Cytopathic Effects Of Viruses Flashcards
Cytopathic effects
Changes made to host cells infected by viruses by varied and complex mechanisms
Not all infections result in new virion production and significant changes could be induced without cell death resulting
Categorisation
Cytocidal (lytic)
Non-cytocidal (non lytic)
Cytocidal infection
Morphological cell changes
Inhib of pro, rna and dna synth
Cell death
Usually virions produced (CPE can occur in non productive infections)
Persistent noncytocidal productive infection
No CPE Little metabolic disturbance Cells cont to grow and divide May cause loss of specialised fx Always (often with red yield)
Persistent noncytocidal nonproductive infection
Usually no effect on cell
No new virion production genome just persists as an episome or is integrated without expression
Teansformational infection
Morphological alterations
Cells survive and become immortalised
Transformed cells may produce tumours
If oncogenic dna virus then they rarely produce new virions but oncogenic rna viruses sometimes do
Shutdown of host macromolecular synth
Many cytocidal viruses cose for pros that shut down hist pro synth (cell rna and dna synth usually affected as a conseq) could be rapid or gradual shutdown
Noncytocidal viruses dont do generalised shutdown at all
Flu macromol shutdown eg
Rna birus repl in nucleus
Needs capped rna as primers to initiate viral rna synth
Nuclear rna pol 2 transcripts are cleaved just before 5’ end by viral cap dep endonuclease (part of virus rna pol)
Aka cap stealing
Cap req for translation
Herpes macro mol shutdown eg
Pro encoded by all herpes viruses redistrib spliceosomes and decr splicing as birus genes predominantly unspliced
HSV birion host shutoff pro is a struct pro carried in the virus that acts in the cytoplasm to resuce mRNa stability and cause an initial decr in amount of cellular mRNA
Enterovirus macromol shutdown eg
Some encode a pro that alters ribosome sonit cant recog 5’ cap
Virus uses IRES for translation initiation so ribosomes preferentially act on viral mRNA
Polio macromol shutdown eg
Encode proteases that cleave initiation factors and polyA binding pro si decr translation of cell mRNA and allows incr viral mRNA cont IRES
Viral interference with apoptosis
Many encode antiapoptotic pros to prev cell death allowing virus to persist or complete replicative cycle
Others induce apoptosis in the infected cell, as a way to reduce inflam resp so red imm resp against virus
Viral interference with cell cycle
Some induce cell to enter cell cycle to ensure replication machinery req by cirus is available
In lytic infections this isnt an issue but if infection is abortive this abnormal activation could lead to a tumour
Viral interference with cell fusion
Glycoproteins that induce virus-cell fusion remain on CM of cell and can induce fusion with neighbouring cells in the same way by glycopro interact with rec on neighbouring cell
Can cause syncytia or polykaryocyte formation (a feature of cell monolayer infected with pox herpes corona or paramyxoviruses)
Viral interference with permeability
Several cell fx triggered by depolarisation, so can be induced following virus infection
These changes may be swamped in lytic infections but can be key in nonlytic ones
Cytoskel fx
Substrate for polyribosomes
Structural integrity
Struct framework for organelle movement
Part of system for cell movement
Viral interaction with cytoskel
Many viral macromolec assoc with cytoskel and is likely that sub cellular compartmentalisation of viral processes relies on cellular organisation of host cell
Also cytoskel disrupt and so polyrib disrupt could partly explain inhib of host macromol synthesis
miRNA fx
Act as key regulators of gene expression in mammals birds and other organisms
miRNA production and process of action
Encoded by genome and expressed as longer RNAs processed by cellular enzymes to prod short hairpin RNAs
These dsRNA can recog a pro called Dicer and are incorporated into an RNA induced silencing complex that allows a strand of miRNA to bind a spec seq in target mRNA causing either degradation or inhib translation
Viral interference with miRNAs
Most notably herpes viruses encode miRNAs that target cellular genes
Mech of release of progeny virus dep on
Viral structure
Nucleocapsid bud through plasma mem prod EC virions or through internal mem (eg organelle mem or inner nuclear mem) and released via fusion of secretion vesicles cont virions
Release from polarised (eg epi) cell
Can be directed to diff surf of cell eg basal or apical surf
Othro and paramyxo at apical surf
VSV and retro at basal surf
Glycopros of the viruses traffiked to the apprpriate surf (an innate property of glycopro struct and mimics cellular glycopro trafficking
Budding of many virions may disrupt the cell mem and cause CPE
