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Disease And Defense > Virology > Flashcards

Virology Flashcards

1
Q

Mucociliary Flow

A

cilia that line the bronchi and trachea - forcing mucus from lungs and sinuses toward pharynx to be swallowed!

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2
Q

Infection

A

relationship between microorganism and human host; good or bad relationship; stable and transient

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3
Q

Infectious disease

A

an infection that results in a disease state

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4
Q

Communicable disease

A

infection that can be transmitted from person to person

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5
Q

Etiologic Agent

A

organism responsible for disease manifestations - direct or indirect (immune response)

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6
Q

Koch’s Postulates

A

criteria for proving that a certain organism is associated with disease 1) specific microbe is present in specific disease lesion 2) microbe can be isolated and grown in vitro 3) microbe can be infected in animals and cause disease 4) can re-isolate from animals and infect new animal host.

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7
Q

Limitations of Koch’s Postulates

A

some ID do not have characteristic lesions, some cannot be grown in vitro, ID is complex interaction between microbe and host

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8
Q

Pathogenicity

A

capacity of microbe to damage host

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9
Q

Pathogenicity

A

microbe causing host damage can be classical or opportunistic

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10
Q

Frank pathogen

A

cause disease to normal host

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11
Q

Opportunisitic pathogen

A

disease to immunocompromised patients

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12
Q

Virulence

A

relative capacity of a colony of microbes to cause a disease - often synonymous with pathogenicity

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13
Q

Virulence Factor

A

component of pathogen that facilitates damage to host.

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14
Q

In what ways doe microbes differ?

A

Same bug might have vastly different concentrations depending on route of infection, genetic differences, whether administred with bicarbonate.

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15
Q

What does administering microbe with bicarbonate do?

A

reduces stomach acidity, causes more virulence.

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16
Q

Stages of infection

A

1) encounter - how agent meets hosts - endogenous/exogenous, route dose 2) entry: colonization or adherence 3) spread: cross musical surface or spread within tissue 4) multiplication 5) damage - caused by agent of immune response 6) outcome - who wins?

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17
Q

Routes of spread

A

1) bodily fluids - saliva, blood, respiratory 2) fecal-oral 3) venereal 4) Zoonses - Vector (biting arthropod), Vertebrate Reservoir (contained within animal population) and Vector-Vertebrate Reservoir - arthropod infecting humans and animals

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18
Q

Entry of Microbes

A

globlet cells produce mucus and normal flora and pathogens are able to penetrate the tissue by: 1) disruption of tight junctions 2) infect the cell with phagocytosed material and transported via vesicles to other side.

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19
Q

what factors affect the microbiome?

A

Diet (breast or bottle feeding, solid food), suppression of microbial flora with antibioties, anatomic abnormalities, genetic differences.

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20
Q

Physiologic Importance of micro biome

A

Effect on tissue/organ differentiiaton, production of vitamins by gut flora, biochemical conversions, competition with pathogens for colonization.

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21
Q

Cholera is an example of a…

A

toxin mediated disease.

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22
Q

Pneumoccal Pneumonia is an example of…

A

acute inflammation caused by invasion, extracellular bacteria

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23
Q

TB is an example of…

A

infection by facultative intracellular bacterium

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24
Q

Rheumatic Fever is an example of..

A

pathology mediated by an immune response.

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25
Q

What is a virus?

A

filterable, sub-microscopic, obligate intracellular parasite. They are not alive, or do not undergo division. Genetic material enters the host cell and directs host to build new virus, which are then transported to another cell to carry out another round of replication.

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26
Q

Capsid

A

small proteinacous particle that contains DNA or RNA genome with the information to initiate and complete the infectious cycle.

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27
Q

How do viruses vary?

A

particle architecture, size, nature, topology of genes, protein coding strategies, cell/tissue tropisms, pathogenesis.

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28
Q

Two different classification of viruses

A

Classical and Baltimore

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29
Q

Classical Viruses

A

grouped according to shared physical properties - name derived from sort fo disease they are associated with

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30
Q

Properties of classical viruses

A

nature of genetic material, symmetry of capsid (helical or icosahedral), Naked or eveloped, dimensions or vision and capsid.

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31
Q

Baltimore Viral Classification

A

understanding how the virus replication and infection works. Based on central dogma.

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32
Q

Minus RNA

A

bottom strand of DNA (3’ to 5’), NDA from which mRNA is copied from

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33
Q

Positive RNA

A

top strand of DNA (5’ to 3’), contains open reading frame that is ribosome ready and able to be translated into protein.

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34
Q

Two principles of Baltimore Classification Scheme

A

1) genomes severe as template for synthesis of progeny genomes 2) function of viral genome is to make mRNA once inside the cell.

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35
Q

DNA Viruses

A

must use minus strand of DNA as genome template. RNA Pol II fills in the gaps of the DNA genome. Process takes place in the nucleus and produces an mRNA that is capped, poly A tailed.

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36
Q

dsDNA viruses

A

polyomaviruses, herpes, pox virus

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37
Q

Gapped Circular dsDNA

A

looks like normal DS, but has a portion of ssRNA, so this requires viral reverse transcriptase to bet to mRNA.

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38
Q

ssDNA

A

parvovirus, ssDNA is copied by host DNA Polymerase to make dsDNA and then to make mRNA and viral proteins.

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39
Q

RNA Viruses

A

have a negative or plus strand that dictates whether the genome alone is sufficient to be replicated. Some require additional proteins.

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40
Q

RdRp

A

RNA dependent RNA polymerase is a noval protein in the RNA viruses that produce both the RNA genome and mRNA from RNA template.

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41
Q

dsRNA

A

contain both + and - strands, can be turned into mRNA immediately; not reliant on host machinery as much

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42
Q

+ ssRNA

A

+ strand is translated directly by host ribosomes into protein, but need RdRp to amplify mRNA numer of subgenomic mRNA.

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43
Q

+ ssRNA with DNA intermediates

A

+ssRNA in virion is a real mRNA, but it is never used. Instead it is converted to dsDNA by viral reverse transcriptase and the sDNA intermediate integrates into host DNA and becomes a permanent part of the host genome.

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44
Q
  • ssRNA
A

very deadly virus, Virus’s can’t be made directly into protein. First copied to make positive strand, always used viral encoded RdRp found inside caspid.

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45
Q

How do we study viruses?

A

infecting eggs,electron microscopty, cell culture, quantification by plaque assay, ELISA, hemoglutination tests infecting susceptible animals, gene sequences.

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46
Q

Capsid definition

A

protective protein sturcture the delivers genome, assembles from components during an infection, two forms: helical and isosahderal; can be surrounded by a lipid envelope.

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47
Q

Nucleocapsid

A

Nucleic acid protein complex in virion that is a substructure of a complex particle.

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48
Q

Envelope

A

host-cell derived lipid bilayer

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49
Q

Spike

A

virus derived membrane bound glycoproteins

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50
Q

Virion

A

infectious virus particle

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51
Q

Helical Capsids

A

a caspid put down in an array that sounds the genome in a disc like fashion; looks like a long strand or bullet shape.

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52
Q

Icosachderal capsid

A

alternative structure where the proteins are arranged in a hollow, quasi-pherieral structure with the genome enclosed inside. Have 2, 3, and 5 fold axis of symmetry.

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53
Q

Envelopes

A

lipid bilayers acquired during viral particle assembly, have glycoproteins embedded. From from budding through host membrane through PM, ER

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54
Q

how do non-enveloped viruses leave the cell

A

lysis

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55
Q

Viral Glycoproteins

A

spikes; integral membrane proteins that function in entry, host range determinants, assembly and egression, evasion from immune system.

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56
Q

How do viruses replicate?

A

in a replication burst - not exponentially - a virus come in, dismantles, makes new viral components, then puts together a lot and buds them outside of the cell or lysis to release contents.

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57
Q

Eclipse Period

A

Period where virus particles are broken down after penetrating cell, releasing their genome as a prerequisite to replication. No longer infectious.

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58
Q

Latent Period

A

time it takes from infection to release of new infectious virus particles.

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59
Q

what are the steps that occur during latent period?

A

attachment of virus to cell; entry of virus into the cell and un-coating of viral genome; viral gene expression; genome replication; assembly of new viruses and release of virus from cell

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60
Q

Attachment

A

specific binding of a virus attached protein with a cellular receptor to epithelial and mucosal surfaces

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61
Q

Susceptible Cells

A

functional receptor that may or may not be able to complete viral replication cycle

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62
Q

Resistant Cell

A

No functional receptor, it may or may not be able to replicate virus

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63
Q

Permissive Cell

A

has capacity of replicate virus, but may or may not have function receptor

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64
Q

Suseptible and Permissive

A

is the only cell that can take up a virus and repllicate it

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65
Q

steps in virus attachment

A

non-specific electrostatic binding to bring in close proximity, and proteins interact to initiate fusion of endocytosis

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66
Q

what are receptors on surface that react with viruses made of?

A

carbohydrates and protein - carbohydrate is less specific

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67
Q

Entry of virus

A

follows quickly after binding to cell surface, is an energy dependent process (cell must be metabolically active)

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68
Q

How does a virus enter a cell?

A

1) endocytosis to form an endosome (with enveloped or non-enveloped viruses, with or without clathrin or caveolin) 2)fusion of virus envelope (enevloped) with cellular membrane

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69
Q

Uncoating

A

virus has entered he cell and virus capsid is completely or partially removed and virus genome is exposed.

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70
Q

Gene expression and viruses

A

all RNA viruses encode a RdRp; RNA viruses need strategy to switch from making mRNA to making genomes.

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71
Q

how does a virus accomplish task of making maximal function with minimal genome?

A

nested mRNA, splicing, ambisense coding, RNA editin

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72
Q

How do viruses make or process proteins?

A

polyproteins, IRES elements, leaking scanning of AUG, suppression of terminal codons, protein processing/conformation change resulting in new activities

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73
Q

Viral Assembly

A

depends on host machinery: cellular proteins to capable or assist in folding; cell transport to move viral proteins and NA to site of assembly; membrane proteins enter secretory pathway, nuclear proteins use nuclear import machinery, subunits more on cytoskeleton using cellular motors

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74
Q

How is helical nucleocaspids assempbled?

A

viral genomic RNA is coated during synthesis of genome

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75
Q

How are icoshedral capsids assembled?

A

around virus genome, or inserted into preformed caspids.

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76
Q

Viral Egression

A

viruses with naked capsids are released from infected cell by lysis.

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77
Q

how do we measure how a virus effects the host?

A

1) result of viral infection on target cell 2) balance with host is necessary for survival 3) innate or primary defenses 4) adaptive defenses are acquired over time

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78
Q

Three general outcomes of a viral infection

A

Abortive infection/failed - no apparent effect on cells

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79
Q

Lytic/acute infection

A

production of virus and death of infected cell

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80
Q

Persistent Infection

A

Chronic production of virus, latent, transforming

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81
Q

Latent virus production

A

no virus is actively produced

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82
Q

Indirect Cell damage by virus

A

Integration of viral genome, induction of mutations in host genome (oxygen radicals), inflammation, host immune response. (these could be by viral design or by accident)

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83
Q

Direct Cell damage by virus

A

diversion of cell’s energy, shut off of macromolecular synthesis, competition of viral mRNA for cellular ribosomes, competition of viral promoters and enhancers, inhibition of interferons

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84
Q

Cytopathic effects by virus

A

changes in cellular morphology: nuclear shrinking, nuclear membrane alterations, cytoplasmic vacuolization, cell fusion, chromosomal breakage, rounding and detachment of tissue culture cells, lysis; Formation of inclusion bodies: Virions and proteins in nucleus, protein and RNA inclusions, Virus protein and nascent virus in cyto, chromatin clumps in nucleus.

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85
Q

How do viruses cause disease?

A

Oncogenic/transforamtion; lytic, persistent infection, latent (slow delay between infection and appearance of symptoms)

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86
Q

Innate Defense mechanisms from virus

A

natural barriers, certain cells, and soluble factors that bring a non-specific and immediate response to infection - primes the adaptive imune response.

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87
Q

Natural innate barriers to viral infection

A

skin, mucosal membrane, ciliated epithelium, gastric acid, tears, bile,

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88
Q

Cells involved in innate defense against viral infection

A

dendritic, NK, PMNs

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89
Q

Soluble factors in innate defense against viral infection

A

interferons, cytokines, complement, chemokines.

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90
Q

Intracellular restriction factors

A

cell factors that block/inhibit virus after entry into cell - widely expressed and potent, however viruses have evolved to antagonize these factors.

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91
Q

APOBEC/TRM

A

both intracellular restriction factors that bind to viral component *shared structure among viral family, and block viral replication

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92
Q

APOBEC

A

human protein that interferes with HIV by damaging viral DNA; not present in every cell - those that lack is are permissive; APOBEC transcription is induced by IFN signaling.

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93
Q

what is APOBEC inhibited by?

A

Vif - an HIV protein that blocks APOBEC from binding or targets it for destruction

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94
Q

TRIM:

A

an intracellular restriction factor that blocks retrovirus activity

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95
Q

Interferons

A

cytokines that are able to protect neighboring cells form viral infections

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96
Q

Type I IFN

A

Alpha or beta; antiviral factors that are made in most cell types

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97
Q

Type II IFN

A

gamma, produced in T cells and NK cells, more restricted than Type I.

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98
Q

Jak/Stat

A

signaling pathway that Type I and II IFN act through to cause the synthesis of antiviral

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99
Q

IFN gamma activates what genes

A

GAS

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100
Q

IFN Alpha and beta activate what genes?

A

IREs

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101
Q

What is the antiviral state?

A

induced by cells that have responded to IFN to alter transcription; is the optimal state to block viral replication

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102
Q

how does anti-viral state block viral infection?

A

temporary blocks cell proliferation, reduces cellular metabolism, potentiates NK acitvity by induction go IFN gamma, increase antigen presenting molecules, apoptosis

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103
Q

what triggers anti-viral state

A

IFN is triggered by dsRNA (which si produced in replication of RNA viruses, is an intermediate in replication of DNA viruses) and intracellular signaling of TLRs and RLHs

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104
Q

what is the result of a anti-viral state?

A

flu-like symptomes

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105
Q

what are the downstream mediators of IFN induced anti-viral state?

A

PKR and OAS

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106
Q

PKR

A

downstream mediator of IFN anti-viral state: phosphorylates and inactivates EIF2alpha translation to decrease protein synthesis

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107
Q

OAS

A

Downstream mediator of IFN anti-viral state; 2-5-oligoadenulate synthetase to activate cellular ribonuclease to degrade mRNA

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108
Q

what transcription is included in antiviral state?

A

adhesion molecules, MHC Class I, P21 for growth arrest, and procaspases (inactivated OAS and PKR)

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109
Q

why are inactivated forms of OAS and PKR formed?

A

inactive precursors that are activated by darn to shut down translation of both cellular and viral mRNA, induce gene products associated with CTL, and arrest cell cycle and induce apoptosis.

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110
Q

what TLRs are responsible for viral infection?

A

3, 7, 9 recognize Nucleic acids (dsRNA, ssRNA, CgP containing DNA)

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111
Q

RHL

A

Retinoic Acid Inducible Gene I: reocognize viral patterns like TLRs do..

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112
Q

what cells are involved in innate immune response to virus?

A

Mononuclear phagocytes, dendritic cells; NK, granulocytes.

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113
Q

Role of mononulcear phagocytes in viral infection

A

innate: phagocytosis, inflammatory mediator, antigen presentation

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114
Q

role of dendritic cells in viral infection

A

migratory cells found in every tissue except brain, present antigen to T and Stimulate B cell differentiation and proliferation, key modulators in development of adaptive immune repsonse, secrete cyotkines

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115
Q

Role of NK cells in viral infection

A

innate; active in response to IFN or macrophage derived cytokines, serve to contain virus infections while adaptive immune system is generated

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116
Q

Granulocytes in viral infection

A

innate: neutrophils, basophils, eosinophils

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117
Q

cytokines in innate defense

A

INF, IL-1, TNFalpha, IL6, IL12, Il18

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118
Q

Chemokines in innate defenese against virus

A

IL8

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119
Q

how does the transition work between innate and adaptive viral response?

A

viral pathogens are recognized by cells in which they replicate, leading to IFN production and inhibiting viral replication. Activation of NK cells. Innate either succeeds in clearing infection or containing it for adaptive response.

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120
Q

Adaptive Immune response to virus

A

activates microbicidal and cytokine secreting properties of macrophages, activate complement, stimulate NK cells, uses cytokines to induce inflammatory response and promote influx of antibodies and effector lymphocytes

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121
Q

what is the adaptive response most important in?

A

cleanup and prevention of infection - cell mediated and humoral immunity.

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122
Q

where are virus antigens present?

A

on virions, surface of infected cells, debris of infected cells, peptide fragments on MHC molecules

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123
Q

Humoral Response

A

adaptive immunity: using B-lymphocytes to make immunoglobin to neutralize and prevent infection. Critical in recognition of virion.

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124
Q

ab Affinity Maturation

A

selection of B-cell producing highest affinity antibody, binding can lead to isotope switching

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125
Q

what antibodies are made during a viral infection

A

lower affinity usually, and most often IgM isotypes.

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126
Q

IgA - viral infections

A

inhibits attachment, neutralizes toxins and enzymes

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127
Q

IgG - viral infections

A

inhibit fusion of enveloped virus, opsonizes virons to engage phagocytosis, facilitate complement lysis

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128
Q

IgM - viral infections

A

opsonize virions to engage phagocytosis, coat and agglutinate virions, facilitate complement lysis

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129
Q

Types of antibodies

A

group or type specific

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130
Q

Group specific antibodies

A

see epitopes that are shared by all viruses in a group

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131
Q

Type specific antibodies

A

see epitopes defining a virus group subset.

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132
Q

Neutralizing antibodies

A

bind to virus attachment proteins that prevent productive infection (re-infection)

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133
Q

Cell mediated response

A

adaptive immunity: rely on CTL to kill virus once inside the cell. Utilize T cells (helper and Cytotoxic killer) that bind to MHC I and II on APCs

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134
Q

what do helper T- cells bind to?

A

MHC Class II and produce cytokines that regulate proliferation

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135
Q

what does CTLs bind to?

A

MHC class I and kill virus infected cells

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136
Q

Results of adaptive immune response

A

secrete IFN by helper and activated NK cells; CTL lysis of cells; NK and macrophage kill directly

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137
Q

Th1 activate moves towards…

A

cell mediated immunity

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138
Q

Th2 activation moves towards…

A

humoral response.

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139
Q

Memory Cells

A

antibody and T-cells decline over time after infection is cleared, reinfection at later time leads to rapid increase in antibody and effect T-cells and infection appears as mild or even inapparent.

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140
Q

how doe viruses evade host defense?

A

antigenic variation, immune tolerance, trestricted expression of virus genes, production of viral molecules that act as inhibitors or decoys, down regulation of host proteins, infection of immunopriveledged sites, direction infection of immune system, inhibition of apoptosis

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141
Q

antigenic variation in virus resistance

A

point mutation of genome shifting to make virus unrecognizable by immune system receptors

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142
Q

Immune tolerance in virus resistance

A

molecular mimicry or infection prior to immune system.

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143
Q

what barriers do airborne viruses overcome in respiratory route?

A

alveolar macrophages, ciliated epithelium mucus secretion, lower temperature

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144
Q

what barriers do viruses overcome in the GI tract?

A

gastric acid, bile salts

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145
Q

what barrier do viruses overcome in the skin?

A

requires a breach of physical integrity or a vector (tick, mosquito)

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146
Q

where do viral infections usually take place?

A

near epithelial surface or barrier

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147
Q

requirements for successful infection

A

sufficient virus, cells at site of entry are susceptible and permissive, local host defense is absent of insufficient.

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148
Q

viral infected cells that are released from apical side tend…

A

to remain a local infection

149
Q

Viral infected cells that are released from basolateral side tend to..

A

gain access to underlying tissue and spread

150
Q

hematogenous stread

A

viral spread by infecting endothelial cells or direct inoculation of blood or lymph

151
Q

Tropism

A

virus likely to infect certain tissues but not others

152
Q

why does tropisms occur?

A

access to tissue, receptors for virus entry, expression of host genes required of virus, production of virus progeny, relative failure of host defense.

153
Q

Enveloped viruses - tranmission

A

fragile and sensitive to pH - only transmitted from close contact

154
Q

Non-enveloped viruses - transmission

A

hardier, sustain dyring, pH, detergents, high temperatures, and are transmitted via fomites, respiratory, fecal/oral routes

155
Q

Incubation period of small pox

A

twelve days

156
Q

Incubation period of common cold

A

2-5 days

157
Q

Incubation period of Measles

A

8-12 days

158
Q

Incubation period of Chicken Pox

A

14-16days

159
Q

incubation perio of Erythema infectiosum

A

13-18 days

160
Q

Incubation period of rosella

A

9-10 days

161
Q

Incubation period of rubella

A

14-21 days

162
Q

Incubation period of influenza

A

1-2 days

163
Q

Virulence definition

A

capacity of the infection to cause a disease; affected by ability of virus to replicate, modify host defense mechanism, facilitate virus spread in and among hosts, directly toxic to host cells

164
Q

Host factors in viral disease

A

receptor, cell type, age of host, genetic background, exposure history and underlying health conditions, immune status

165
Q

what is the optimal age of flu for host infection?

A

Elderly >65 or children

166
Q

underlying predispositions for the flu

A

asthma, COPD, cardiovascular disease, obesity, diabetes

167
Q

What viruses are associated with cancer

A

HepB, HepC, retrovirus, EBV, papilloma, papovavirus, JC, BK, Wu, KI, HIV1, KSHV

168
Q

outcome of a viral infection..

A

acute, persistent, latent/reactivated infection

169
Q

Localized infections

A

rhinovirus, rotavirus, papillomavirus

170
Q

Rhinovirus

A

UPR

171
Q

rotavirus

A

local insetinal epithelium

172
Q

Papillomavirus

A

local epidermis

173
Q

systemic viral infections

A

enterovirus and herpes virus

174
Q

enterovirus

A

primary: intestinal epithelium, secondary lymphoid tissue and CNS

175
Q

Herpse Virus:

A

primary: propharynx or GU tract; secondary: lymphoid cells of CNS

176
Q

Acute Local infections

A

only infect epithelium, short incubation period 1-2 days, induces secretary IgA, often have many different serotypes that are dependent on host age, history, immune status, Reinfections are common due to short lived immunity.

177
Q

Acute Systemic Infection

A

primary infection in epithlium, secondary: in spleen, lung, liver with viremia. Incubation period of 10-21 days, lifelong duration of immunity; secrete IgG and secIgA for antibodies.

178
Q

Transforming Viral Infection

A

activate viral or host oncogenes, cause host DNA damage and activation of oncogenes or inactivation of tumor suppressor to cause inflammation and tumorgenesis.

179
Q

what viruses are most susceptible to re-infection

A

local acute infections

180
Q

Serotypes

A

a single infection that can result in a variety of syndromes - most often associated with local acute infections

181
Q

Epidemic

A

local outbreak

182
Q

Pandemic

A

global outbreak

183
Q

Endemic

A

outbreak that occurs commonly and frequently in given population

184
Q

Viral Gastroenteritis signs and symptoms

A

diarrhea, nausea, vomiting, intestinal cramps (muscle aches, fever, rarely headaches, malaise), dehydration.

185
Q

Viral gastroenteritis incubation

A

1-2 DAYS

186
Q

viral gastroenteritis duration

A

1-2 DAYS

187
Q

site of infection for viral gastroenteritis

A

local inestinal epithelial cells

188
Q

Viruses that cause gastroenteritis

A

rotavirus, adenovrius, astrovirus, norovirus

189
Q

Norovirus

A

source is by contaminated water/food, shellfish, person to person spread and possible respiratory spread.

190
Q

Norovirus incubation

A

15 hours to 2 days

191
Q

Duration of illness of norovirus

A

1-2 days

192
Q

Stool contaisn how many viruses - norovirus

A

10,000,000 viruses/ml

193
Q

Infectious dose of norovirus

A

10 to 100 viruses

194
Q

Attack rate of norovirus

A

up to 50% in 2 days

195
Q

Examples of persistent or latent viruses

A

Rubella, HepC, HepB, rotovirus, herpes, papillomavirus, parvovirus

196
Q

Latent virus definition

A

dormant state in which virus is not replication

197
Q

examples of latent viruses

A

Herepes slimplex, EBV, HPV

198
Q

Herpes virus lays dormant in..

A

dorsal root gangion

199
Q

EBV lies dornant in..

A

the B lymphocytes

200
Q

HPV lies dormant in..

A

basal epithelial cells

201
Q

Hep B incubation time

A

60-90 days

202
Q

Clinical signs of HepB

A

jaundice, chronic infection, incidence differs with age.

203
Q

Fatality for Hep B

A

0.5-1% acute fatality, premature mortality due to liver disease in 15-25%

204
Q

Spectrum of chronic disease with HepB

A

chronic persistent heptatits *asymptomatic), chornic active hepatitis, cirrohsis, hepatocellular carcinoma.

205
Q

General outline of herpes viruses

A

Primary infection, latent period, reactivation

206
Q

Structure of Herpes

A

Enveloped with glycoproteins, Tegument layer, icosahedral capsid with dsDNA.

207
Q

What is the tegument

A

middle layer of herpes virus that contains proteins that control entry, gene expression and immune evasion; evasion is without cell lysis

208
Q

Herpes Simplex Virus Manifestations

A

Painful vesicles on skin at sight of inoculation

209
Q

Primary site of infection for HSV

A

most often silent, HSV1 is during childhood. Oropharyngeal for 1, Genital for 2

210
Q

Which are more severe, primary or secondary lesion for HSV?

A

if symptomatic, primary.

211
Q

Length of incubation time in primary HSV infection

A

1-3 days after exposure, if immunocompromised may spread

212
Q

Secondary HSV

A

also known as recurrent, causes encephalitis, keratitis, mucocutaenous, labia and genitals

213
Q

Latency period of HSV

A

inside sensory ganglia (trigeminal for Orofacial) and Sacral ganglia for Genital

214
Q

What provokes reactivation of HSV?

A

Sunlight, stress, menstruation, immunosuppression.

215
Q

Prognosis/outcome of secondary HSV infection?

A

more localized lesions and heal more rapidly; still infections; may even be silent (still infectious)

216
Q

Diagnosis of HSV

A

for gum, oral, genital - clinically; but cal do a viral culture, direct IFA, PCR

217
Q

Treatment of HSV

A

oral acyclovir for oral or genital; C-section for women with active lesions; for severe IV Acyclovir

218
Q

Prophylaxis for HSV

A

antiviral suppression, but no vaccine

219
Q

Gingiovostamitis

A

complication/symptom of HSV, oral secretions, mouth ulcers on lips, gums, tongue. Fever and enlarged nodes

220
Q

Herpetic Whitlow

A

Innoculation of HSV from oral secretion onto finger - med professionals

221
Q

Encephalitis

A

HSV complication, predilaection for temporal lobes to cause hemorrhagic necrosis, slow mental capabilities, hallucinations. Primary or reactivation

222
Q

Herpes keratitis

A

HSV infection of cornea vie ophthalmic branch of trigeminal N. Primary or reactivation

223
Q

Genital Herpes

A

HSV, 10-14 days duration, very painful. primary or reactivation

224
Q

Neonatal HSV

A

Transmitted via materanal secretions of active lesion or asymptomatic viral shedding, more often primary than reactivated.

225
Q

Forms of Neontal HSV

A

1) Skin, eye, mucous mem (SEM) 2) CNS 3) Disseminated

226
Q

SEM

A

neonatal HSV, site of lesions, corneal ulcers, blindness

227
Q

CNS - Neonatal HSV

A

severe encephalitis, 5% mortality with acyclovir

228
Q

Disseminated HSV

A

neonatal HSV that is widespread - pneumonitis, hepatitis, intravascular coagulation, encephalitis, skin rash, eye involvement. Most lethal, 30% mortality with acyclovir

229
Q

Varicella-Zoster Virus Transmission

A

Respiratory, aerosolized, lesion contact

230
Q

VZV incubation

A

10-21 days

231
Q

Symptoms of VZV

A

fever, malaise, headache, cough rash

232
Q

Rash of VSV

A

vesicular of face/trunk that spreads to limbs, lesions appear in successive waves (crops). Multiple stages of lesions throughout body

233
Q

Duration of VZV

A

1w

234
Q

Pathogenesis of VZV

A

Respiratory entry, spread via lyphatics. Replication in lymph nodes (primary). Viral replication in liver, spleen, sensory ganglia, Secondary to cause rash

235
Q

Complication of VZV

A

Strep, pneumonia, necrotizing fasciitis, encephalitis, encephalomyelitis, hepatitis

236
Q

Treatment of VZV

A

self limiting, acyclovir accelerates resolution if given 48-72 hours of onset. Vircella zoster immune globulin for high risk individuals

237
Q

VZV prophylaxis

A

Live attenuated varicella vaccine (varivax) 2 doses as 12-18 months and 4-6 years

238
Q

Latency and Ractivation of VZV

A

latent in sensory ganglia; asymptomatic shedding DOES NOT occur ing reactivation. Leads to Herpes Zoster (Shingles in 30%)

239
Q

Herpes Zoster

A

Singles, Radicular pain along dermatome that does not cross midline. Itchy, very painful, but heals in 2 weeks.

240
Q

Complication of Herpes zoster

A

skin infections, Ophthalmicus, encephalitis, never palcies, Post-herpetic neuralgia

241
Q

PHN

A

complication of things - Post-herpetic neuralgia- debilitating neuropathic pain that lasts weeks to months

242
Q

Immune response to VZV

A

depends on cell mediated immunity - why is occurs in immunocompromised and elderly

243
Q

Treatment of Herpes Zoster

A

acyclovir within 48-72hours and NSAIDS, steroids for PHN

244
Q

Prophylaxis for HZ

A

live attenuated vaccine (Zostavax) for >50

245
Q

Diagnosis of VZV/HZ

A

clinical signs; possible direct IFA, PCR, Culture

246
Q

Cytomegalovirus

A

type of herpes that is generally asymptomatic except in immunocompromised - opportunistic infection of most organs

247
Q

Transmission of Cytomegalovirus

A

infected body fluids, in untero, organ transplants

248
Q

body fluids of cytomegalovirus transmission

A

saliva, breast milk, sex, blood, tears, urine

249
Q

Infection rate of cytomegalovirus

A

high, almost 80% in >40

250
Q

Pathogenesis of cytomegalovirus

A

infects epithelial cells in salivary and genital tract, persistent infection and viral shedding - distribution to other organs and tissues

251
Q

Latency of cytomegalovirus

A

latent in monocytes and lymphocytes, reactivated virus occurs in urine and saliva. Usually asymptomatic reaction unless immunocompromised

252
Q

Pregnancy and cytomegalovirus (CMV)

A

3-5% tranmission, 1/3 are infected in utero, 10-15% symptomatic

253
Q

Congenital CMV

A

congential Cytomegalovirus that causes low birth weight, microceohaly, hearing loss, mental impairment, HPM, blueberry muffin spots, jaundice

254
Q

Immunocompromised CMV

A

severity parallels cell mediated immunity, pneumonia, colitis, retinitis, hepatitis, encephalitis

255
Q

Diagnosis of CMV

A

Serology IgM or IgG, culture, PCR,DFT

256
Q

CMV histoloty

A

intranuclear inclusion bodies and intracytoplasmic inclusions

257
Q

Treatment of CMV

A

no treatment for normal; IV gancyclovir or oral valcancyclovir for immune compromised, IV gancyclovir for congenital; high titer for CMV antibodies (CMV-IG) for pregnant and transplant patients

258
Q

Prophylaxis for CMV

A

no vaccine, CMV-IG

259
Q

Herpes viruses

A

HSV, VZV, Cytomegalovirus, HHV6, HHV-7, HHV8/KSHV, EBV

260
Q

Influenza Virus scutures

A

RNA virus with segmented genome, 8 different single stranded RNA pieces, enveloped. Hemagglutinin, neuraminidase glycoproteins

261
Q

Hemagglutinin

A

glycoprotein on influenza virus used for cell entry

262
Q

Neuraminidase

A

glycoprotein on influenza virus used for cell except

263
Q

Pathology of Influenza

A

binds to sialic acid, enters cells, replication, release

264
Q

Type A Influenza

A

severe illness, epidemics and pandemics, rapidly changes in lots of aniamls and humans

265
Q

Type B influenza

A

less severe symptomes, epidemics only, only in humans

266
Q

Type C influenza

A

mild or asymptomatic, minimal public health impact. Only in humans

267
Q

Naming of Type A

A

Virus Type/geographic origin/strain number/year (virus subtype)

268
Q

Naming Type B

A

same, but lacks subtypes

269
Q

Antigenic Drift

A

grandual minor change (point mutations) in DNA that changes hemagglutinin or neuraminidase surface antigens. Creates a new strain and cause ongoing flu vaccine changes. creates epidemics

270
Q

Antigenic Shift

A

type A influenza virus with a completely novel hemagluttinin or neuramidinase segment introduced into humans (from other species) - due to two infections in a being. Less frequent but more dramatic impact. Pandemic

271
Q

waterfowl transmit flu to..

A

aquatic mammals, horses, poltry, humans, pigs.

272
Q

What transmits flu to humans

A

waterfowl, poultry, pigs

273
Q

Transmission of flu

A

droplet, aerosols, fomites, hand and feet

274
Q

how long does flu virus live on hand

A

5m

275
Q

how long does flu virus live on cloth/paper

A

8-12 hours

276
Q

how long does flu virus live on plastic

A

24-48 hours

277
Q

how does flu cause symptomes

A

desquamation which leads to upper and lower airway inflammation, high rates of secondar infection

278
Q

Flu symptoms in neonates

A

Fever, lethargy, decreased eating, mottling, apnea

279
Q

Flue in infants/tollders

A

GI, fever >103, anorexia, respiratory, malaise, headache, sore throat

280
Q

Flu in children/adutls

A

rapid onset, high fever, cough, chills, muscle aches

281
Q

General drugs for flu treatment

A

Matrox protein inhibitors and neuraminidase inhibitors

282
Q

Matrix Protein inhibitors action

A

diable M2 proteins to prevent uncoating useful for A viruses

283
Q

Neuraminidase inhibitors action

A

inhibit release of visions and promote clumping, Used on A and B

284
Q

Swine Flu

A

H1N1, started in mexico and spread around the world. Highest incidence in 5-24 years olds , then 0-4 year olds; caused Acute respiratory distress in humans

285
Q

Bird Flue

A

domestic poultry most effected. H5N1 is high virulence in poultry and occasionally humans, high pathogenic, most prevalent in asia.

286
Q

Pandemic Flu Requirements

A

1) new virus subtype 2) must infect humans and cause serious illness 3) sustained transmission and spread easily

287
Q

Inactivated Flu Faccine

A

IM or ID, killed; >6 months. Trivalent and quadrivalent.

288
Q

Live Attenuated Vaccine

A

intranasal, live, >2 years-49 years, quadrivalent.

289
Q

Efficacy of flu vaccines

A

70-90% effective in well matched years, less for elderly (but reduction in hospitalization and death)

290
Q

CDC Flu vaccine recomendations

A

> 6 months or older who do not have contraindications

291
Q

RSV

A

Respiratory Syncytial Virus

292
Q

RVS epidemiology

A

infants and young chilldren, LRI annually during winter and spring

293
Q

RVS spread

A

large lipid droplet spread - lives on surface for 1 hour (no vaccine)

294
Q

Structure of RSV

A

singled stranded non,segmented RSV, antigenic variablity, drift,F-protein and Gprotein

295
Q

F-protein

A

Fusion of viral envelope to host or fusion of membranes of infected cells taught syncytia (RSV)

296
Q

G protein

A

initial binding of RSV to host

297
Q

Subtypes of RSV

A

A and B, A is usually worse

298
Q

Pathophysiology of RSV

A

invades conjuctivat and nasopharynx, spreads to lower respiratory tract by inhalation of secretions. Constriction of smooth muscle bonchioles to get edema/inflammation, hypoxia, emphysema, hyper expansion by mucous plugging

299
Q

RSV incubation

A

3-5 days

300
Q

Clinical signs of RSV

A

Respiratory distress, wheeze/rhonchi, hypoxia, copious secretions

301
Q

Testing of RSV

A

culture - not practial, Direct antigen detection - not sensitive, PCR

302
Q

RSV Immunology

A

recurrent infections are common, immune proetextion is complete, drift occurs, may be associated with wheeze or asthma later in life

303
Q

RSV treatment/prevention

A

Formalin-inactivates RSV vaccine of 60’s did not provide immunity and was worse off, new vaccines on horizaon. Palivizumab and motavizumab are prophylaxis.

304
Q

Palivizumab

A

human pooled antibody of highh RSV titers to decrease severity and hosptializations. IM injection during season to high risk

305
Q

Motavizumab

A

higher affinity RSV titer that binds tighter to F protein - inferior to palivizumab and very expensive

306
Q

Mechanisms of Anti RSV

A

do not inhibit pre-fusion to hairpin formation, questionable to inhibit pre-hairpin to hairpin, confirmed inhibition of hairpin to post-fusion formation

307
Q

steps in antivirals

A

Block attachment and entry; blocks uncoating; blocked NA syntehsis, Blocks protein synthesis and process, Blocks viral release

308
Q

Pathophysiology of Influenza

A

Binds to airway epithelial and is endocytosed and forms endosomes. Acidified to promote conformation change in hemagglutinin to medial fusion between Flu viral envelope and endosome membrane. Proton influx through viral M2 proton channels elects RNA genome release for replication and assembly. New visions are tethered to PM via Hemagglutinin and sialic acid. Nueroaminidases cleave silica acid and release

309
Q

Oseltamivir and Zanamivir- Action

A

Inhibition of Neuraminidiase to cleave Sialic acid to prevent egression. Causing aggregation on PM surface.; impairs viral penetrate through mucin

310
Q

Types of NA inhibitors

A

Oseltamivir (tamiflu), Zanamivir, Peramivir

311
Q

Oseltamivir resistance

A

rare from mutations in Hemagglutinin or NA

312
Q

Pharmokinetics of Oseltamivir

A

Oral prodrug, eliminated as renal secretion

313
Q

Pharmokinetics ofZanamivir

A

Inhalation renal elmination, but be over 7 YO

314
Q

Pharmok of Peramivir

A

single IV dose

315
Q

Use of Oseltamivir or Zanamivir

A

48 hours of symptoms to decrease severity and duration of A or B in adults and children. Can be prophylactic in contacts

316
Q

Adverse reactions to Oseltamivir

A

N,V, headache, fatigue, diarrhea

317
Q

Adverse - zanamivir

A

bronchospams, ough, nasal and throat discomfort

318
Q

Adverse Peramivir

A

GI, diarrhea, neutropenia, skin reactions

319
Q

Drugs that inhibit flu uncoating

A

Amatiadine, Rimantadine

320
Q

Amatiadine and Rimatadine actions

A

Blocks M2 (H+) channel to prevent intracellular changes for uncoating

321
Q

Resistance to Amatiadine and Rimatadine

A

Occurs due to muataions in M2

322
Q

PK of Amatadine

A

Oral, excreted in urine (unchanged, requires renal function dosage change). Excreted in break milk too

323
Q

PK for Rimatadine

A

Oral, elemianted in liver; excreted in breast milk too

324
Q

Use of Amatadine and Rimatadine in flue

A

Prophylaxis for Flu A, give 1-2 days prior, and 6-7 durings to reduce insidence and severity. Only slightly effective after 48 hours of symptoms

325
Q

AR to Adatadine

A

Insomnia, difficulty concentration, lightheadded, headache

326
Q

AR to Rimatadine

A

better tolerated, poor CNS penetration

327
Q

Drugs for Herpes target

A

DNA polymerase (viral) and penetration

328
Q

Herpes mechanism

A

Cell attachment, uncoating, transfer DNA to host nuclei for transcription and syntethesis, Assmbly and packaging, budding

329
Q

Inhibitors of Viral DNA polymerase

A

for herpes, most are nucleoside analogs that target viral genome replication and inative viral DNA pol and viral RT; purine and pyrimidine analogs covered to triphosphates forms by intracellular kinases

330
Q

Highest degrees of selective toxicity in Viral DNA polymerase inhibitors

A

is due to necleoside analogs that are activated by viral kinases rather than host kinases

331
Q

Types of nucleoside analogs

A

Acyclovir, vidarabine, foscarent, ganciclovir

332
Q

Mechanism of Acyclovir

A

Phosphorylation of analog is mediated by viral thymidine kinase to convert to Triphosphate form. TP competes for binding with DNA polymerase and is incorporated into viral DNA strand. Termination. DNA with acyclovir TP irreversibly binds and inactivates viral DNA pol

333
Q

Resistance to acyclovir

A

reduced expression of viral thymidine kinase, alters thymidine kinase substrate specificity, altered viral DNA pol acitvity - rare only in immunocompromised

334
Q

PK of acyclovir

A

oral is poor (15-30%), but also available in topical or IV

335
Q

PK of valacyclovir

A

Prodrug of acyclovir, given orally for higher plasma levels (3-5x)

336
Q

PK of peniciclovir

A

Acyclic guanosine analog, poor oral abosprotion, topical only (better than acyclovir topical)

337
Q

PK famiciclovir

A

pinciclovir prodrug that increase oral bioavaliability

338
Q

Elimination of Acyclvir

A

renal, neonatal under 1 year is 1/3 f clearance

339
Q

Use of acyclovir with HSV

A

oral shortens symtomes for primary and recurrent and reduces pain duration of recurrent labialis. Topical is not effective. good secondary prevention.

340
Q

when is acyclovir HSV used?

A

HSV encephalitis, neonatal HSV, serious HSV or VZV infections

341
Q

Treatment of VZV antivirals

A

oral acyclovir decreases number of lesions and duration for varicella and zoster, but higher dose required. Zoster: increases lesion healing, decreases pain, lessens incidence

342
Q

AR to acyclovir

A

Headache, nausea, vomit, renal dysfunction.

343
Q

IV acyclovir AR

A

tremors, hallucinations, seizures, coma (encephalopathy)

344
Q

Inhbiitors of Herpes penetration

A

Ducosonal (abreva))

345
Q

Ducosonal Mechaism

A

long chain sat alcohol that inhibits rep of lipid enveloepd virus and prevents fusion for viral entry.

346
Q

Ducosanol PK

A

topical begun within 12 hours of symptomes to reduce healing time.

347
Q

RSV drugs

A

Ribavirin, purine nucleoside analog

348
Q

Mechanism of Ribavirin

A

not understood. Covered to TP by cellular kinases, inhibits 5’ capping of viral mRNA to decrease stability, increase viral mutation.

349
Q

Resistance in ribavirin

A

none yet

350
Q

PK ribavirin

A

oral, with fatty meals. Eliminated via hepatic and renal excretion. Other routes inhalation for kids

351
Q

AR to ribavirin

A

conjuctival or bronchial irritation when inhaed, Oral: Hemolytic anemia, should not ge given during pregnancy or administered by pregnant HC workers

352
Q

Use of Ribavirin

A

for RSV and penuomia, but only severe or immunocompromised patients

353
Q

Palivizumab action

A

human monoconal antibody to RSV F glycoproein used for immnoprophylaxis in infants and children with heart disease. exepnsive, mostly IM

354
Q

Drugs for cytomegalovirus

A

Canciclovir, Valganciclovir, Foscarnet, Cidofovir

355
Q

Methods of treating CMV

A

viral DNA pol inhibition

356
Q

Ganciclovir mechanism

A

uptake regulated by viral protein kinase UL97 (selectivity), cellular kinases convert MP to TP binds to viral DNA polymerase, terminates strand.

357
Q

Resistance to Ganciclovir

A

UL97 mutations, mutation in viral DNA pol

358
Q

PK of Ganciclovir

A

Poor oral, but good IV. excreted unchanged via urine

359
Q

Valganciclovir PK

A

prodrug of ganciclovir that is converted to active ty GI and hepatic esterase’s

360
Q

Clinical use of ganciclovir

A

CMV retinits HSV keratits in immuncompromised and for transplant patients.

361
Q

AR in ganciclovir

A

Myelosuppresion, neutropenia, thrombocytopenia, N/D, fever, rash, HA, isnomia, GI headache, seizures.

362
Q

Cidofovir

A

does not require activation by viral kinases, so can be used against acyclovir or ganciclovir resistant strains; nucleotide analog

363
Q

Cidofovir PK

A

IV only, long half life, renal excretion. must be administered with probenecid to block secretion and decrease nephrotoxicity.

364
Q

Cidofovir AR

A

nephrotoxicity, neutropenia

365
Q

Foscarnet mechanism

A

inorganic pyrophosate analog, very unique. Does not require cellular activation. Noncompetitivey binds to pyrophosphate BS of RNA and DNA pol and inhibits cleavage of pyrophosphate from TPs to block viral replication.

366
Q

Resistance in Foscarnet

A

alterations in DNA polymerase, combines use with ganciclovir is useful

367
Q

PK of Foscarnet

A

poor oral, good IV. Eliminated unchanged in urine

368
Q

Clinicical use of foscarnet

A

CMV retinitis in immunocompromised patients, used in Gancyclovir or acyclovir resistant infecitons

369
Q

AR of foscarnet

A

nephrotoxicity, hypocalcemia, heachace, tremor, seizure.

Disease And Defense (7 decks)

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