• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/93

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

93 Cards in this Set

  • Front
  • Back
Localized Infection
newly released virus infects adjacent cells
Systematic Infection
Organs, wide spread
Neurotropic
Virus can infect neural cells
Tropism
predilection of virus to infect certain tissues and not others.

4 parameters: susceptibility, permissibility, accessibility, local immune responses.
Epidemiology
The study of occurrence of disease in a population.
Fomite
object that can transmit infection
Neutralization tests
A test to determine the antimicrobial activity of a serum by inoculating a susceptible animal with a mixture of the serum and the virus or other microbe being tested.
Acute Infection
rapid production of infectious virus followed by rapid resolution and clearing of infection by the host.
Chronic Infection
Persistent infections that are eventually cleared.
Polarized release
Directional release of virions from polarized cells
Hematogenous Spread
Spread throughout the body via blood. 2 phases of viremia.
Viremia
presence of infectious virus particles in blood
Primary viremia
virus released into the blood after initial replication at the site of entry. Initial sites of entry: skin, mucous membrane, Resp. T, GI Tract. Move through blood to
Replication sites: muscle, liver, spleen, blood vessels.
Secondary viremia
Secondary viremia delayed appearance of infectious virus in the blood as a consequence of disseminated infections.
Replication sites: skin, mucous membrane, lungs, kidney, GI tract, brain.
Neural Spread
spread of virus through neurons.
Enter the neuron at axon, sensory terminal or cell body.
Replication occurs in cell body (transcription and translation). Assemble virus particles egress from neuron in a directional manner.
Virus replicates in ganglea.
Infection of nervous system
3 types of infections: neurotropic, neuroinvasive, neurovirulent
Neurotropic
Virus can infect neural cells.
Neuroinvasive
virus can enter CNS after infection of a peripheral site.
Neurovirulent
Virus can cause disease of nervous tissue, manifested by neurological symptoms and often death.
Virus Shedding and transmission
Shedding: release of infectious viruses from an infected host.
Respiratory secretions: measles
Saliva: rabies, feline leukemia
Feces: Polio
Blood: Ebola, Marburg
Urine: Hanta
Semen: HIV, HEP B
Skin lesions: Herpes Simplex
Virulence (viral)
capacity of infection to cause disease.

Virulent
Avirulent: no disease
Atenuated: not that severe
Zoonosis
disease shared by animal and humans
Vertical transmission
transfer of viruses between parent and offspring.
Iatrogenic transmission
activity of healthcare worker leads to infection.
Nosocomial transmission
individual infected in a hospital or medical facility
Mechanisms of transmission
Aerosol
Food and water
Fomites
Body secretions
Sexual activity
Birth
Transfusion or transplant
Zoonoses
Herd immunity
failure of disease to progress due to natural immunity of herd or through vaccination of certain members of the herd.
Controlling spread
Quarantine
Vector elimination
Immunization
Antivrals
Patterns of infection
Acute
Inaparent
Persistent
Latent, reactivating
Chronic, Slow
Transforming
Acute Infection
Rapid production of infectious virus, followed by rapid resolution and clearing of infection
Persistent infection
infected cells or virions are not cleared efficiently by adaptive immune response, and virus particles or viral gene products continue to be produced for long periods.
Chronic
persistent infections that are eventually cleared.
Latent
persistent infections that last the life of a host.
Transforming
special class of persistent infection. Infected cells may exhibit altered growth properties and begin to proliferate faster than uninfected cells.
Prodromal
spread before obvious symptoms, but shedding. Period can be extremely infectious.
What are the most common methods for viral entry into a host?
Respiratory tract: mechanical barriers (cilium, mucus, protective structure)
Alimentary tract: epithilial cells, villi, microvilli on intestine lining.
Urogenital tract
Eyes
Skin
List 4 parameters that determine viral tropism
Susceptibility: receptor
Permissivity: virus may require particular protein
Accessibility: acess to tissue
Local immune response: different areas different responses
Describe most common mechanisms for shedding a virus
Respiratory secretions
Saliva
Feces
Blood
Urine, semen, and milk
Skin
Describe ways that viruses can overcome plant cell walls.
Viruses can use channels between cells that allow movement.
Proteins also allow virus to move through plasmodesma.
What are some of the common signs of virus infection in a plant?
Local lesions like chlorotic and necrotic spots and ringspots, systemic symptoms like yellowing, dwarfing, mosaics.
Describe the mechanisms for establishment of a persistent infection
Ineffective intrinsic or innate immune response.
Perpetuation of persistent infection by modulating the adaptive immune system.
Infection of tissues with reduced immune surveillance.
Direct infection of the cells of the immune system.
Vaccines
Stimulate immune memory.
Active or passive immunization.
Types of Vaccines
Live attenuated virus
Inactivated or "killed" virus
New vaccine technologies
Adjuvants and vaccine delivery systems
Advantages and disadvantages of Live virus vaccine
Advantages: generalized immune system activation, polyclonal, immunity is long-lived and cross reactive.

Disadvantages: contaminants, low level virulence, back mutations, interference, secondary spread, unstable.
Examples of Live virus vaccines
adenovirus, measles, mumps, polio (Sabin), rubella, smallpox, varicella, yellow fever.
Inactivated virus vaccines +, -
(+)Low risk of contamination, more stable

(-)More doses and boosters, no local immunity, high concentration is needed, potentiation of disease.
Examples of Killed virus vaccines
hep A, polio (Salk), flu, rabies
New Vaccine Technologies
subunit vaccines, DNA vaccines, live virus vectors
Subunit vaccines
Include only the antigens that best stimulate the immune system, lower risk of adverse reactions
Examples of subunit vaccines
HEP B, HPV
DNA Vaccines
Use genes that code for antigens, transfection, syringe or gene gun.

No need for developing delivery method.
Adjuvants
Immunostimulatory substances
-Presentation of antigen as particles
-Localization of antigen to the site of inoculation
-Direct stimulation of the innate immune system
Delivery Systems
Hypodermics, air guns, emulsions, artificial particles, direct injection of fine powders under skin, oral delivery, edible particles
Vaccines as immunotherapy
patients already infected with virus.
Can provide patient with cytokines, antibodies, or lymphocytes
Recombinant vaccine
Recombinant vaccines are created by utilizing bacteria or yeast to produce large quantities of a single viral or bacterial protein. This protein is then purified and injected into the patient, and the patient's immune system makes antibodies to the disease agent's protein, protecting the patient from natural disease.
Targets for antivirals
Attachment
Penetration and uncoating
Synthesis of viral proteins
Replication of viral nucleic acids
Integration
Viral morphogenesis
FDA Approval process
Preclinical: Lab and animal studies
Phase I trial: establishes drug is neither lethal nor toxic
Phase II trial: compare to existing treatment or placebo, 200-300 patients.
Phase III trial: measured against established therapies, 1,000-3,000 patients
Parallel track
Mutation
As nucleic acids replicate, mistakes occur. Changes in the genome are caled mutations.
Field isolate
virus strain that is isolated from natural host
Wild Type
the prevalent type of a virus in the host population before genetic manipulation or mutation; before lab

Original strain for study
Mutant
has a genome mutation that varies from original
Spontaneous mutation
naturally happening without the use of known mutagen, low rate of mutation
Induced mutation
induced artificially
Hemadsorption
the adherence of red blood cells to other cells or surfaces; a process in which a substance or an agent, such as certain viruses and bacilli, adheres to the surface of an erythrocyte. The process occurs naturally, or it may be induced for laboratory identification of bacteriologic specimens.
Complementation
Genetic interaction of viral gene products. Two different viruses by themselves can't replicate if defective. Together they can produce viruses.
Ex. Polymerase from one virus, capsid from another assemble in a cell.
Recombination
physical interaction of viral genomes, intramolecular or reassortment

Genomes interaction progeny can change genotype
Genetic Reactivation
special case of recombination or reassortment. Marker rescue.
Temperature sensitive
Virsuses are temperature sensitive.

Permissive and non-permissive temperature
Defective viral genome
Gene transfer and expression, regulatin of virus lethality, evolution of host and virus
Defective viral genome types
integrated defective, staellite virus, pseudovirons, conditional defective, DI particles
Types of mutation
Plaque morphology
Host range
Temperature sensitive
Cold sensitive
Deletions
Others
Pleiotropism
single viral gene has effects on several viral properties.
Satellite virus
replication defective, require gene products of other virus, often show no homology to helper virus
Defective Interfering Particles
Subgenomic deletion mutants, helper virus dependent, helper and DI particle are homologous
Therapeutic index
is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes death (in animal studies) or toxicity (in human studies).

Therapeutic ration = LD50/ED50
Comparison of transcription in RNA viruses
(+)sense RNA ->Translation->Viral protein

(-)sense RNA->virion transcriptase->mRNA->Translation->Viral protein

Double sense RNA->virion transcriptase->mRNA->Translation->Viral protein
Picornaviridae Physical Characteristics
-Naked virion
-Icosohedral
-30nm in diameter
-single-stranded (+) sense RNA
-9 genus, indistinguishable in EM
Types of Picornaviridae
Apthovirus->F&M
Caridovirus->encephalomyocarditis
Enterovirus->polio, coxsackievirus, enterovirus, echovirus
Hepatovirus->Hep A
Parechovirus->Human parechovirus
Rhinovirus->103 Rhinoviruses
Genome organiztion of Picornaviridae
(+)sense ss RNA
Poly (AAA) tail at end
VPg at end
if AAA clipped off, not infectious
Capsid of Picornaviridae
Icosohedral T=1
Proteins VP1,2,3,4
60 copies of VP4 per virion
VP1 is antireceptor helps attachment
Attachment of Picornaviridae
Electrostatic attachment
Specific receptors on cell surface
Penetration of Picornaviridae
-Virion binds to receptor. As more receptors are recruited, the membrane is drawn around the particle.
-Receptor-mediated conformational change occurs, leading to the production of altered (A) particles.
– VP4 is lost.
Translation of Picornaviridae
• RNA can act as mRNA when it
enter the cell.
• One ORF, translated as a
single polyprotein.
• Viral proteins derived by
cleavage
• Inefficient
Transcription of Picornaviridae
• Replicative intermediates
Need replicase before transcription
• 3 possible fates of
+RNA:
– Act as mRNA
– Template for more
-RNA
– Genome for new
virion
Assembly of Picornaviridae
• Protomers self-assemble into pentamers.
• Pentamers assemble into empty procapsids.
• After RNA is encapsidated, VPO
cleaves and infectious virion is complete.
Effect of picornavirus infection on host cell
• Susceptible cell contributes:
– Energy
– Precursors for synthesis of viral components and cellular machinery
– Receptors for infection
– Membranes
• Virus inhibits cellular RNA synthesis and protein synthesis
Inhibition of cellular translation by picornavirus
• Inhibits 5
Non-Polio Enteroviruses
• Very common: 10-15 million symptomatic infections annually in the US.
• Pathogenesis
– May play a role in autoimmune disease
– Implicated in the etiology of diabetes
– Important etiologic agent of viral myocarditis
– Meningitis
Polio
Attacks:
-muscles that straighten or bend hips
-shoulders
-straighten knee
-lift foot
-thumb muscles
-back muscles
-respiratory problems (iron lung)
-Post polio (recovery to breath)
Hep A
-Ingestion
-Replication in GI tract
-Transported to liver (major replication site)
-Shed in bile, transported to intestine
-Shed in feces
-Brief viremia
-Cellular immune response
Caliciviridae
-Icosohedral
-38nm
+ ssRNA
-5' VPg and 3'poly(A) tail
-Larger than picorna
-1 coat protein
-Subgenomic RNA
-2 RNA transcripts, Genomic and subgenomic
Norovirus
-90% of epidemic non-bacterial outbreaks of gastroenteritis around the world.
-Produces gastroenteritis
-Incubation and disease very short
Hepatitis E
Formerly Caliciviridae, no formal family assignment.
• Genome organization and size
resemble calicivirus.
• Causes epidemic water-borne
hepatitis.
• Found in Asia, Africa, southern
Europe, Mexico
• Disease is severe but mortality
is low
– Fatality rate higher in
pregnant women.