main steps of Viral Replication

A 
Attachment
- to host cell via specific receptor on cell membrane
Penetration
- entry into host cell 
- sheds protein shell
Replication of Viral Genome
- production of mRNA
- production of early viral proteins
Production of late viral proteins
Assembly of progeny virions
Release of virions from cell (budding or lysis)
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6
Q

Bacteriophage different Life Cycles

A

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 host chromosome
- may enter lytic cycle

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7
Q

What are the two ways viruses can cause disease?

A
  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
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8
Q

CPE - Syncytia

A

Cell fusion
Certain viruses produce specified fusion proteins which mediate entry into cell
Also cause plasma membrane
Formation of giant multinucleated cells (Syncytia)

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9
Q

CPE - Inclusion Bodies

A

Bodies that appear in cells as a result of viral infection
They are:
- an aggregation of mature viral particles
- altered staining patterns at sights of virus synthesis
- degenerative changes due to infection

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10
Q

CPE - Transformation

A

Some viruses produce cancerous or pre-cancerous like changes

These viruses may act together with other cellular proteins and can cause mutations

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11
Q

What is Cytopathic Effect (CPE)

A

The effect of virus replication in the host cell

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12
Q

Cytokines and the Cytokine Storm

A

Cytokines released by immune system in response to viral infection
Attract T cells and macrophages
Controlled by feedback loop
Cytokine storm is the sudden outpour of various cytokines in response to viral infection
Feedback loop uncontrolled and results in tissue damage

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13
Q

HIV

A

Causes depression of immune response by destroying helper T-cells
Destruction of adaptive immune response
Causes opportunistic infections and tumors

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14
Q

Types of Skin Rashes

A

Vesicular Eruptions - replication of virus and direct damage to epithelial cell (Herpes)
Maculopapular Rash - due to destruction of virus infected cells by cytotoxic T-cells (Measles)
Purpuric Rashes - associated with fall of platelets due to viral infection (Rubella)
Hemorrhagic Rashes - due to disseminated intravascular coagulation resulting from viral infection (Dengue)

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15
Q

How do viruses evade the immune response?

A

Some viruses:

  • don’t display enough antigen on cell surface
  • inactivate B cells, T cells and macrophages
  • interfere with expression of MHC proteins
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16
Q

Acute non-persistent, Persistent and Latent Infections

A

Acute
- usually self limiting and will resolve without intervention
Persistent
- infection not terminated by immune response
- persistence of viral DNA in host
Latent
- some never cause disease
- during latent phase infections sub clinical
- some reactive causing episode of illness

17
Q

Insidious Infection

A

Prion diseases

  • abnormally protein configuration
  • can occur during spontaneous mutations
  • abnormal protein contacts normal protein and will convert to abnormal conformation (recruitment)
  • fatal
18
Q

Herpes Virus

A

Group 1 - dsDNA
Icosahedral
Replicates in nucleus of host cells
Enveloped - phospholipid rich with viral glycoproteins for cell attachment
Form latent infections which may reactivate at later stage

19
Q

HSV Entry

A

Attachment via envelope glycoproteins
- triggers fusion of viral envelope of cell
Nucleocapsid enters cytoplasm
Goes to nucleus and viral DNA released

20
Q

HSV Gene Expression

A

VP16 protein in tegument activates alpha phase genes
Needs to bind to host Oct1 and HCF which are cellular proteins
Genes expressed in phases
alpha - immediate early, regulators of gene expression
beta - early, proteins for DNA replication
gamma - late, structural proteins
One phase activates the next, inhibits the previous phase
Assembly in nucleus
Released through ER

21
Q

HSV Latency

A

Activation of HSV genes in neurons is limited
- failure to express alpha genes
Reasons why failure to express alpha genes in neurons:
1. Latency Associated Transcripts
- short RNA fragments from virus that interfere with alpha genes
2. VP16 fails because HCF is cytoplasmic in sensory neurons

22
Q

Influenza Virus

A

Class 5 - ss(-)RNA segmented genome
Enveloped
Helical
Has surface peptides haemagglutinin and neuraminidase

23
Q

Influenza Infection Process

A

Binding to cell
- haemagglutinin on surface of virion
- binds sialic acid residues on mucous membrane
- also causes fusion and entry
Release of Viral Genome
- M2 protein forms channel allowing H+ ions to enter
- low pH weakens M1 (matrix protein) bond to release nucleocapsid
Each segment of RNA is bound to nucleocapsid protein (NP) which transports it to nucleus

24
Q

Influenza Replication

A

Occurs in nucleus
After transporting to nucleus
- negative RNA is template for + RNA which is mRNA
- mRNA sent to cytoplasm for translation
- progeny nucleocapsid sent to cytoplasm where assembly occurs at plasma membrane
- neuraminidase releases virions

25
Q

Types of Influenza

A 
A 
- bird virus crossed into mammals
- haemagglutinin undergoes minor changes
- neuraminidase variation
- epidemics 1-2 yrs
B
- human only host
- epidemic 3-5 yrs
C
- human 
- rare 
- mild illness
26
Q

Influenza Genetic Variation

A

Antigenic Drift
- minor changes due to host immune selection of mutants with slightly altered haemagglutinin and neuraminidase
- types A and B
Antigenic Shift
- major change in haemagglutinin and neuraminidase due to recombination between human and animal types
- segmented genome increases chances of reassortment
- type A

27
Q

Sub Clincal Diseases

A

Most common viral infection
No signs or symptoms
Immune system clears virus in same way as other infections

Medical Microbiology (7 decks)

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