Virology Essay


2. Includes picornavirus (polio, rhinovirus, HepA, coxsackievirus, echovirus), calcivirus (Norwalk virus), astroviridae (astrovirus), flaviviridae (HepC, yellow fever), togaviridae (rubella virus, sindbis), coronaviridae (SARS virus), significant # of plant malware (TMV, TRV, BMV, PVX, TEV, PVY) * All have great sense genomic RNA acting directly as mRNA pertaining to protein activity; all consist of RNA, protein and no lipid envelopes; herb and microbe viruses consist of single form of coat healthy proteins (animal picornavirus contain four types of coat protein) * Following entry to host cell an uncoating, protein activity start straight from viral RNA and and then replication and packaging 5. Translational tactics used: 1) synthesis of subgenomic RNAs (e. g, TMV), 2) formation of polyprotein, followed by post-translational control to generate useful proteins (e. g. picornavirus) LECTURE 20: PICORNAVIRUS

2. Picornavirus structure

* Icosahedral, T=1

2. 27-30 nm in diameter

* four structural protein, 60 replications of each every virion

2. VP1, two, 3 kind canyon where cellular radio binds, VP4 only visible on inside particle, exactly where contacts genomic RNA 2. Genome

* Ss (+) sense RNA, poly-A tail at 3' end, VPg (Virion healthy proteins genomic) covalently linked to 5' end in place of cap 5. VPg

* Attached with 5' terminal pUpU of viral RNA via phosphodiester linkage with tyrosine-OH group * Function in buffering viral RNA toward ribosome for translation & part in duplication * Monocistronic genome (contain 1 ORF) which encode large polyprotein polyprotein cleaved to yield structural and nonstructural aminoacids * Proteolytic cleavage

* Polyprotein first cleaved into a few protein precursors: P1, P2 and P3 * P1: precursor pertaining to capsid healthy proteins; P2 and P3 precursors for polymerase and proteases * QG (glutamine-glycine) target for cleaved (viral protease 3C) * Translation

* 5' noncoding (untranslated) place usually very long and include high level of secondary structure * Cap-independent

2. Picornavirus focus on cellular mRNA to prevent their translation through cap-binding protein which usually inactivate (cap-dependent) cellular mRNA translation by cleaving eIF-4G * Translation of viral RNA then strong reduction in host cell mRNA 2. Poliovirus has internal ribosomal entry site (IRES) where they inside initiate translation 2 cell phone proteins (P52 and P57) bind to IRES and enable ribosome to bind 5. Replication

* Following virus entry and uncoat, poliovirus RNA directly converted to produce healthy proteins necessary for replication in cytoplasm * a few virus particular RNA constructions associated with membranous vesicles 5. 1) ssRNA lacking VPg

* 2) replicating intermediates (RI): negative stranded template 2. 3) replicative form (RF): end product of RNA replication * Proteins 3D is definitely RNA based mostly RNA polymerase, proteins 2B, 2C, 3AB, 3CD as well involved 5. All nascent RNA located with VPg attached at their very own 5' end * Designs for part of VPg in virus replication

* 1) VPg turn into uridinylated and acts as special primer for – RNA synthesis * 2) host component add poly-U to poly-A tail, varieties hairpin and primes elongation of – strand, then cleaved 2. Circular RNP complex accustomed to initiate – RNA activity * Virus-like proteins 3CD and VPg, poly-A joining protein (PABP) and poly(rC) binding protein (PCBP) connect to each other and ends of viral RNA to form rounded RNP intricate * Inhibited of translation initiation allow clearance of viral RNA over time simply by elongation of translating ribosome to 3' end of coding pattern * When template RNA cleared of translating ribosome, VPg-pUpU relate with several end of viral...


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