Micro Unit 3

obligatory intracellular parasites

microbe that can only reproduce in a host

virion

complete, fully developed virus

capsid

protein coat that protects nucleic acid

envelope

covers capsid, made of carbohydrates, lipids, proteins

spikes

carbohydrate-protein complexes projecting from envelope

antigenic drift

mutations in a viruses’ genes over time

helical viruses

long rods, helical nucleic acid in cylindrical capsid

polyhedral viruses

capsids with many faces

enveloped viruses

layer outside capsid

complex viruses

more than one shape

viral species

group of viruses with same genetic info and host range

plaque method

host cells grow into a monolayer, phages are added and form plaques

plaques

clearing in bacterial lawn from lysis

cytopathic effect

death of host cells due to viruses

primary cell lines

human tissue cells that only grow for a few generations

diploid cell lines

human embryo cells, can grow for 100 generations

continuous cell lines

immortal, cancerous cells

serological tests

identify viruses by reaction with antibodies

lytic cycle

attachment, penetration, biosynthesis, maturation, release

lytic cycle attachment

virus attaches to bacterial receptor with tail

lytic cycle penetration

virus injects DNA, tail releases lysozyme to break down cell wall

lytic cycle biosynthesis

in cytoplasm, make viral nucleic acids and proteins

eclipse period

viral multiplication is incomplete

lytic cycle maturation

phage dna and capsids assemble into complete virions

lytic cycle release

lysis using lysozymes

lysogenic bacteria

attaches, injects dna, linear phage dna becomes circular, recombine with bacterial dna

prophage

phage dna inserted to host’s dna

phage conversion

host genetically changes due to phage

specialized transduction

prophage’s dna can transfer to another cell

induction

prophage can excise from host chromosome and become lytic

animal virus receptor site

proteins and glycoproteins of plasma membrane

how to animal viruses enter a cell

receptor-mediated endocytosis or fusion

fusion

viral envelope fuses with membrane and releases capsid into cytoplasm

uncoating

separation of nucleic acid from protein coat

animal viral multiplication

attachment, entry, uncoating, biosynthesis (nucleus for dna, cytoplasm for rna viruses), latency, release

how are animal viruses released

enveloped viruses bud, nonenveloped rupture membrane

adenoviridae

acute respiratory disease

poxviridae

skin lesions

herpesviridae

cold sores

papovaviridae

warts, tumors, vacuolation

Hepadnaviridae

hepatitis, viral reverse transcriptase

coronaviridae

colds, enveloped single-stranded rna viruses

plus strand

can be used as mrna

minus strand

template, cannot be used as mrna

Togaviridae

mosquitoes, enveloped, single-stranded rna

rhabdoviridae

rabies, bullet-shaped, single stranded rna

reoviridae

respiratory and enteric systems

reverse transcriptase

use viral rna to make dna

provirus

viral dna from reverse transcriptase integrates to host cell chromosome

budding

envelope develops around capsid by pushing through cell membrane

sarcoma

cancer of soft tissue

adenocarinomas

cancer of glandular epithelial tissue

transformation

tumor cells have features different from normal cells

tumor specific transplantation antigen

viral antigen on transformed cell

oncolytic viruses

tumor destroying

latent infection

virus remains in host without causing disease for many years

persistant viral infection

gradually increase in severity

viroids

short, naked pieces of rna without protein coat, infect plants

virusoids

viroid with protein coat

prion

infectious self-replicating protein without nucleic acid

prion activity

converts host’s PrPc to PrPsc, accumulate, cell damage

pathogenesis

how a disease develops

hygeine hypothesis

lack of exposure to microbes during childhood decreases immunity and increases allergies

microbial antagonism

competitive exclusion, normal microbiota prevents harmful ones by competing for resources

symptoms

subjective changes

signs

observable changes

syndrome

group of signs and symptoms in a disease

incidence

how many develop a disease in a period

prevalence

how many have a disease at one time

endemic disease

constantly present in a population

subacute disease

between acute and chronic

sepsis

immune system overworks from severe infection, blood vessels leak, form clots, damages organs

infection fatality ratio

deaths/infected

case fatality ratio

number of deaths within a period

focal infections

infection injects enter blood or lymph vessels and spread

septicemia

blood poisoning, pathogens multiply in blood

disease development

incubation, prodromal, illness, decline

prodromal period

early mild symptoms

reservoir of infection

source, living or nonliving

chronic carriers

recovered but can still spread it for a long time

passive carriers

medical professionals who accidentally transmit

zoonoses

diseases mainly in wild animals but can infect humans

congenital transmission

mother to fetus or newborn by crossing placenta or fluid contact in delivery

vehicale transmission

by medium like air or water

mechanical transmission

transport pathogens through body parts like feet

biological transmission

ingesting pathogen

universal precautions

reduce transmission in healthcare

standard precautions

prevent transmission at all times

transmission-based precautions

contact, droplet, airborne

EIDs

new or changing, increasing or potential to increase

antigenic drift

minor, gradual mutations in viral RNA

antigenic shift

sudden, major change from two strains mixing

reproductive number

average number of people who will get a disease from 1 individual

descriptive epidemiology

collecting all data to find the cause

analytical epidemiology

determine cause and risk factors

morbidity

incidence of specific notifiable diseases

vehicle transmission

indirect, nonliving carriers