Download viruses 16 kb viruses

Give example of viruses that infect eukaryotic cells. How are these viruses structurally organised and
what effects do they have on infected cells?
Intro:

Viruses=intracellular parasites, subversion of host machinery for repro.

20-300nm

Genome types= double strand DNA, positive/negative sense single strand RNA, retroviruses.


Mechanisms of attack: lytic, lysogenic.
General action: injection of virus/genome into host, genome replication, synth viral proteins,
self assembly, release.
Structural organisation:
Human papillomavirus (HPV):


capsid=72 capsomeres=2 viral proteins=L1+L2. Rough sphere.
Circular, double stranded DNA, 800 bp.

Overlapping ORFs so alternative splicing used for gene expression, however in HIV, length of
ORFs dictates protein type. long=viral proteins short= cell cycle regulators.
Human immunodeficiency virus (HIV):





Retrovirus, +ve strand RNA, own reverse transcriptase.
120nm diameter, rough sphere
2 separate strands (recombination=rapid response to stress)
Enclosed in conical capsid (protein p24) with integrase and rev trans enzymes.
lipid membrane (enveloped) from budding of host membrane by action of viral spikes.
Tobacco mosaic virus (TMV):

HIV needed integrase+rev trans, TMV uses host enzymes as +ve strand RNA.

+ve = direct translation in cytosol unlike -ve (eg. rabies virus) which uses viral polymerase to
make +ve.
6.4kb +ve single strand RNA in core surrounded by rod-like helical capsid= 2130 molecules coat
protein.


codes 4 proteins: 2xreplicate viral RNA, transportation of RNA, capsid.
Effects on host cells:
HPV:




Infects basal cervical epithelial cells, uncoats and DNA enters nucleus.
E6+E7 transformation genes, first genes expressed.
E6=inhibits p53 (a cell cycle repressor / apoptosis activator when DNA is damaged). Also triggers
telomerase (reset bio clock of cell).
E7=inactivates Rb, a tumour suppressor.

High rate of cell division=tumour growth=cancer.


latent so HPV DNA remains incorporated into all new cell nuclei as a plasmid.
Cells differentiate, E1/E2 switched on. DNA binding proteins: E1=helicase, E2=transcription
factor.
L1/2 encode viral proteins.

HIV:

Like HPV, HIV is also latent.

Targets CD4+ T helper cells, macrophages and dendritic cells.



Adsorption of glycoproteins to membrane= endocytosis of enzymes and RNA.
RNA to DNA by rev trans. Integrase to insert DNA into host chromosome to be transcribed.
High error rate (new strains easily formed)

Many rounds, then lytic cycle begins.


Certain transcription factors must be present, viral genome encodes 2, Tat/Rev=+ve feedback.
Budding of host plasma membrane, viral glycoproteins inserted into lipid membrane to form
envelope.
HIV kills T helper cells=lower immune defence=higher chance of AIDS=susceptible to cancer.

TMV:



Unlike HIV, TMV doesn't incorporate it's genome into host's. (lytic straight away)
Infection, replication genome (RNA dep RNA pol to make -ve sense template), translation,
assembly.
Produces p30 movement protein to enlarge plasmodesmata and facilitate entry to neighbor
cells.
can spread through phloem for longer distances/contact with diseased plant.

Causes stunted growth of tobacco plant.

Conclusion:


Baltimore classification, sense, enveloped.
Despite small size of virus and genome, major detrimental effects on cellular and organism level.


Viral polymerases have no exonuclease activity= high error rate=rapid response to stress=drug
resistance.
Ultimately, viruses propagate own genomic material by subverting host cell cycle to favour
transcription/translation of viral proteins.