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Medicine Unit 3 > Microbiology pathogenicity: Viruses > Flashcards

Microbiology pathogenicity: Viruses Flashcards

1
Q

3 main components of a virus’ structure

A

genetic material (essential)
protein coat (capsid and is essential)
lipid membrane (envelope, optional)

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2
Q

genetic material in a virus

A

DNA or RNA
double or single stranded

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3
Q

protein coat/capsid in a virus

A

helical
icosahedral, 20 sided
more complex shapes

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4
Q

HIV as an example of a virus

A

retrovirus: enveloped, ssRNA genome
protein components: nucleocapsid, capsid, matrix

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5
Q

bacteriophage

A

viruses that infect bacteria
role in bacterial virulence- spread pathogenicity genes
used in phage therapy of bacterial infections
useful model system to study viral replications

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6
Q

lytic cycle

A

phage infects a cell
phage DNA circularises, remaining separate from the host DNA
phage DNA replicated and phage proteins are made
new phage particles assembled
cell lyses
releasing phage

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7
Q

lysogenic cycle

A

phage infects cell
phage DNA becomes incorporated into the host genome
cell divides and prophage DNA is passed onto daughter cells
under stressful conditions the phage DNA is excised form the bacterial chromosome and enters the lytic cycle
the phage DNA replicated and new phage proteins are made
new phage particles assemble
cell lyses
releasing the phage

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8
Q

viral pathogenesis

A

process by which a viral infection leads to disease
abnormal situation of no value to the virus
majority of viral infections are subclinical, not in the interest of the virus to severely harm or kill the host
consequences of viral infections depend on the interplay between a number of viral and host factors

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9
Q

2 outcomes of viral infection

A

acute infeciton
chronic infection

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10
Q

acute viral infection

A

recovery with no residue effects
recovery with residue effects
death
proceed to chronic infection

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11
Q

chronic infection

A

silent subclinical infection for life, CMV/EBV
long silent period before disease, HIV/SSPE/PML
reactivation to cause acute disease, herpes/shingles
chronic disease with relapses and excerbations, HBV/HCV
cancers

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12
Q

factors in viral pathogenesis

A

effects of viral infection on cells
entry into the host
course of infection
cell/tissue tropism
cell/tissue damage
host immune response
virus clearance or persistence

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13
Q

how do cells respond to viral infections

A

no apparent change
death
transformation

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14
Q

what may direct cell damage and death from viral infection result from

A

diversion of cells energy
shutoff of cell macromolecule synthesis
competition of viral mRNA for cellular ribosomes
competitions of viral promoters and transcription enhances for cellular transcriptional factors such as RNA polymerases and inhibition of interferon defence mechanisms

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15
Q

what can indirect cell damage result from

A

integration of the viral genome
induction of mutations in the host genome
inflammation
host immune response

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16
Q

what is tropism determined by

A

cell receptors for virus
cell transcription factors that recognise viral promoters and enhancer sequences
ability of the cell to support virus replication
physical barriers
local temperature,ph and oxygen tension enzymes and non-specific factors in body secretions
digestive enzymes and bile in the gastrointestinal tract that may inactivate some viruses

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17
Q

cell damage with viruses

A

viruses may replicate widely throughout the body without any disease symptoms if they don’t cause significant cell damage or death

18
Q

cell damage with retroviruses

A

don’t usually cause ell death
being. released form the cell by budding rather than by cell lysis
cause persistent infections

19
Q

cel damage by picornaviruses

A

cause lysis and death of cell in which they replicate
leading to fever and increased mucus secretion in in the case of rhinoviruses paralysis or death

20
Q

two types of chronic persistent infections

A

true latency
persistence

21
Q

true latency

A

virus remains completely latent following primary infection
HSV or VZV
genome may be integrated into the cellular genomes or exists as episomes

22
Q

persistence

A

virus replicates continuously in the body at a very low level
HIV, HBV, CMV, EBV

23
Q

mechanisms of viral persistence

A

antigenic variation
immune tolerance
restricted gene expression
down regulation of MHC class 1
down regulation of accessory molecules
infection of immunopriviliged sites within the body
direct infection of the cells of the immune system

24
Q

immune tolerance

A

causing reduced response to an antigen
may be due to genetic factors, pre-natal infection, molecular mimicry

25
Q

down regulation of MHC class 1 expression

A

results in lack of recognition of infected cells
adenoviruses

26
Q

down-regulation of accessory molecules involved in immune recognition

A

LFA-3
ICAM-1
by EBV

27
Q

infection of immunopriviliged sites within the body

A

HSV in sensory ganglia in the CNS

28
Q

direct infection of the cells of the immune system itself

A

herpes virus
retroviruses
often results in immunosuppression

29
Q

examples of viral pathogenesis

A

hepatitis B

30
Q

what is hepatitis b

A

member of hepadnaviridae family
contains partially double stranded, relaxed circular DNA

31
Q

viral pathways of hepatitis b

A

rcDNA delivered to the nucleus
converted into fully double stranded DNA
converted by ligation into covalently closed circular DNA (cccDNA)
stable for of HBV DNA that is responsible for its persistence in infected hepatocytes and transmission to progeny cells

32
Q

spectrum of chronic hepatitis B diseases

A

chronic persistent hepatitis- asymptomatic
chronic active hepatitis- symptomatic exacerbations of hepatitis
cirrhosis of the liver
hepatocellular carcinoma

33
Q

orthomyxovirsues biology

A

influenza
ssRNA consists of 10 genes coded onto 8 different RNA segments
3 types, A,B and C
A causes most infections
virus attaches to, multiplies in the cells of the respiratory tract
finished viruses are assembled and budded off

34
Q

influenza a

A

acute and highly contagious respiratory illness
seasonal pandemics
respiratory transmission
binds to ciliated cells of respiratory mucosa
causes rapid shedding of cells, stripping the respiratory epithelium leading to severe inflammation
fever, headache, myalgia, pharyngeal pain, shortness of breath and coughing
weakened host defences predispose patients to secondary bacterial infections, especially pneumonia

35
Q

actual process of influenza inside the body

A

virus adsorbs to respiratory epithelium by hem agglutinin spikes and fuses with the membrane
virus is endocytose into vacuole and uncrate to release 8 nucleocapsid segments into the cytoplasm
nucleocapsids transported into the nucleus, - sense RNA strand transcribed into + sense strand that will be translated into viral proteins that make up capsid and spikes
+ sense RNA used to synthesise glycoprotein spikes inserted into the host membrane
+ sense RNA used to synthesise - sense RNA, assembled into nucleocapsids and transported out of the nucleus to the cell membrane
release of mature virus occurs when viral parts gather at cell membrane and are budded off with envelope containing spikes

36
Q

glycoprotein spikes in influenza

A

hemagglutinin
neuraminidase

37
Q

hemagglutinin

A

H
15 subtypes
most important virulence factor
binds to the host cells

38
Q

neuraminidase

A

9 subtypes
hydrolyses mucus and assists viral budding and release

39
Q

antigenic drift

A

constant mutation
gradually changing amino acid composition

40
Q

antigenic shift

A

one of the genes or RNA strands is substituted with a gene or strand from another influenza virus form a different animal host

41
Q

COVID-19 viral pathway

A

spike proteins bind to ACE2 receptors
cleavage of S glycoprotein between S1 and S2 domains completed by the protease trans-membrane serine protease 2 and lysosomal cathepsin enabling cell membrane viral fusion and viral RNA release
either creates pore to allow viral RNA and RNA-associated proteins to gain access to cytoplasm or may be internalised by endocytosis and uncoated in acidic lysosomal environment to release ssRNA into cytosol
viral genome replicated
translated into viral proteins
envelope glycoproteins processed in the Golgi
further assembling of viral particles which are released by vesicular exocytosis

Medicine Unit 3 (28 decks)

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