Introduction Flashcards
Virion
Extracellular virus particle
Inc nucleic acid and protein coat (and sometimes lipoprotein membrane envelope)
Size: 20-300 nm
Common features of viruses
Obligatory intracellular growth (virion = vehicle)
Replication - via synthesis in host vs binary fission
Contain one kind of nucleic acid (RNA or DNA)
Eclipse period
Virion undetectable within hours after initial infection of cell
- virion disintegrates -> releases nucleic acid (=”eclipse”) -> subsequently assembled into new virions
Baltimore classification
Via type of genome and type of replication ex: dsDNA (Adeno, Herpes, Pox) ssDNA (Parvo) \+ssRNA (Picorna, Toga) - "+" is mRNA -ssRNA (Orthomyxo, Rhabdo) - "-" is nRNA/template ssRNA-RT (Retro) dsDNA-RT (Hepadna)
Steps of viral replication cycle
Asorption Penetration Uncoating -> eclipse period Synthesis Assembly -> ends eclipse Maturation (usu involves enzyme) Release
Requirements for viral growth
Cell:
- machinery (ribosomes, tRNA), ATP, precursors (nucleotides, amino acids), various enzymes, transport pathways (lysis, vesicle, etc)
Virus:
- genes for virion
- non-virion genes -> replication enzymes, manipulation of host cell
Susceptible vs permissive
Describe host cell infectability
Susceptible
- presence of host cell surface receptor (adsorption and entry)
Permissive - can virus replicate after entry
- innate cellular defenses can be overcome
- machinery for replication cycle (synthesis, transport)
Viral challenges
- must encounter host cells
- must evade physical defenses (skin, mucous, etc)
- must overcome defense mechanisms (intrinsic, innate, adaptive)
Protein coat structure
Symmetrical
Identical capsomeres
Helical Icosahedral (like geodesic dome)
Nucleocapsid
= nucleic acid + capsomer protein coat
Enveloped viruses
Lipoprotein membrane around nucleocapsid
Viral antigens
Only proteins!
Unenveloped nucleocapsid -> capsomer
Enveloped -> envelope proteins
Detection methods
Detection - clinical methods - cytopathic or transforming effect - inclusion bodies - plaques - syncytia Cultivation is slow, labor intensive, still doesn't provide specific identity
Cytopathic effect
Viral infection -> change in size, shape, motility, attachment
-> lysis
Visualize with light microscopy as infection spreads
Transforming viruses
Abnormal proliferation -> piles or mountains from single layer culture
- aka tumor viruses
Inclusion bodies
Sites of viral replication
Requires histologic staining
Location may be characteristic (cytoplasm vs nuclear)
Plaque formation
Zone of dead cells from cytopathic virus
PFU = plaque forming unit = only quantitative method for measuring virions in sample
Syncytia
Virus envelope includes “fusion” protein ->
large multinucleated cell
Ex RSV
Viral identification
Usually relies on detection of virion:antibody match
- neutralization
- complement fixation
- hemagglutination (not all viruses)
- fluorescent antibody
- radioimmunoassay, ELISA, etc
Diagnosis of viral disease
Antibodies
- isolate virus -> interaction with known antisera (Ig)
- Seroconversion - acute (prior) vs convalescent antibody levels
= may have “window period” - active infection but not seropositive (Hep B, HIV)
Rapid - presence of viral components
- protein antigens (via antibody)
- nucleic acid (via PCR) - works during window period
Neutralization
Tight binding of antibody:virion surface
- high affinity, essentially irreversible dt repeating epitopes
- > can’t adhere/enter cells
- doesn’t impact intracellular multiplication
- ex local IgA in resp or GI
- > also use for diagnosis (fewer PFUs)
- only works for infectious virions
Simple nucleocapsid viruses
All icosahedral Stable in env't (don't require direct contact for transmission) RNA -> assembled in cytoplasm DNA -> assembled in nucleus (enveloped are different...)
Host range
Species that can be infected
Determined by adsorption (cell receptors)
Ex - polio -> humans and higher primates
Tissuetropism
Range of tissue that can be infected
Adsorption
Virions bind to receptor protein
Highly specific
Determines host range and tissuetropism
Can be bypassed experimentally (ex polio RNA -> chicken cell -> synthesis of virions)
Polio replication
RNA-dependent RNA polymerase (no DNA, not inhibited by DNA-> RNA block via actinomycin)
Cytoplasm
Inhibits host synthesis
mRNA (+ strand) -> large protein -> cleavage -> capsomer and enzymes (inc polymerase)
- > complementary (-) strand = template -> synthesis of new + strand
- >
- strand + capsomers -> new virions
Patterns of pathogenesis
- growth in cells at site (no illness) -> viremia
- incubation weeks/months
- immunity reliable, decades/life
- growth at site -> illness (mucosal)
- incubation days
- immunity via IgA, less effective, 3-10 years
- less severe illnes
- growth at site -> neural spread (rabies)
Patterns of infection
Acute - occurs then clears
Persistent - virus and/or infection not clears
- inc latent and slow
May be asymptomatic (aka subclinical, inapparent, silent)
Incubation period
Length of time between infection and symptoms
Defined by symptoms - may have detectable antigen or antibodies
Window period
Infection without detectable antigen or antibodies
Depends on sensitivity of tests (higher sensitivity can shorten but not eliminate)
Eclipse period
Time between phagocytosis of virus and release of new virions
Defined on cellular vs organism basis
