Microbiology pathogenicity: Viruses Flashcards
3 main components of a virus’ structure
genetic material (essential)
protein coat (capsid and is essential)
lipid membrane (envelope, optional)
genetic material in a virus
DNA or RNA
double or single stranded
protein coat/capsid in a virus
helical
icosahedral, 20 sided
more complex shapes
HIV as an example of a virus
retrovirus: enveloped, ssRNA genome
protein components: nucleocapsid, capsid, matrix
bacteriophage
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
lytic cycle
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
lysogenic cycle
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
viral pathogenesis
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
2 outcomes of viral infection
acute infeciton
chronic infection
acute viral infection
recovery with no residue effects
recovery with residue effects
death
proceed to chronic infection
chronic infection
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
factors in viral pathogenesis
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
how do cells respond to viral infections
no apparent change
death
transformation
what may direct cell damage and death from viral infection result from
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
what can indirect cell damage result from
integration of the viral genome
induction of mutations in the host genome
inflammation
host immune response
what is tropism determined by
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
cell damage with viruses
viruses may replicate widely throughout the body without any disease symptoms if they don’t cause significant cell damage or death
cell damage with retroviruses
don’t usually cause ell death
being. released form the cell by budding rather than by cell lysis
cause persistent infections
cel damage by picornaviruses
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
two types of chronic persistent infections
true latency
persistence
true latency
virus remains completely latent following primary infection
HSV or VZV
genome may be integrated into the cellular genomes or exists as episomes
persistence
virus replicates continuously in the body at a very low level
HIV, HBV, CMV, EBV
mechanisms of viral persistence
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
immune tolerance
causing reduced response to an antigen
may be due to genetic factors, pre-natal infection, molecular mimicry
down regulation of MHC class 1 expression
results in lack of recognition of infected cells
adenoviruses
down-regulation of accessory molecules involved in immune recognition
LFA-3
ICAM-1
by EBV
infection of immunopriviliged sites within the body
HSV in sensory ganglia in the CNS
direct infection of the cells of the immune system itself
herpes virus
retroviruses
often results in immunosuppression
examples of viral pathogenesis
hepatitis B
what is hepatitis b
member of hepadnaviridae family
contains partially double stranded, relaxed circular DNA
viral pathways of hepatitis b
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
spectrum of chronic hepatitis B diseases
chronic persistent hepatitis- asymptomatic
chronic active hepatitis- symptomatic exacerbations of hepatitis
cirrhosis of the liver
hepatocellular carcinoma
orthomyxovirsues biology
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
influenza 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
actual process of influenza inside the body
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
glycoprotein spikes in influenza
hemagglutinin
neuraminidase
hemagglutinin
H
15 subtypes
most important virulence factor
binds to the host cells
neuraminidase
9 subtypes
hydrolyses mucus and assists viral budding and release
antigenic drift
constant mutation
gradually changing amino acid composition
antigenic shift
one of the genes or RNA strands is substituted with a gene or strand from another influenza virus form a different animal host
COVID-19 viral pathway
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
