Viral Reproduction and Infection Mechanisms

Extracellular is inactive DNA or RNA surrounded by proteinIntracellular – active inside a host cell/ viral reproductionprotein capsid - Viral nucleic acid presentcapsomere- protects genetic materialretroviruses: ss RNA hepadnaviruses: dsRNA enveloped”- membrane lipid bilayer (host)& proteins (virus)naked-+ viral DNA complex viruses- icosahedral head/ helical tail/ Tail fibers attach to host cellviral replication: the virion attaches host specific/ proteins interact w/ receptors on surface/ if receptor not present= can’t infect. 2. Phages often complex3.active/intracell/ production of new virions/ viral mRNA is required SS DNA ->DS DNA -> mRNA / DS DNA= mRNA (w/polymerase) RNA polymerase” to make mRNA from viral RNA/ SS RNA (+) = read as mRNA/ (-) RNA) - need polymerase->synthesize complementary strand-> mRNA. 4&5 /Temperate phages-Lytic - virions replicated & lyses (virions released)/

lysogene: bacteria that has viral particle / lambda is DS DNA / Lysogenic –DNA->in host/ most of viral genome not expressed; replicates w/ host

Animal viruses: *Retroviruses- RNA/ replicate w/ DNA intermediate./ reverse transcriptase (dna from rna)/ gene therapy

*Are highly diverse, many enveloped

Both are plus sense, but are H-bonded together so are not read as mRNA

*4 classes- effect on host cellreplication: 1. virion enters (endocytosis) 2. Reverse transcriptase either by a. synthesizes

1.Virulent infection (host cell lyses when released complementary DNA from RNA templateb degrades the RNA of the RNA/DNA(as ribonuclease)

2.Latent infection (viral NA not replicating – c. during degradation of RNA synthesizes complementary DNA to produce viral DS DNA

a delay between infection and reproduction3) DNA integrates into the host genome (using viral integrase)

3.Persistent infection (host cell remains alive, 4) Transcription of viral DNA to viral/genomic mRNA 5) make viral nuccapsid in host cytoplasm

virions produced slowly over a long period) 6. Release by budding through the host cytoplasmic clel membrane (envelope acquired)

4.Transformation (transform normal cells to cancer cells)

influenza viruses- (-) SS RNA/ orthomyxovirus- “myxo” -mucus or slime of a host cell/ enveloped virus & “polymorphic”(no defined shape)/ Acquires envelope by budding through host cell / protein spikes on the surface that interact with the host cell /Hemagglutinin- binds to sialic acid in mucus cell Neuramindase -breaks down sialic acid/ Replication occurs in both the nucleus and the cytoplasm/ Viral RNA is replicated in the nucleus using viral replicase and viral endonuclease( brought in)/Influenza RNA (8) “segmented genome”/ Codes for 10 proteins/ antigenic shift-different segments be packaged together- changes virion surface properties-- no longer recognized by host antibodies when released/ antigenic drift” – accumulation of mutations that change virion surface properties

Viroids - smallest/ infect plants (wound)/ small, circular, SS RNA/ no capsid/ extracellularly/ naked RNA/ Do not code for any proteins – only viral RNA/ dependent on host machinery /Prions: infective proteins- no NA/ extracellular stage/ not killed by radiation/ animals/ holes in the brain/ Normal hosts have gene that codes for a prion-like protein/ first organisms=methanogens-anaerobic/ molecular phylogeny: carl woese 1970s/ analyzed three domains based on RNA/ 16S RNA =prokaryotes/ 18S RNA= eukaryotes/ prokaryotic species=no sex/ 97% + similar 16s RNA gene

*E- donor oxygenic photosynthesis: H2O/ anoxygenic photosynthesis electron donors include H2, Fe2+, H2S, S2O32- and S°