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1.19.3.10 - Introduction to Viruses - Coggle Diagram
1.19.3.10 - Introduction to Viruses
virus
Small infectious agent that replicates by infecting the cells of a host organism
obligate intracellular pathogens
range in size from 20-300nm
has to replicate inside cells
cannot easily sruvuve outside cells
most can only infect specific cell types
tropism
nucleic acid surrounded by a protein coat
DNA or RNA
importance
epidemic
emerging diseases
diseases in individuals or groups
mild or life threatening
cancer
shapes
icosahedral
e.g. foot and mouth disease
helical
e.g. rabies
complex
e.g. poxvirus
structures
nucleic acid/genome in the middle
surrounded by a protein coat
surface of the virus may have embedded proeins which help the virus to enter cells
some viruses have lipid envelopes
enveloped viruses
derived from cell membranes by budding
plasma membrane
nuclear membrane
internal organells
relevant - enveloped viruses are easier to get rid of from the environemnt
less stable
genome
either RNA/DNA
single/double stranded
circular/linear/segmented
single stranded
positive sense/negative sense
posivite can encode directly for virus protein
negative - reverse complement - doesn't typically code for protein
variable size
limited compared to eukaryotes
proteins
functions
structural
capsid - the outer coat of the virus which protects the nucleic acid and may also serve to allow the virus to bind to target cells
nucleocapsid - simpler structure – proteins closely associate with virus genome
envelope glycoproteins - embedded in lipid membrane of enveloped viruses mediate recognition of host cells and entry
non-structural
Mediate replication of genome i.e. polymerases
role in suppressing the immune system (e.g. NS1 in influenza) or changing the cellular environment
accessory
Have special functions, usually in restricted cell types e.g. orfA in feline immunodeficiency virus promotes replication in lymphocytes
present in more complex viruses
classifications
DNA/RNA
single/double stranded
-ve/+ve sense
genome type influences how viruses make mRNA
Baltimore - splits viruses into groups by their nucleic acid
using phylogenetics to establish relatedness
grouped together based on similarity of genome sequence
determined by ICTV
Order - Family - Genus - Species
replication
viral entry
spike proteins
uncoating
transcription
translation
viral assembly and release
virsus must infect cells which supirt heir replicaton in order to multiply
able to enter cells i.e. have appropriate receptors
cell physiology appropriate
supplies replicative enymes
virus isolation and diagnosis
many viruses cnanot be grown in culture
slow- days/weeks to get reuslt
rquires specialist lab
often requires secondary confirmation e.g. test for viral proteins or nucleic acid
replication strategies
viruses need to rxploit normal cell porceses
ingect specific cells/cell compartments which provide what htey need
or encode proteins that they require or which alter the cell metabolism
polymerase enzymes
replicate genetic material to produce mRNA protein and genomic nucleic acid
provided vy cell or by virus
if suitable prolymerase not provided by cell or not provided in compartment in which virus replilcates virus must supply its own polymerase
encode own DNA polymerase so can control replication independent of cellular DNA replication
transcription of DNA viruses by cellular RNA polymerase
ssDNA viruses require active host DNA polymerase to replicate genome
they use host RNA polymerases to produce mRNA
DNA virses produce less replication errors than RNA viruses
+v snese virsuses
-ve sense viruses
virus RNA cannot act directly as mRNA
virions contain and genome encodes for:
RNA dependent RNA polymerase
genergates +ve sense mRNA
typically replicatei n the cytoplasm
genome also replicated by viral RNA polymerase, via positive sense intermediate
retroviruses
different
viral RNA is reverse transcribed
this cDNA integrates into the chromosome by viral ntegrase enzyme
the integrated DNA then produces RNA and protein using normal cell machinery
lots of retroviruses will produce tumours
integration is permanent for the rest of cell life
virus infection has idfferent outcomes on the celular level
transformation of normal cells to tumour cells
lots of viruses wull kill by lysis
persistent infection
latent infection
outcomes are different
clinical disease
cell death
tissue damage
secondary bacterial infections
host response to infection
cancer
subclinical infection
transmission to susceptible animals
undetected effects
latent viruses
can casue problems trying to contro ldisease in a population
factors affecting outcome
virus
virus strain
virus load
host
genetic
age
pre-existing immunity
physiological status
concurrent infection
environment
overcrowding
ventilation
genentic variation of viruses
genetic changes occur during replication
replication in host leads to spread of virus
virus needs to reproduce to survive
spontaneous mutuation
mistakes during replication
RNA have a higher rate of mutation
very high mutation rate of some RNA viruses means very large numbers of mutant viruses
gene transfer between virsuses of cells
gene reassortment
segemtned viruses
rapid evolution of virus variants
when two different viruses infect a cell
consequences
lethal mutation
silant mutation
growth advantage/disadvatage
selection pressure favours the establisment of new strains
clinical relevance
antigenicity
vaccines dont work, naive population
virulence
clinical consequences
host range/ tropism
disease in new host
susceptibility to antiviral drugs decreases
retroviruses
viral RNA is reverse transcribed
cDNA
cDNA integrates into the chromosome of the hot cell
host cell then produces viruses using cell machinery