4.10 Viral Pathegenosis Flashcards

1
Q

What must viruses do in order to be maintained in nature?

A
  • Shed into the environment
  • Taken up by an arthropod vector or needle
  • passed congenitally
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2
Q

What are the routes of entry of a virus?

A
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3
Q

How do viruses enter through the respiratory tract?

A
  • most important (and most frequent) site of entry
  • many protective mechanisms
  • mucus, cilia, alveolar macrophages
  • viruses attach to specific receptors on epithelial cells • can remain localised or spread further
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4
Q

How do viruses enter via the alimentary tract?

A
  • Ingested viruses can either be swallowed or infect the oropharynx and then be carried elsewhere but the oesophagus is rarely infected
  • intestinal tract has mucus which prevents attachment to host cells but constant movement of contents allows some virus to contact specific receptors
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5
Q

What sort of viruses infect the alimentary tract?

A

Viruses that infect the intestinal tract are normally acid and bile resistant and (generally) do not have an envelope

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6
Q

Once in the alimentary tract what disease do viruses cause?

A
  • Some viruses cause diarrhoea, others do not cause disease in the intestinal tract but spread from there to cause generalised infection
  • HIV can infect via the rectal route
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7
Q

Which two viruses can enter via the alimentary tract?

A
  • Herpes simplex virus 1 cold sores: acquired by direct contact of infected saliva with damaged skin of mouth
  • Epstein Barr virus: infectious mononucleosis, aquired by direct contact of infected saliva with oropharynx
    • Babies sucking contaminated objects or adolescents kissing
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8
Q

What viruses enter through the skin?

A
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9
Q

What other ways can viruses enter the body?

A
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10
Q

What are the mechanisms of viral spread throughout the body?

A
  • Local spread on epithelial surfaces
  • Sub-epithelial invasion and lymphatic spread
    • HIV infect the rectal tract and gain access to T lymphocytes in underlying tissue and proliferate
  • Sub-epithelial invasion and neuronal spread
    • Rabies, infected animal bite through skin and pass virus to nerves and brain
  • Spread via bloodstream - viraemia
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11
Q

What is the difference between systemic and disseminated infection?

A
  • Disseminated infection is spread beyond primary site
  • Systemic infection is many organs infected
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12
Q

How can viruses stay free in plasma?

A
  • primary and secondary phases
  • produced by infected vascular endothelium or released in large amounts from eg, liver and spleen
  • neutralised by developing Ab response and removed by macrophages (duration usually 1-2wks)
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13
Q

What are cell associated viruses?

A
  • Cell-associated viruses (leukocytes, platelets, erythrocytes)
  • eg. measles spread by monocytes
  • can persist from months to years if viral genome becomes latent to avoid CTL attack
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14
Q

How does viraemia occur?

A
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15
Q

Explain this

A
  • direct injection of virus into the blood through mosquito or needle passive
  • Virus attached to epitheliul cells, remove from bloodstream need to get into host cells = primary viraemia
  • Go to secondary lymph tissues, secondary viraemia until cleared from the host
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16
Q

Why do we feel sick when having a virus?

A
  • Viral damage to tissues and organs
  • Consequences of the immune response
17
Q

How does viral damage to tissues and organs occur?

A
  • Cytocidal virus: disease may result directly from the cell death caused by viral replication
  • tissue specific cell killing in rotavirus diarrhoea (enterocytes), and influenza virus infection (epithelial cells in respiratory tract).
18
Q

How does sars-cov-2 cause viral damage to tissues and organs?

A
  • It is a non-cytocidal virus where cells may lose their ability to perform particular functions
  • Angiotensinogen is secreted by the liver and gets converted to Ang I by renin, which is mainly produced in the kidneys.
  • Ang I gets cleaved by ACE to result in Ang II.
  • Ang II is a ligand for the AT1 receptor and promotes vasoconstriction and hypertension.
  • Alternatively, Ang II can bind to the AT2 receptor to inhibit vasoconstriction.
  • ACE2 processes Ang II to Ang 1–7 which binds to the Mas receptor to induce vasodilation.
19
Q

How can consequences of the immune response cause sickness?

A
20
Q

What does the mass release of cytokines cause?

A
  • “Cytokine storm” increases:
  • IL-6 and others
  • Immune activation
  • Vascular permeability
  • Inflammatory Monocytes & neutrophils
  • Liver / kidney damage
  • Hypoxia (< 80% saturation)
  • Mechanical ventilation
  • Death
21
Q

How can the susceptibility of the host impact the progression of the disease?

A
  • Genetic factors such as polymorphism in a receptor gene (CCR5 and HIV)
  • Age: newborns and aged are more susceptible to severe disease (immature and waning response) but young suffer less from immunopathy
  • Malnutrition decreases resistance such as vitamin A and measles
  • Hormones and pregnancy where males and pregnant women are more susceptible
  • Dual infections may result in more severe disease such as Hep B and D co-infection
22
Q

What are the outcomes of a virus infection?

A
  • Fatal: viral diseases where man is not the natural host have very high mortality rates eg. Ebola
  • Full recovery: virus completely cleared by host’s immune system eg influenza
  • Recovery but permanent damage: virus cleared but left with symptoms eg. poliomyelitis, cancer
  • Persistent infection: virus not cleared and can resurface to cause disease
23
Q

Why can we get some diseases over and over again?

A
  • ineffective immunity eg. warts
  • effective immunity but multiple serotypes of virus eg. rhinovirus
  • constantly evolving virus
    • over time within the population eg. influenza
    • over time within a single patient eg. HIV
24
Q

What are viral genomes continually changing as a result of?

A
  • mutation (errors in copying the nucleic acid esp. RNA viruses)
  • If two closely related viruses infect the same cell then:
    • recombination (exchange of nucleic acid sequence)
    • reassortment (swapping of segments for viruses that have segmented genomes)
25
Q

What is the result of antigenic drift?

A

Antigenic drift resulting from RNA copying errors and selection of influenza virus with mutations in HA under the pressure of neutralising antibody giving rise to new seasonal epidemic strains

26
Q

What is an example of a latent infection?

A
  • eg. Varicella-zoster virus (Herpesviridae) (chickenpox and shingles)
  • Latent in the spinal chord
27
Q

How is HIV a latent disease?

A
  • eg. Human Immunodeficiency virus (Retroviridae)
  • AIDs
  • HIV integrates in T cells in genome and latent infection slowly kill T cells