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How do viruses cause disease in humans Flashcards

1
Q

What is the basic reproduction number (R0)

A
  • Is an approximate measure of how many new infections one person will generate during their infectious period
  • Note that R0 values are approximate, and can vary by outbreak, mode of transmission and location
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2
Q

What is the duration of infection period divided into

A
  • Incubation period and symptoms
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3
Q

What is the serial interval

A
  • Time between the onset of symptoms in the primary cause and onset of symptoms in secondary cause
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4
Q

What is zika virus associated with in pregnant women

A
  • Virus causes birth defects in babies born to some infected pregnant women including microcephaly
  • Microcephaly is when babies are born with underdeveloped heads and brain damage
  • Zika has also been linked to guillian-barre syndrome, a condition in which the immune system attacks the nerves
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5
Q

What is zika mainly transmitted via

A

mosquitoes

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6
Q

What is a virus

A
  • Particle made of nucleic acid and a protein coat

- Obligate intracellular - only replicates inside living cells

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7
Q

How can viruses infiltrate skin

A
  • Abrasions
  • Insect/animal bites
  • Needle punctures
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8
Q

How can viruses enter alimentary tract

A
  • Gastroenteritis viruses

- Movement facilitate viral entry

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9
Q

How is the alimentary tract protective against viruses

A

Hostile environment

  • Extreme acidity/alkalinity
  • Digestive enzymes
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10
Q

How can viruses enter the urogenital tract

A

Abrasions facilitate viral entry

  • HPV - local lesions
  • HIV - viral spread
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11
Q

Urogenital tract - protective factors

A
  • Mucus membranes

- Low pH

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12
Q

Eye - viral entry

A
  • Localised infection - conjunctivitis

- Viral spread - eye blindness/CNS

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13
Q

Baltimore system for viral classification

A 
I  dsDNA 
II ssDNA 
III dsRNA 
IV +ssRNA 
V -ssRNA 
VI +ssRNA with DNA intermediate 
VII gapped dsDNA
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14
Q

Viral spread

A

After replication at the site of infection

  • Some remain localised within epithelium or within one system
  • Some cause disseminated or systemic infection (inflammation compromises integrity of cell basement membrane)
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15
Q

Viral release

A
  • Apical e.g. flu - facilitate viral dispersal, but virus does not invade underlying tissues
  • Basolateral e.g. rabies - provides access to underlying tissues and may facilitate systemic spread
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16
Q

Haematogenous spread - ways of viral entry to blood

A
  • Directly through capillaries
  • By replicating in endothelial cells
  • Through vector bite
  • By lymphatic capillaries

Once in the blood, virus has access to almost every tissue

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17
Q

Viraemia

A

Presence of infectious virus in the blood

  • Passive/active viraemia
  • Primary/secondary viraemia

Diagnostic value - measuring viral replication
Practical problem - need to screen blood donors

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18
Q

Neural spread

A

Less common than haematogenous spread
Viruses can go either way
- From peripheral sites to CNS
- From CNS to peripheral sites

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19
Q

Infection of the CNS

A

Neurotropic - virus can infect neural cells
Neuroinvasive - virus can enter CNS following infection of a peripheral site
Neurovirulent - Virus can cause disease of nervous tissue

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20
Q

Comparison of viruses - Neuroinvasiveness vs neurovirulence

A

NI NV
HSV + ++++
Mumps ++++ +
Rabies ++++ ++++

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21
Q

Tissue tropism - determinants

A

Limited or pantropic

  • Cell receptors - HIV/CD4+
  • Cellular proteins that regulate viral transcription - JC/viral enhancers in oligodendrocytes
  • Cell proteases - flu/serine protease
22
Q

What makes virus virulent

A

Viral genes affecting virulence

  • Those that affect the ability of virus to replicate
  • Those that modify host’s defense mechanisms (eg. virokines/viroreceptors)
  • Those that enable virus to spread
  • Those that have intrinsic cell killing effects
23
Q

How do cytolytic viruses injure cells

A
  • Inhibition of host protein and RNA synthesis - leads to loss of membrane integrity
  • Syncytium formation
  • Induction of apoptosis
24
Q

How do non-cytolytic viruses injure cells

A
  • CD8+ mediated
  • CD4+ mediated
  • B cell mediated
25
Q

How else can viruses injure cells

A
  • Cell injury associated with free radicals
26
Q

Routes of viral transmission

A
  • Skin/mucous membrane
  • Respiratory tract
  • Faecal oral
  • Blood borne
  • Sexual transmission
  • Vertical transmission
27
Q

Skin/mucous membrane examples

A
  • HSV-1/2

- VZV

28
Q

Resp tract examples

A
  • Influenza
  • Parainfluenza
  • RSV
29
Q

Faecal oral examples

A
  • HAV

- Norovirus

30
Q

Blood borne examples

A
  • HIV
  • HBV
  • HCV
31
Q

Sexual transmission examples

A
  • HIV

- HSV-1/2

32
Q

Vertical transmission examples

A

Mother to baby - eg HIV, CMV

  • antenatal eg. transplacental
  • Perinatal
  • Postnatal - eg. breast milk
33
Q

Effects of rubella infection during 1st trimester

A
  • Congenital infection syndrome

- Cataracts, heart defects, micro-cephaly, mental retardation, deafness

34
Q

Types of infection

A
  • Acute
  • Persistent
  • Latent, reactivating infection (continuous replication, latency - restricted viral gene expression)
  • Slow virus infection
35
Q

Acute infection examples

A
  • Rhinovirus
  • Rotavirus
  • Influenza virus
36
Q

Persistent infection example

A
  • Lymphocytic choriomeningitis virus
37
Q

Latent, reactivating infection example

A
  • Herpes simplex virus
38
Q

Slow virus infection examples

A
  • Measles virus SSPE

- Human immunodeficiency virus

39
Q

What is SSPE

A
  • Subacute sclerosing panencephalitis (SSPE) is a progressive neurological disorder of children and young adults that affects the central nervous system (CNS). It is a slow, but persistent, viral infection caused by defective measles virus
40
Q

Features of latent infection

A
  • DNA viruses or retroviruses
  • Persistence of viral DNA (extra-chromosomal element - herpes viruses or integrated within the host genome - retroviruses)
  • During cell growth, viral genome is replicated along with the host cell chromosomes
41
Q

Herpes simplex virus reactivation presentation

A
  • Fever

- Blisters or cold sores

42
Q

What might retrovirus infection result in

A
  • Transformation of the cell leading to cancer
43
Q

Host response against acute infection

A
  • Establishment of infection
  • Induction of adaptive response
  • Adaptive response
  • Memory
44
Q

Control of acute vs chronic infection

A

Acute infection - non equilibrium process (host response and virus infection change continually until resolution)

Chronic - equilibrium between virus and host - balance until equilibrium changes

45
Q

How do viruses evade immune system

A
  • Inhibition of antigenic processing
  • Production of cytokine receptor homologues
  • Production of immunosuppressive cytokine
  • Infection of immunocompetent cells - HIV
46
Q

Inhibition of antigenic processing - mechanism

A
  • Blockage of transporter associated with antigen processing - HSV
  • Removal of MHC-1 molecules from endoplasmic reticulum - CMV
47
Q

Production of cytokine receptor homologues - mechanism

A
  • IL-1, IFN-gamma - Pox viruses, vaccinia

- Chemokine - CMV

48
Q

Production of immunosuppressive cytokine - mechanism

A
  • IL-10 - EBV
49
Q

How do influenza viruses evade host defense mechanisms

A
  • The virus can change its surface antigens - the immune response no longer able to identify them
  • Mechanisms of antigenic variation HA and NA - antigenic drift and shift
50
Q

Antigenic shift

A

Antigenic shift is the process by which two or more different strains of a virus, or strain of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains.

51
Q

Antigenic drift

A

Antigenic drift is a mechanism for variation in viruses that involves the accumulation of mutations within the genes that code for antibody-binding sites

302/308 (22 decks)

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