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Viruses sgu

lecture 13-18

QuestionAnswer
Viral properties associated with all living organismssmaller than bacteriamust use metabolic machinery of living host to replicatecore of NA surrounded by protein coatsymmetrical nucleocapsidmetabolically inert
virion complete viral infectious particle
Capsid found in all viruses, protects the genomeprotein shell surrounding NAmade of protomers that aggregate to make capsomersreduced need for genetic info and promotes self assembly
Function of capsids provides NA protection from digestion by enzymesallows attachment of virion to host cellprovides proteins that enable virion to penetrate host cell membranehelps inject infectious NA
Helical capsid rod shaped capsomers arranged ina coildiameter determined by protomerslength determined by length of NA
isocahedral capsid shape and dimension depends on protomersring or dome shaped, capsid spherical or cubical20 sided polygontriangular hexons: 6 capsomersround penton: 5 capsomersvariable=adenovirus (252), poliovirus (32)
viral envelope some viruses have an envelopeprotein phospholipid layerexternal to nucleocapsidlipids taken from host cell membranemakes viral partical sensitive to lipid dissolving agents
matrix proteins link envelope to capsid, stabilize virus, mediate interaction between capsid proteins and envelope
surface proteins exposed capsid proteins or envelopeglycoproteins-attachment (spikes)antigenic determinantsex: hemagglutinin and neuraminidase
nucleoproteins stabilize NA during replication or have enzymatic functionfound in the corerequired for replication strategies
nucleoprotein core NA (DNA or RNA) and nucleoproteins
classification originally based on symptomsmethod of transmissionsymmetry of capsidtissue or organ affected
Today classified by ICTV type of NAsymmetry of capsidpresence/absence of envelopesize of virus particle
baltimore system complements ICTVmRNA production centricbased on NA content and how mRNA is formed
virus detection Cytopathic effect: plaque assay, EMBiochemical: enzymatic assays, PCR/NA hybridizationSerological: IF, IP, IB, ELISA, RIA
viruses as tools life sciencesmedicine (gene therapy, immunology, etc)weapons, biodefense
viruses of prokaryotes bacteriophage=infect bacteriamostly dsDNAhead surrounds the NAstructure acts as an injectorfacilitates injection of phage NA into the prokaryotic cell
defective virus complete virion but unable to replicate without helper virus
pseudovirions contains host DNA, infectious, but no replication
viroids subviral particles, infectious agentscircular ssRNA moleculesmainly cause plant diseaseswith or without capsid or envelopeex. Hep D
prions small proteinaceous infectious particles that resist inactivation by most proceduce which modify NANO NAPrP gene-found on most body tissues, increased in CNS
pathogenesis of prions slow infectionresults in neurodegenerative diseasespongiform changes with neuronal lossspongiform encephalopathyno inflammatory response
epidemiology of prions tansmitted naturally by peripheral routesCJD most common disease, 10%of cases familial
clinical symptoms of prions Scrapie, Kuru, BSE, CJDrapidly progressive, loss of muscle control, shivering, myoclonic jerks and tremors, loss of coordination and rapidly progressing demetia and deathno lab diagnosis (direct)no treatment
Viral life cycle no typical growth patternsproduced from assembly of preformed viral structural components synthesized in host cellsno energy production, metabolism, gene replication, or protein synthesisalter structure/function of host cell
Viral replication phases eclipse phase: cannot be seen or recovered from infected cells, ends when first viral particle is observedMaturationLatent phase: progeny virus accumulates intracellularly, ends when first free virus is released
Viral attachment requires physical contactVAPs recognize specific receptors, determine susceptibilty (does not = permissiveness)most receptors are glycoproteinsentry by: clatharin coated, fusion, macropinocytosis, or phagocytosis like
viral penetration enveloped viruses: fusion of viral membrane with cellular plasma membrane, endocytosis-> fusion with cellular vacuolesnon eneveloped: adsorptive endocytosis, other ill defined pathwaysget uncoating: releases viral genome for functional expression
protein and NA synthesis transcription/translation: syntheis of viral mRNA, production of viral proteinsreplication: progeny viral genomes produced by DNA/RNA dependent polymerasesnaked genome DNA/+ssRNA: infectious NA-initiate replication on injection
assembly and packaging assembly into virions takes place in nucleus (DNA except poxvirus) and cytoplasm (RNA except orthomyxoviruses)type of genome and glycoprotein sequence determine site of buddingnaked viruses assemble preformed units, enveloped viruses formed from units
maturation and virion release released after lysis by budding from plasma membrane or exocytosismatrix proteins arrange alongside modified cell membranenucleocapsid moves toward the matrix protein area, complex buds out
Class I: dsDNA(adenoviruses, herpesviruses, poxviruses, polyomaviruses) host enzymes recognize dsDNA, transcribe mRNA, produce IE proteins, transcribe more mRNA, produce E proteins, replicate parental DNA and more mRNA, produce L proteins, assemble capsids, incorporate viral DNA to make mature viruses
characteristics of class I smaller genomedecreased number of proteins it can encodeinvade nucleusPox viruses: replicate in cytoplasm, responsible for human diseaseAdenovirus: replicate in nucleusHerpesvirus: replicates by rolling circle mechanism, some can transform cells
E proteins tend to be regulatory in nature
L proteins assemble into capsid (incorporate viral DNA to make mature viruses)
Class II: ss+ sense DNAparvoviruses host cell proteins synthesize da viral DNA, mRNA produced and translated, viral proteins polymerize to make capsid, viral DNA encapsidatedreplication in nucleus- sense strand serves as template for + sense strand
Class III: dsRNAreovirus, rotavirus segmented dsRNA genomeshave RNA dependent RNA polymerase (RDRP)genome with 10-12 separate dsRNA moleculesviral mRNA transcribed by RDRP, mRNA translated, viral proteins form immature capsid, copied to form dsRNA, more mRNA made
Class IV: ss+ sense RNApicornaviruses (poliovirus, calcivirus, flavivirus, togavirus, coronavirus) ss+ sense RNA that is polyadenylatedinfectious by itself during replication genomic RNA copied into -strand, which can act as a templateclass a(polyprotein) and b (no polyprotein)
Class V: ss- sense RNAortho and paramyxoviruses, rhabdoviruses, filoviruses, bunyaviruses, and arenaviruses rabies and influenzaviral mRNA copied into mRNA by enzyme in virionVa: non segmented, measles/mumps, virus specific RNA polymerase catalyzes synthesis of many RNAsVb: influenza, segmented, each segment is template strand for mRNA
Class VI: ss+ sense RNA with DNA intermediateretroviruses enveloped, 2 identical + strands of RNA (retroviruses), directs formation of DNA molecule (ss- then complementary +strand), dsDNA integrated into chromosomal DNA of infected cell, transcribed by cell into +RNA
Class VII: dsDNA with RNA intermediatehepadenoviruses cantain DNA genomes, use reverse transcriptase to make genomic DNA from RNA copyupon infection the gapped genome is repaired (using virus associated DNA polymerase)
mechanism of viral pathogenesis 1.curcumvent protective barriers of the body 2. evade immune control 3. kill cell directly or trigger a destructive immune and inflammatory response have speceific tissue tropism (can cause one or multiple diseases) encode virulence factors
basic steps of viral disease 1. acquisition 2.initiation of infection at primary site 3. incubation period 4. replication in target tissue 5. immune response 6. virus production in tissue that releases virus 7. resolution or persistent infection
infection of target tissues virus enters body through breaks in the skin or across mucoepithelial membranes inhalation most common route replicates in cells that express viral receptors and have the appropriate biosynthetic machinery
cytopathogenesis nature of the infection-determined by characteristics of the virus and target cells nonpermissive: does not allow replication permissive: cells provide biosynthetic machinery, supports replication
possible outcomes of a viral infection 1. failed (susceptible but not permissive) 2. cell death (lytic) 3. infection without cell death (persistent)
determinants of lytic infection access to target tissue, stability of body, ability to cross skin/mucous epithelial cells, ability to establish viremia, ability to spread through the RES, target tissue
persistent infections occurs when a cell is not killed, may result from DNA virus infection may be chronic, latent, recurrent, ortransforming
cytopathic effects (CPE) due to infection with virus inclusion bodies, rounding, cell lysis, necrosis, apoptosis, syncytial formation
non-specific defenses 1.IFN: confers cellular resistance to infection, transcription of IFN genes occurs after exposure (RNA best inducer) first line of defense 2. complement: results in lysis 3. cytokines: produced bya ctivated macrophages, anti-viral activities
specific defenses Ab production, IgG, IgM, and IgA play role in immunity
immunopathology immune response can sometimes cause tissue injury ex: fixation and deposition of immune complexes
viral diseases mostly mild/no symptoms, may target essential tissues and organs, severity determined by a patients 1. ability to prevent/resolve infection 2. target tissues and virulence of virus, and 3. ability to repair damage to the body
exposure many viruses are ubiquitouspoor/close living conditions promote exposure to respiratory and enteric viruses
transmission direct contact animals can be vectors non-enveloped can withstand drying, detergents, extremes of pH and temp (generally transmitted by fomites) enveloped: fragile, spread in respiratory droplets, blood, etc, injection, or organ transplants
maintenance depends on general health, nutrition, genetic make up, age, and immune status of a population
geographica./seasonal considerations geography is determined by presence of cofactors, and immunological status of population seasonal differences correspond with behaviors that promote the spread of the virus
outbreak introduction of a virus into a new location originating from a common source, often can be stopped if the source is identified
epidemic occur over a larger geographical area, result from introduction of a new strain of virus into an immunologically naive population
pandemic worldwide epidemic
oral/respiratory tract infections oropharynx/respiratory tract=most common sites of infection spread via droplets, food, water, saliva, close contact primary infection or can spread URT and LRT infections
GIT infections results in gastroenteritis, vomiting, diarrhea, or no symptoms infect SI, damage epithelial lining and absorptive villi generally self limiting more significant on infants spread promoted by poor hygiene
Exanthems and hemorrhagic fevers virus induced skin disease through mucosa, cuts, as secondary infections, or from inflammation. childhood-roseola, fifth, varicella, measles, and rubella by enterovirus infections, dengue, yellow fever, ebola, lassa, sin nombre (infect endothelial)
organ and tissue infections symptoms from tissue damage or inflammatory response spread in blood, macrophages, may infect skin or muscle first find mononuclear cells, low PMN and normal to slightly reduced glucose (vs. bacterial)
STI sexual contact: HPV, HSV,CMV, HIV, HTLV1, HBV, HCV, HDV establish chronic and latent recurring infections and disease with asymptomatic shedding
eye infections results from direct contact with virus or viremic spread
hematological disease lymphocytes and macrophages-not permissive for viral replication, viruses establish persistent infections may elicit large T cell response macrophages are vehicles for spread
syndromes of possible viral etiology MS, kawasaki disease, arthritis, diabetes, chronic fatigue syndrome
chronic infections occur when immune system has difficulty resolving the infections DNA viruses (except parvo and pox viruses) and retroviruses cause latent infections with potential for recurrence CMV, herpes, and retroviruses cause chronic productive infections
Oncogenic viruses viruses can induce cancer by carrying a copy of genes in which altered expression can lead to loss of growth control, or they can alter expression of the cell's copy of regulatory genes (p53, RB)think of path and all the associations
immunocompromised patients more susceptible to infection with enveloped viruses severe T cell deficiencies atypical and more severe presentations IgA deficiency=more problems with respiratory/GI viruses
controlling the spread of viruses 1. quarantine: limits nosocomial spread 2. good hygiene 3. changes in lifestyle 4. elimination of a vector 5. immunize the population (more difficult to inhibit without being toxic to the host) 6. education
control of an outbreak 1. identify the source 2.cleanup 3.quarantine 4. immunization
vaccines inactivated/live attenuated (yellow fever, MMR)killed(flu, hep A)subunit (HPV)prophylactic vs.therapeutic
stimulators of host innate immune protective responses agents that bind tolllike receptors stimulate the release of cytokines, activate NK cells leading to cell mediated immune response interferon and interferon inducers facilitate treatment of some chronic viral infections antibodies prevent viral spread
problems with antivirals when symptoms become obvious the virus has already replicated viruses are dependent on host cell enzymes and processes
groups of antivirals attachment (neutralizing Ab, receptor antagonists), penetration (fusion inhibitors), uncoating (blocked by Amantadine), replication (NA and/or enzymes, blocked by nucleoside analogues (acyclovir), RT (AZT) and protease inhibitors),
more antivirals... RNA synthesis (blocked by ribavirin), release (blocked by neuraminidase inhibitors (oseltamivir) and protease inhibitors (sawuinavie, indinavir))
activation of antivirals acyclovir must be converted from acyclovir monophosphate to acyclovir triphosphate started by a viral thymidine kinase, finished by cellular thymidine kinases inhibits DNA polymerase by preventing elongation
resistance to antivirals due to changes in enzymes that would normally be targeted mutations, deletions, or substitutions replication rate prevention of resistance....Cocktail of drugs
Created by: kamarsh