H2 Biology 15 - Virus reproduction

viruses acellular; don't contain cytoplasm, cellular organelles >

dont carry out metabolism/respiration, grow, divide outside host cells >

can replicate only by using host cell's metabolic machinery & cellular organelles(enzymes,ribosomes, amino acids) >

only reproduce in host cell >

dont synthesise own proteins >

not capable of movement, no means of moving themselves >

dont feed >

not affected by drying/freezing >

survive within host cell, crystallise outside of host cell >

contain either DNA/RNA but never both

virulent; lytic

A; attachment sites r&a specific receptor sites on HBCW

P; tf anchor bpp to cell surface >

conformational changes in bp, ts; ts contracts, drive hollow tube thru BCW > phage DNA injected into bact cytoplasm

R; phage genes expressed w/ host metabolic machinery, resources; codes for enzymes-disrupts normal host cellular fn by terminating bact macromolecular synthesis; nucleases-hydrolyse bact chromosome, nucleotides released used for new phage DNA copies >

host metabolic machinery used, synthesise > phage enzymes, structural components

M; sufficient components synthesised, phage components assemble, enclose newly replicated phage DNA, forms new phages

R; phage directs lysozyme production, breaks down peptidoglycan cell wall of bact, osmotic lysis of bact >

newly assembled bacteriophages released

temperate; lysogenic+lytic

A; attachment site on tf used to r&a specific receptor site on HBCW

P; ts contracts, drive hollow tube thru BCW >

phage DNA injected into bact cytoplasm >

phage DNA circularises inside bact, prevents degradation from host exonucleases

R; phage DNA incorporated into specific sites of host bact chromosome; inserted phage DNA called prophage >

repressor protein prophage gene expressed; represses GE of other prophage genes controlling phage replication >

phage replication blocked, phage dormant >

bact divides, phage DNA replicates as host bact DNA, passed to each daughter cell >

enables viruses to propagate w/o killing host they depend on

I; env factors induces phage to enter lytic cycle,find new host for replication >

repressor proteins no longer made, phage DNA excised from bact chromosome, switches lysogenic->lytic & lyses host

A; HA r&b to specific SAC receptors on HCPM

P,U; virus enters host by RME, HCPM invaginates, pinches off; places virus in endocytic vesicle, enters cytoplasm >

acidification -> viral envelope fuse w/ endocytic vesicle membrane, nucleocapsid released >

uncoating; capsid degraded by cellular enzymes, viral NA+RDRPol released

R; viral NA template for synthesis of cRNA strand by RDRPol >

cRNA strand template for synthesis of new viral RNA copies >

fn as mRNA, undergoes t/l produce viral proteins

M; gp synthesised by ribosomes on RER transported to PM via vesicles, incorporated into HCPM, clustered in patches as exit pts for viral progeny >

capsid assembled around viral RNA, RNA dependent RNA pol

R; new viruses bud off from HCPM @ exit pts by budding, get viral envelope >

NA cleaves SA residues from HA, facilitates release of newly replicated viruses

A; gp120 r&b CD4 on HCPM >

induces gp120 conf change, enables binding of gp120 to HC chemokine receptor(CCR5/CXCR4) >

induces gp41 conf change, allows HIVE+HCPM fusion

P&U; genetic material, capsid enter HC >

cell enzymes remove capsid; release vRNA, RT & IT

R; RT cat. syn. of cDNA, RNA strand degraded >

2nd DNA strand syn. comp to cDNA, dsDNA formed >

dsDNA -> nucleus, incorp. as provirus by IT >

t/c, host RNA pol transcribes provirus genes into RNA molecules, serves as mRNA for proteins, genetic material for new virus particles

M&R; viral mRNA t/l -> synthesis of gp, IVPP >

gp & IVPP transported, emb. in HCPM by transport vesicles from RER >

RNA assembles w/ proteins, form new viral particles >

virus particles bud off from HCPM, acquires HPM w/ gp emb. >

HIV protease cleaves IVPP into fn proteins, virus mature

diff virus strains infect same host simultaneously >

random assembly/genetic reassortment of RNA segments from diff virus strains leads to novel combinations of viral genes coding for viral proteins, forming new strain, leads to antigenic shift

point mutations in gene coding for viral protein can occur during replication of viral RNA >

accumulation of mutations results in slight changes to viral protein shape(e.g. HA) >

host immune system no longer recognises antigenic sites on new strain HA >

new HA shape allows it to be complementary to other membrane receptors on new types of host cells, allows for infection >

leads to antigenic drift