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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
How do viruses get into the body?
Either through exogenous or endogenous routes e.g. conjunctiva, respiratory tract, alimentary tract, urogenital tract, anus, arthropod, capillary, scratch or injury, skin
26
Skin as a method of virus entry
abrasions, insect/animal bites, needle punctures
27
Alimentary tract as a viral entry route
Gastroenteritis viruses gut motility facilitates viral entry hostile environment - extreme acidity/alkalinity and digestive enzymes
28
Urogenital tract as a viral entry route
mucus membranes with low pH | abrasions facilitate viral entry e.g. HPV - local lesions, HIV - viral spread
29
Eye as a viral entry route
localised infection e.g. conjunctivitis | Viral spread can lead to blindness/CNS
30
Baltimore system for viral classification
``` 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
Viral spread
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
Viral release
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
Haematogenous spread - ways of viral entry to blood?
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
Viraemia
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
Neural spread
less common than haematogenous spread Viruses can go either: from peripheral sites to CNS from CNS to peripheral sites
36
CNS infection
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
CNS infection viruses
HSV - not very neuroinvasive, massively neurovirulent Mumps is very neuroinvasive but not very neurovirulent Rabies is very neuroinvasive and neurovirulent
38
Tissue tropism
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
What makes viruses virulent?
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
How do viruses injure cells?
Can be cytolytic or non-cytolitic viruses | Cell injury is associated with free radicals
41
Cytolytic viruses
Inhibition of host protein and RNA synthesis - leads to loss of membrane integrity Syncytium formation Induction of apoptosis
42
Non-cytolytic virus cell injury
CD8+ mediated CD4+ mediated B cell mediated cell injury associated w free radicals
43
Routes of transmission
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
Types of vertical transmission
vertical transmission is mother to baby antenatal e.g. transplacental perinatal postnatal e.g. breast milk
45
Types of infection
Acute infection e.g. rhinovirus Chronic/persistent: -continuous replication -latency - restricted viral gene expression
46
Latent infection
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
Host response against acute infection
Entry of virus then: innate defences, establishment of infection, induction of adaptive response, then adaptive response until virus is cleared, then memory.
48
Control of acute vs chronic infection
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
How do viruses evade the immune system?
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
Influenza virus type A structure
``` Matrix protein Segmented RNA genome Neuraminidase (NA) Haemaglutinin (HA) M2 ion channel protein ```
51
How does influenza virus evade host defence mechanisms?
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
Antigenic drift
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
Antigenic shift
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)

BSMS302 (10 decks)

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