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PID > Virus pathogenesis > Flashcards

Virus pathogenesis Flashcards

1
Q

What are the steps in the virus life cycle?

A

A. Attachment
B. Entry
C. Uncoating
− At the plasma membrane
− In endosome by changes in pH
D. Viral Gene Transcription
E. Genome Replication
F. Translation
G. Assembly
H. Release
− Non enveloped viruses by cell lysis
− Enveloped viruses by budding from the
plasma membrane

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2
Q

How do viruses attach?

A

Highly specific process
−Involves complimentary receptors on the surface of a susceptible host cell
−Receptor can be protein or carbohydrate
−Initial binding is reversible
−May cause a conformational change that then allows binding to a co-receptor

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3
Q

How do viruses enter?

A

− Receptor mediated endocytosis
− Cell membrane fusion (non-endocytic pathway)

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4
Q

What is cell membrane fusion?

A
  • Virus membrane fuses with plasma
    membrane and nucleocapsid is released
    into cytoplasm
  • Occurs at neutral pH (pH independent
    fusion)
  • Examples - HIV, herpes virus
  • Some enveloped virus require proteolytic cleavage of envelope glycoprotein for activation of fusion domain, e.g influenza haemagglutinin (HA) spike protein
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5
Q

What is receptor mediated endocytosis?

A
  • Virus particle binds to host cell receptors
  • Enters cell in an endosome
  • Virus membrane fuses with membrane of the
    endosome and nucleocapsid is released into cytoplasm
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6
Q

How does Herpes simplex virus enter the cell?

A

Cell membrane fusion
1. Initial binding gB or gC to heparin sulphate (a
complex carbohydrate expressed on the surface of
many cell types)
2.Attachment of gD to
* HveA (lymphocytes, epithelial cells, fibroblasts)
* Nectin 1 & 2 (neurons, epithelial cells,
fibroblasts)
3. Fusion of the viral envelope with cell membrane

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7
Q

How does HIV enter the cell?

A

Cell membrane fusion
1. Binding of HIV gp120 to CD4+ T cells
* Induces conformational change in
gp120
2. Enables binding of gp120 to CCR5 or CXCR4
* Causes the gp120 trimer to break apart
* Allows gp41 to be pulled towards the
cell membrane
3. Fusion of gp41 with cell membrane
* Releases nucleocapsid into the
cytoplasm
4. Nucleocapsids are targeted to nucleus

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8
Q

How does influenza enter the cell?

A

Receptor mediated endocytosis
1. Binding of haemagglutinin (HA) to sialic acid receptor
2. Internalisation in clathrin coated pit
3.Movement into endocytotic vacuole which fuse with
lysosomes
4. Low pH triggers conformational change in HA trimer
5. Exposes fusion domain which allows fusion of viral
membrane and endosome membrane
6. Release of nucleocapsids into cytoplasm

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9
Q

What is uncoating?

A
  • Release of viral nucleic acid from viral capsid
  • Process is variable: For some viruses
  • nucleic acids may still be in a nucleoprotein complex
  • the capsid is only partially disintegrated
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10
Q

How do viruses replicate?

A

DNA viruses
*dsDNA viruses use host machinery in the nucleus (except poxviruses)
to make more ds DNA
*ss DNA converted to ds DNA then replicates like ds DNA
RNA viruses
* replicate in the cytoplasm (except influenza and retroviruses)
* All make viral mRNA which then migrates into the cytoplasm to
synthesis viral proteins using the host ribosomes

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11
Q

How do viruses assemble?

A
  • Translation of viral proteins in the cytoplasm
  • Assembly of virus capsids from newly synthesised
    components (de novo assembly)
  • Encapsidation of the viral nucleic acid
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12
Q

How do viruses enter the body & initiate infections?

A
  • Skin
  • Respiratory tract
  • Alimentary tract (GI tract)
  • Urogenital tract
  • Eye
    Viruses attach to cells at these locations by attaching to receptor molecules on certain cells
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13
Q

What are innate defences in the skin?

A
  • Is an effective barrier
    (keratinised)
  • Must be breached by
    abrasions or bites
  • Macrophages, neutrophils,
    dendritic cells, natural killer
    cells
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14
Q

What are innate defences in the respiratory tract?

A
  • Specialised ciliated epithelium & mucus: MUCOCILIARY ESCALATOR (in Upper Respiratory Tract
    (URT) and bronchi)
    − Filters out large particles
  • Sneezing & coughing
  • Innate immunological defences (e.g. alveolar macrophages, complement, cytokines, natural killer
    cells)
    Virus entry occurs via aerosolized droplets expelled by an infected individual
    − Spread by coughing or sneezing
    − Contact with saliva from an infected individual
    Examples of viruses entering via respiratory route are Influenza and Foot and Mouth Disease Virus
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15
Q

What are innate defences in the GI tract?

A

− Low pH in stomach (Denatures protein and kills most microorganisms)
− Bile and proteolytic enzymes in intestines
− High pH in the duodenum (rapid change)
− Mucous
Virus Entry via oral route (ingestion)
Examples of viruses entering via the GI tract are Rotavirus and Norovirus

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16
Q

What is viraemia?

A

Where viruses can spread to distant sites in the body, by entering the bloodstream via the lymphatic system.
Primary viraemia (clinically silent – increases virus levels allowing infection of distant organs)
Secondary viraemia (virus replication in other organs leads to high concentrations of virus in circulation)

17
Q

How do viruses spread to the CNS? (Rabies)

A
  • Entry: Bite of a rabid animal or contamination of scratch wounds by virus-infected saliva.
  • Rabies replicate in peripheral tissues (striated or connective tissue) at site of infection
  • Can remain at site of infection for days/weeks or longer
  • Virus enters peripheral nerves. (Infects
    unmyelinated nerve endings in muscle)
  • Spreads to CNS and enters brain (causes behaviour changes)
  • Migrates to salivary glands (replicates) and excreted in saliva
  • This also allows rabies to evade the immune system.
18
Q

What is virus tropism?

A

Specificity of a virus for a
particular host, tissue or cell that determines the host range of
virus.

19
Q

What are factors affecting tropism?

A

For virus infection to occur, the cell must be:
* Susceptible - appropriate cell surface receptors for entry
* Permissive − Able to support replication of the virus; may need particular cellular proteins to complete infection; may need to be in a particular cell type, E.g. Canine parvovirus needs rapidly
dividing cells

20
Q

How does protease cleavage by digestive enzymes occur?

A
  • Reoviruses are activated into
    infectious virions by cleavage
    with digestive enzymes
  • Cleavage of VP4 spike to
    VP8 and VP5
  • Conformational change
    permitting virus to bind to M
    cells in the gut
21
Q

What are the different temperatures at which viruses replicate?

A
  • Most human viruses replicate at
    37°C
  • Upper respiratory tract has a lower
    temp – about 33°C
  • Rhinoviruses replicate efficiently at
    33°C but poorly at 37°C
  • This limits their ability to spread
    beyond the upper respiratory tract
22
Q

Apart from temperature, what are two other barriers to viruses?

A
  • Gastrointestinal tract presents a harsh environment
    −Acid pH of stomach
    −Alkaline pH of intestine
    −Destructive effects of pancreatic enzymes
  • Ability of virus to breach barriers
    such as blood brain barrier will limit
    their distribution, e.g. poliovirus/ West Nile virus
23
Q

How can virus spread be studied experimentally?

A

First study of serial daily titration of virus content of various organs & tissues to trace where the virus went in the body
Inoculated groups of mice in the foot pad with mouse pox (caused lesions in the skin) - Frank Fenner
−At daily intervals looked for virus in
* Inoculated foot pad
* Lymph nodes
* Spleen
* Skin
* Blood
Mouse poxvirus spreads from skin -> lymph nodes -> blood -> spleen/liver -> blood -> skin -> primary lesion -> early rash, papules -> severe rash, ulcerations

PID (15 decks)

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