viral latency Flashcards
what is viral latency
when viruses remain in the host without proliferating and causing damage to the cells
it is present in the body but exists in a resting state
what part of the viral life cycle does viral latency lay
the lysogenic part
what is the lytic cycle
when circular dsDNA is replicated, transcirbed and translated into proteins to make the components of viral progeny which is then released by lysis
what is the lysogenic cycle
when circular dsDNA is integrated into the chromosome forming a prophage which is replicated with the host chromosome and passed to daughter cells until chnages in the environment excise it and the lytic cycle begins
what are the types of latency
1) integrated/proviral
2) episomal
what is integrated/proviral latency
when the viral genome gets into the nucleus and inserts itself into the host genome
what are the advantages and disadvantages of integrated latency
+automatic host cell division results in replication
+ near impossible to remove without killing the cell
-needs to enter the nucleus
-increased difficulty to remain latent
what is an episome
an extrachromosomal element which replicates alongside the host genome
what occurs in episomal latency
the virus circulates the cell in an episome
latency associated nuclear antigens tether the episome to the cell chromosome
the viral episome replicates once in concert with cell DNA
it is replicated but new viral particles are not produced and the infected cell dies
what are the advanatges and disadvantages of episomal latency
+ easier to maintain and reactivate that proviral latency
- more exposure to cell defences leading to possible degredation of virus by cellular enzymes
what is an acute infection
when the virus infects the host and takes over the cellular machinery
what is latent infection
when the viral genome is replicated with the host genome but the viral gene expression is silenced
what is reactivation
acute expression may occur later resulting in symptoms appearing long after the virus is acquired
what are the different outcomes of a viral infection
1) persistant infection
2) transformation
what is a persistent infection
when the virus replicates at a rate the immune system can tolerate but at some point the immune system wears down allowing increased replication leading to symptoms
what is meant by transformation
when a virus carries a gene which promotes cell proliferation such as onconogenes whcih integrate into the host genome and produce tumours
why do viruses remain latent
1) avoid killing the cell allowing prolonged survival
2) keep gene expression undercontrol
what is apoptosis
programmed cell death
outline how the herpes virus invades the mucous membrane
1) comes in contact with the membrane
2) binds to epithelial cells
3) viral proteins change conformation which releases energy driving the fusion of viral and host membrane
4) a fusion pore is generated and the viral capsid slips into the cytoplasm
how does the herpes virus generate new virions in the epithelial cells
1) capsid reaches the nucleus
2) capsid docks in a nuclear pore and delivers DNA
3) numerous lytic cycles result in a blister on the skin
how does the herpes virus reach the nucleus
1) host dynein motor proteins transport the virus towards the minus end of the microtubule to the microtubule organsising centre
2) once there the kinesin motor proeins move the virus to the plus ends of another microtubule and to the nucleus
what are the to transport proteins associated with the entry of the herpes virus to the nucleus
1) dynein
2) kinesin
how does the herpes virus deliver DNA
1) DNA circularises
2) recrutes factors which silence viral DNA to prevent inferon cell receptors recognising it and triggering cell mediated immunity
how do HSV lesions reappear again and again
1) once epithelial cells are infected HSV travels to the neurons which innervate these mucous membranes
2) here they become latent by recruiting chromatin assembly factors to pack DNA
3) it becomes repressed expect for the gene which codes for latency associated transcript
4) it is reactivated when host cells sense stress which reinitiates viral gene expression and therefore replication
what does latency associated transcript do
stimulates heterochromatin packaging and prevents the cell triggering apoptosis
what are syncytins
- retroviral envelope proteins which allow cell to cell fusion and adopted by the host for their ability to promote development of the placenta
what is an oncogene
a mutated gene which contributes to the development of cancer, its unmutated state is referred to as an proto-oncogene which plays a role in cell division
what are the three genes which code for a retro virus
1) gag= codes for structural virion proteins
2) pol= codes for reverse transcriptase
3) env= codes for envelop glycoproteins
4) a long terminal repeat which is a non-coding sequence at the end of the genome
what is the LTR needed for in retroviruses
integration into the host chromosome as well as encoding gene expression
what is the difference between a normal retrovirus and a cancer causing retrovirus
transforming viruses are vairents where part of the viral sequence has been replaced by an oncogene (the pol and env gene)
outline how onocogenes are aquired by retroviruses
1) viruses integrate near a host oncogene
2) it is integrated and packed into the virion
3) virus infects a new host carrying onco gene with it
what is a viroid
not a virus
- smaller in size
- not enclosed in a protein shell
- causes disease by inducing RNA silencing of host mRNA alterimg gene expression
- only causes disease in plants
what is a prion
not a virus
- proteins whihc undergo conformational transition into an insoluable form
- they accumulate in the brain cells causing brain impairments
- resistant to proteases and high temps
