Viruses Flashcards
Characteristics
Can be considered as living or non-living
Non-living:
Acellular and does not have organelles
Cannot replicate or synthesise proteins autonomously
Do not carry out metabolic processes like respiration outside of host cell.
Living:
Capable of reproduction by using host cell machinery
Has own genetic material in the form of RNA or DNA
An obligate parasite as it requires a host cell to complete its life cycle and reproduce.
T4 Bacteriophage
When the tail fibres of T4 phage attaches to specific cell receptors on the bacteria cell wall, it releases lysozyme which digests the peptidoglycan cell wall. Released molecules induces conformational change in the phage base plate, Its tail sheath contracts and thrusts through the cell wall, injecting viral DNA genome into the cell.
Once in the cell, enzymes coded for my viral DNA immediately hydrolyse host bacterial genome. Virus takes over host cell machinery, using host DNA polymerase to replicate viral genome and using host RNA polymerase, ribosomes and amino acids to synthesise viral proteins. New phages are assembled and enzymes hydrolyse the peptidoglycan cell wall of the bacteria, causing bacteria to lyse and release the phages which can now infect other bacterial cells.
Lysogenic
Same except viral DNA is integrated into the bacterial genome as a prophage where it remains latent but is replicated along with the bacterial genome until it is found in many progeny cells.
When exposed to irradiation, spontaneous induction occurs and prophage is excised. Prophage DNA is replicated and phage components are synthesised using host cell machinery. Enzymes coded by prophage genome hydrolyse host bacterial genome and peptidoglycan cell wall, causing bacteria to lyse, releasing phages after they have assembled.
T4 Bacteriophage vs Lysogenic bacteriophage
1) T4 bacteriophage degrades host cell DNA immediately upon virus entry while lysogenic phage does not upon virus entry.
2) T4 bacteriophage does not have a latent stage and virus replicates immediately while lysogenic phage undergoes a latent stage with no replication.
3) T4 bacteriophage does not incorporate its DNA into the host bacterial genome while lysogenic phage does, now called a prophage.
4) T4 bacteriophage takes full control of host macromolecular synthesis for synthesis of DNA and proteins while lysogenic phage only takes partial control to synthesise repressor proteins
5) T4 bacteriophage, no repressor proteins are encoded or synthesised while lysogenic phage genome expresses two repressor proteins which prevent immediate expression of other genes for replication.
6) T4 phage propagates by lysing the host cell and releasing phages to infect other cells while lysogenic phage propagates by having its viral genome replicated along with host bacterial cell’s until it is found in many bacterial progenies during latent stage.
Influenza
8 segments of ssRNA/-
Haemagglutinin
Neuraminidase
RNAdep RNA polymerase
Haemagglutinin glycoprotein on influenza viral envelope binds to the sialic acid receptor on epithelial cells. This causes cell surface membrane to invaginate and pinch off, transporting the virus into the cell by an endocytic vesicle.
The vesicle fuses with a lysosome. The pH drop causes viral envelope to fuse with membrane of vesicle, releasing viral nucleocapsid which is digested by cellular enzymes to release viral RNA genome into the cell.
Viral RNA genome is used as a template for transcription of +/mRNA by host DNA polymerase and ribonucleoproteins and ATP.
mRNA can then be transported to the cytosol to be translated into viral proteins by host ribosomes and tRNA or as template for replication to be used as new -/RNA strand viral genome.
At the RER, glycoproteins haemagglutinin and neuraminidase are translated and packaged into secretory vesicles that are transported to the cell surface membrane where the glycoproteins are embedded.
New viral RNA genome and ribonucleoproteins associate with capsid proteins to initiate budding. New virions acquire the cell surface membrane with glycoproteins embedded as they bud off and neuraminidase cleaves sialic acid to release virions which can now infect other cells.
HIV
Retrovirus
2 ssRNA/+
gp120 and gp 41
R.I.P. enzymes
Gp120 binds to CD4 receptor on cell surface membrane of T4 helper cells, exposing gp41 which stimulates fusion of viral envelope with cell surface membrane, releasing viral nucleocapsid which is degraded by cellular enzymes to release viral RNA genome.
Viral reverse transcriptase synthesises double-stranded viral DNA by first using viral RNA as template for synthesis of one complementary DNA strand by complementary base pairing to form RNA-DNA hybrid, then using DNA strand as template for synthesis of another complementary DNA strand. Integrase integrates viral DNA into the host cell genome as a provirus where it remains latent and is replicated along with the host cell.
Upon activation, provirus excised and transcribed to RNA which exits the nucleus. RNA can be used as new viral RNA genome or as mRNA to be translated to viral polyprotein by host cell machinery. At the RER, glycoproteins gp120 and gp41 are synthesised and packaged into secretory vesicles which are transported to the cell surface membrane where the glycoproteins are embedded. Viral polyprotein and genome assemble, and viruses bud off, acquiring the host cell surface membrane with glycoproteins embedded. Within the virus, host protease then cleaves the polyprotein into functional proteins and viruses are encapsulated with protein coating forming capsid so now the virions are released to infect other cells.
Virus similarity
Enveloped virus
Have glycoproteins embedded on envelope
Single-stranded RNA genome
New strains
Antigenic drift
New strains of viruses form from an accumulation of mutations of the genome leading to change in the ribonucleotide sequences. As a result of lack of proof-reading ability of RdRp and high rate replication and single-strandededness of RNA resulting in lack of back-up copy to be used as a template for repair.
Antigenic shift
When two different strains of virus infect the same cell and their respective capsids are degraded, reassortment of different RNA segments can result in new virions with recombinant genomes.
New glycoprotein conformation
