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bsms302 > 5. How viruses cause disease > Flashcards

5. How viruses cause disease Flashcards

1
Q

What percentage of leading causes of death are infectious diseases?

A

25% of leading causes of death worldwide are due to infectious diseases, with acute resp infections, AIDS and diarrhoeal diseases causing the top three

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2
Q

What does a primary case of infection feature?

A

Infection followed by incubation period during which person becomes infectious
Then onset of symptoms during which person stops being infectious
Then end of infection

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3
Q

What is the difference between primary and secondary infection

A

Shorter duration of infection than a primary infection

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4
Q

What is the basic reproduction number (R0)?

A

the transmission rate for selected disease outbreaks - can be thought of as how many people can this infect in a uninfected population

doesn’t necessarily mean fatality - e.g. ebola has low basic reproduction number of 2 (isn’t that infectious) but high fatality, whereas measles has R0 of 16

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5
Q

The zika virus harms which specific population group worldwide?

A

pregnant women and their unborn babies
Virus causes birth defects in babies born to infected pregnant women

include microcephaly, and has been linked to Guillian Barre syndrome.

Spread through mosquitos, and potentially sexually.

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6
Q

What is a virus

A

Particle made of nucleic acid and protein coat
Small in size - around 100x smaller than our cells - 20-400nm EM
Obligate intracellular - can only replicate inside living cells

Infect wide range of organisms- humans, animals, plants, bacteria

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7
Q

Virion structure

A

nucleic acid as genetic material - can be DNA or RNA, ds or ss, +ve/-ve or ambisense

protein coat

can be enveloped or unenveloped

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8
Q

nucleocapsid vs virion

A

nucleocapsid = nucleic acid and protein coat
virion - complete intact virus particle (physical particle in extra-cellular phase which is able to spread to new host cells)

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9
Q

Viruses causing encephalitis/meningitis

A 
JC virus
Measles
LCM virus
Arbovirus
Rabies
HSV1/2
VZV
Enteroviruses
Parechoviruses
Mumps
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10
Q

Common cold viruses

A

rhinoviruses
parainfluenza virus
respiratory syncytial virus

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11
Q

pharyngitis viruses

A

adenovirus
EBV
CMV

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12
Q

Gingivostomatitis viruses

A

HSV1

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13
Q

Hepatitis viruses

A 
Hepatitis virus types A, B, C, D, E
HSV1/2
VZV
Enteroviruses
Parechoviruses
Mumps
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14
Q

Skin infection viruses

A 
VZV
Human herpesvirus 6
smallpox
molluscum contagiosum
hpv
parvovirus b19
rubella
measles
Coxsackie A virus
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15
Q

STD viruses

A

HSV2
HPV
HIV

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16
Q

Pancreatitis viruses

A

Coxsackie B virus

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17
Q

Gastroenteritis viruses

A 
adenovirus
rotavirus
norovirus
astrovirus
coronavirus
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18
Q

myelitis viruses

A

poliovirus

HTLV1 (human T lymphotrophic virus 1)

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19
Q

pneumonia viruses

A 
influenza virus types A and B
parainfluenxa virus
Respiratory syncytial virus
Adenovirus
SARS coronavirus
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20
Q

Parotitis virus

A

mumps virus

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21
Q

Eye infection viruses

A

HSV
Adenovirus
CMV

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22
Q

Problems a virus must solve

A

must know what cell(s) to enter and how
must know how to replicate inside a cell
must know how to exit & move from one infected cell to a new cell and to anew host in order to persist in nature
must develop mechanisms to evade host defences

23
Q

Viral pathogenesis

A

process by which virus causes disease in a host
two components of viral disease:
effects of viral replication on host
effects of host response on virus and the host

24
Q

Pathogenesis journey

A

Encounter: virus meets host
Entry: virus enters host
Multiplication: virus replicates in the host
Spread: virus spreads from site of entry
Damage: virus, host response or both cause tissue damage
Outcome: virus or host wins, or they coexist

25
Q

How do viruses get into the body?

A

Either through exogenous or endogenous routes
e.g. conjunctiva, respiratory tract, alimentary tract, urogenital tract, anus, arthropod, capillary, scratch or injury, skin

26
Q

Skin as a method of virus entry

A

abrasions, insect/animal bites, needle punctures

27
Q

Alimentary tract as a viral entry route

A

Gastroenteritis viruses
gut motility facilitates viral entry
hostile environment - extreme acidity/alkalinity and digestive enzymes

28
Q

Urogenital tract as a viral entry route

A

mucus membranes with low pH

abrasions facilitate viral entry e.g. HPV - local lesions, HIV - viral spread

29
Q

Eye as a viral entry route

A

localised infection e.g. conjunctivitis

Viral spread can lead to blindness/CNS

30
Q

Baltimore system for viral classification

A 
I: dsDNA e.g. adenovirus or HSV
II: ssDNA e.g. parvovirus
III: dsRNA e.g. reovirus
IV: +ssRNA e.g. poliovirus
V=ssRNa e.g. influenza virus
VI+ssRNA with DNA intermediate e.g retrovirus
VII: gapped dsDNA e.g. Hep B
31
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 the integrity of the cell basement membrane
32
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

33
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, the virus has access to almost every tissue

34
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

35
Q

Neural spread

A

less common than haematogenous spread
Viruses can go either:
from peripheral sites to CNS
from CNS to peripheral sites

36
Q

CNS infection

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

37
Q

CNS infection viruses

A

HSV - not very neuroinvasive, massively neurovirulent
Mumps is very neuroinvasive but not very neurovirulent
Rabies is very neuroinvasive and neurovirulent

38
Q

Tissue tropism

A

Limited or pantropic

Determined by:
cell receptors e.g. HIV/CD4+
cellular proteins that regulate viral transcription - JC/viral enhancers in olgiodendrocytes
Cell proteases - flu/serine proteases

39
Q

What makes viruses virulent?

A

Viral genes affect virulence:

  • those affecting virus’ ability to replicate
  • those that modify host’s defence mechanisms e.g. virokenes/viroceptors
  • those that enable virus to spread
  • those that have intrinsic cell killing effects
40
Q

How do viruses injure cells?

A

Can be cytolytic or non-cytolitic viruses

Cell injury is associated with free radicals

41
Q

Cytolytic viruses

A

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

42
Q

Non-cytolytic virus cell injury

A

CD8+ mediated
CD4+ mediated
B cell mediated

cell injury associated w free radicals

43
Q

Routes of transmission

A

Skin/mucous membrane e.g. HSV-1/2, VZV
Resp tract e.g. influenza, parainfluenza, RSV
Faecal oral e.g. HAV, norovirus
Bloodborne e.g. HIV, HBV, HCV
Sexual transmission e.g. HIV, HSV1/2
Vertical transmission - mother to baby e.g. HIV, CMV

44
Q

Types of vertical transmission

A

vertical transmission is mother to baby
antenatal e.g. transplacental
perinatal
postnatal e.g. breast milk

45
Q

Types of infection

A

Acute infection e.g. rhinovirus
Chronic/persistent:
-continuous replication
-latency - restricted viral gene expression

46
Q

Latent infection

A

DNA viruses or retroviruses
Persistence of viral dNA:
-extrachromosomal element (herpes viruses) - reactivation can lead to fever, blisters or coldsores
-or integrated within the host genome (retroviruses) - can result in transformation of cell leading to cancer

During cell growth, the viral genome is replicated along with the host cell chromosomes

47
Q

Host response against acute infection

A

Entry of virus then: innate defences, establishment of infection, induction of adaptive response, then adaptive response until virus is cleared, then memory.

48
Q

Control of acute vs chronic infection

A

acute infection - non-equilibrium process - host response and virus infection change continually until resolution

Chronic is more of an equilibrium between virus and host, with a balance until the equilibrium changes

49
Q

How do viruses evade the immune system?

A

Antigenic variation e.g. flu, HIV, rhino

Inhibiting antigenic processing e.g. HSV blocking antigen-processing transporter or CMV removing MHC-1 molecules from the ER

Production of cytokine receptor homologues e.g. pox viruses and vaccinia with IL1 and IFN-g, and CMV with chemokines

Production of immunosuppressive cytokine e.g. EBV with IL-10

Infection of immunocompetent cells - HIV

50
Q

Influenza virus type A structure

A 
Matrix protein
Segmented RNA genome
Neuraminidase (NA)
Haemaglutinin (HA)
M2 ion channel protein
51
Q

How does influenza virus evade host defence mechanisms?

A

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

52
Q

Antigenic drift

A

These are small mutations in the genes of influenza viruses that can lead to structural changes in HA, which stops antibodies being able to bind

53
Q

Antigenic shift

A

Abrupt, major change in an influenza A virus which results in new HA and/or new NA proteins. Can happen when an influenza virus from animals gains ability to infect humans by recombining gene segments.

Can result in a new influenza A subtype in humans that most people do not have resistance to (e.g. H1N1 swine flu)

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