How do viruses cause disease in humans Flashcards

(51 cards)

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
How else can viruses injure cells
- Cell injury associated with free radicals
26
Routes of viral transmission
- Skin/mucous membrane - Respiratory tract - Faecal oral - Blood borne - Sexual transmission - Vertical transmission
27
Skin/mucous membrane examples
- HSV-1/2 | - VZV
28
Resp tract examples
- Influenza - Parainfluenza - RSV
29
Faecal oral examples
- HAV | - Norovirus
30
Blood borne examples
- HIV - HBV - HCV
31
Sexual transmission examples
- HIV | - HSV-1/2
32
Vertical transmission examples
Mother to baby - eg HIV, CMV - antenatal eg. transplacental - Perinatal - Postnatal - eg. breast milk
33
Effects of rubella infection during 1st trimester
- Congenital infection syndrome | - Cataracts, heart defects, micro-cephaly, mental retardation, deafness
34
Types of infection
- Acute - Persistent - Latent, reactivating infection (continuous replication, latency - restricted viral gene expression) - Slow virus infection
35
Acute infection examples
- Rhinovirus - Rotavirus - Influenza virus
36
Persistent infection example
- Lymphocytic choriomeningitis virus
37
Latent, reactivating infection example
- Herpes simplex virus
38
Slow virus infection examples
- Measles virus SSPE | - Human immunodeficiency virus
39
What is SSPE
- 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
Features of latent infection
- 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
Herpes simplex virus reactivation presentation
- Fever | - Blisters or cold sores
42
What might retrovirus infection result in
- Transformation of the cell leading to cancer
43
Host response against acute infection
- Establishment of infection - Induction of adaptive response - Adaptive response - Memory
44
Control of acute vs chronic infection
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
How do viruses evade immune system
- Inhibition of antigenic processing - Production of cytokine receptor homologues - Production of immunosuppressive cytokine - Infection of immunocompetent cells - HIV
46
Inhibition of antigenic processing - mechanism
- Blockage of transporter associated with antigen processing - HSV - Removal of MHC-1 molecules from endoplasmic reticulum - CMV
47
Production of cytokine receptor homologues - mechanism
- IL-1, IFN-gamma - Pox viruses, vaccinia | - Chemokine - CMV
48
Production of immunosuppressive cytokine - mechanism
- IL-10 - EBV
49
How do influenza viruses evade host defense mechanisms
- 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
Antigenic shift
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
Antigenic drift
Antigenic drift is a mechanism for variation in viruses that involves the accumulation of mutations within the genes that code for antibody-binding sites