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45 Cards in this Set

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VIRION
extracellular infectious virus particle
vehicle to transport viral nucelic acid from cell to cell

consists of: the viral nucleic acid with a protein coat.

some have an outer LIPOPROTEIN membrane envelope

small (20-300 nm in diameter, measured by filtration or electron microscope)
LIPOPROTEIN
lipid + protein

makes up envelope surrounding some virion
OBLIGATORY INTRACELLULAR GROWTH
explains the necessary location for virus growth (i.e. in a cell, not in a virion)
Replication of viruses
by synthesis and assembly of component parts

ATTACHEMENT virion attaches to the host cell

PENETRATION virus particle penetrates into host cell

ECLIPSE PERIOD virion proteins covering the nucliec acid are uncoated (virion is not recognizable, occurs in first few hours following infection of a cell)

VIRUS GENE EXPRESSION: The virus (now represented by nucleic acid molecule(s) now directs the synthesis of new viral components

ASSEMBLY of viral components into new virions

RELEASE of many new virions

** this synthesis and assembly mode of replication distinguishes viruses from other small intracellular parasites that multiply by simple cell division)
Nucleic Acid in virion
virions contain only one kind of nucleic acid
Types of nucleic acid in viruses
single-stranded RNA
double-stranded RNA
single-stranded DNA
double-stranded DNA
What does the cell supply for virus growth?
1. Energy (ATP)
2. Low molecular weight precursors: nucleotides and amino acids
3. The protein snythetic machinery: ribosomes, tRNA, etc...
What odes the virus supply for virus replication?
1. GENES FOR VIRION PROTEINS (capsomer proteins, page A5, and envelop proteins, page D1)

2. GENES FOR PROTEINS THAT DO NOT END UP IN VIRION

3. GENES FOR PROTEINS INVOLVED IN GENOME REPLICATION/ MAY CONTRIBUTE TO VIRION Genes for one or more proteins that play a role in the replication of the viral genome and may or may not end up in the virion (depends on particular virus)
basis for virus classification
chemical composision

structure

mode of replication
cytopathic effect
CPE = morphological effect of virus infection

virus infected cells typically change shape (usually round up as they die)

infected cells are released from their normal attachment to the culture vessel surface (on which they were growing before the virus was added to the culture
cytopathic effect is caused by:
infectious virions
method used to quantify infectious units
CPE in tissue culture (agar medium is used to count infectious viriions)
PLAQUES
circular zones of dead cells representing the cell-to-cell spread of virus from the originally infected cell at the heart of the plaque.
PFU
plaque forming units (used to determine infectious virus in the sample)
eclipse period
period in which the virus particle disappears as virus nucleic acid continues to function
latent period
defined from the onset of infection to the appearance of the virus extracellularly
inclusion bodies
aggregations of proteins, represent site of viral replication or assembly (nucleus or cytoplasm)

their presence as well as their location may be characteristic of a particular virus
NEUTRALIZATION
method for detecting the reaction of virions and specific Ab in virus identification

Virions complexed with Ab are neutralized in their infectivity for animals, embryonated eggs, or tissue cultures

Abs bind very tightly and essentially irreversibly to virions

*only works on infectious virions that can cause CPE or PFU
Most common ways of detecting rxn of virions and specific Ab
a. NEUTRALIZATION
b. Complement fixation
c. Hemagglutination inhibition (not general though)
d. Fluorescent Ab
e. Radioimmunoassay, ELISA, and other very sensitive methods
acute sera
serum taken before immune response has been mounted against virus
convalescent sera
serum taken after the immune response to a virus
SEROCONVERSION
change in serum from having no antibody against a certain virus to having antibody against a certain virus
SEROPOSITIVE
having antibody against a certain virus
SERONEGATIVE
lacking antibody for a certain virus
WINDOW PERIOD
temporary interval where antibodies or viral infection should be, but are not yet detectable
rapid viral diagnosis
achieved by detecting the presence of specific viral components from appropriate specimens (works for certain viruses)

a. viral protein antigens can be detected using fluorescent Ab

b. viral nucleic acid can be identified by PCR
capsomers
protein subunits that make up symmetrical protein coat surrounding nucleic acid of a virion
nucleocapsid shapes
symmetrical
helical
or
icosohedral (20-sided)
assembly of the nucleiocapsid w/in an infected cell results from:
recognition of the viral genome by capsomers

and

formation of complexes betwen them
enveloped viruses
have lipo-protein membrane around the nucleocapsid
PLUS-STRANDED RNA VIRUS
virus with virion RNA that can serve as mRNA (plus-stranded RNA)

e.g. Polio virus
MINUS-STRANDED RNA virsus
have virion that contain RNA complementary to mRNA
viremia
infectious virions in the blood
incubation period
the length of time (days to years) between infection and the onset of specific symptoms
ACTIVE IMMUNITY
patient makes antibody as a result of previous natural infection or immunization with a vaccine
PASSIVE IMMUNITY
patient receives antibody from someone else, antibody can be injected by a physician or corss the placenta from mother to fetus (immunity is short term)
PASSIVE --> ACTIVE IMMUNITY
patient is infected while passively immune and gets mild or subclinical disease which results in active immunity
Polio virus pre-vaccination era
most mom's were highly immune

passively immunized their infants
who then became infected and aquired passive --> active immunity
SUBCLINICAL INFECTION
inapparent, typical of most polio infections (asymptomatic)
ASEPTIC MENINGITIS
non-paralytic polio (headache, stiff neck, fever, increased leukocytes in spinal fluid)
SPINAL POLIO
class of paralytic poliomyelitis:

destruction of motor neurons
BULBAR POLIO:
class of paralytic poliomyelitis:

attack on the respiratory centers in the medulla and cranial nerves
SEROTYPES
really antigenic types (called serotypes because distinction was originally made serologically w/ specific antibodies)
INACTIVATED (KILLED) VACCINES
prepared by chemical (usually formaldehyde) treatment

formaldehyde reacts with amino groups
LIVE-ATTENUATED VACCINES
1. multiple-site mutants
2. mutants are selected for greater virulance (i.e. capacity for growth) in a new host species or in a different tissue
3. In some cases the mutations that permit this greater virulance also result in reduced virulence for humans
4. since this is blind selection, potential vaccine strains must be tested for a) virulance in humans and B) antibody response in humans against the homologous wild (virulent) virus