Introduction To Viruses

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VIRION

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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)

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LIPOPROTEIN

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lipid + protein

makes up envelope surrounding some virion

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OBLIGATORY INTRACELLULAR GROWTH

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explains the necessary location for virus growth (i.e. in a cell, not in a virion)

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Replication of viruses

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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)

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Nucleic Acid in virion

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virions contain only one kind of nucleic acid

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Types of nucleic acid in viruses

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single-stranded RNA
double-stranded RNA
single-stranded DNA
double-stranded DNA

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What does the cell supply for virus growth?

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1. Energy (ATP)
2. Low molecular weight precursors: nucleotides and amino acids
3. The protein snythetic machinery: ribosomes, tRNA, etc...

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What odes the virus supply for virus replication?

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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)

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basis for virus classification

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chemical composision

structure

mode of replication

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cytopathic effect

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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

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cytopathic effect is caused by:

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infectious virions

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method used to quantify infectious units

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CPE in tissue culture (agar medium is used to count infectious viriions)

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PLAQUES

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circular zones of dead cells representing the cell-to-cell spread of virus from the originally infected cell at the heart of the plaque.

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PFU

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plaque forming units (used to determine infectious virus in the sample)

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eclipse period

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period in which the virus particle disappears as virus nucleic acid continues to function

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latent period

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defined from the onset of infection to the appearance of the virus extracellularly

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inclusion bodies

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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

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NEUTRALIZATION

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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

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Most common ways of detecting rxn of virions and specific Ab

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a. NEUTRALIZATION
b. Complement fixation
c. Hemagglutination inhibition (not general though)
d. Fluorescent Ab
e. Radioimmunoassay, ELISA, and other very sensitive methods

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acute sera

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serum taken before immune response has been mounted against virus

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convalescent sera

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serum taken after the immune response to a virus

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SEROCONVERSION

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change in serum from having no antibody against a certain virus to having antibody against a certain virus

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SEROPOSITIVE

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having antibody against a certain virus

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SERONEGATIVE

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lacking antibody for a certain virus

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WINDOW PERIOD

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temporary interval where antibodies or viral infection should be, but are not yet detectable

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rapid viral diagnosis

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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

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capsomers

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protein subunits that make up symmetrical protein coat surrounding nucleic acid of a virion

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nucleocapsid shapes

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symmetrical
helical
or
icosohedral (20-sided)

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assembly of the nucleiocapsid w/in an infected cell results from:

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recognition of the viral genome by capsomers

and

formation of complexes betwen them

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enveloped viruses

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have lipo-protein membrane around the nucleocapsid

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PLUS-STRANDED RNA VIRUS

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virus with virion RNA that can serve as mRNA (plus-stranded RNA)

e.g. Polio virus

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MINUS-STRANDED RNA virsus

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have virion that contain RNA complementary to mRNA

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viremia

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infectious virions in the blood

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incubation period

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the length of time (days to years) between infection and the onset of specific symptoms

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ACTIVE IMMUNITY

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patient makes antibody as a result of previous natural infection or immunization with a vaccine

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PASSIVE IMMUNITY

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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)

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PASSIVE --> ACTIVE IMMUNITY

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patient is infected while passively immune and gets mild or subclinical disease which results in active immunity

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Polio virus pre-vaccination era

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most mom's were highly immune

passively immunized their infants
who then became infected and aquired passive --> active immunity

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SUBCLINICAL INFECTION

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inapparent, typical of most polio infections (asymptomatic)

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ASEPTIC MENINGITIS

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non-paralytic polio (headache, stiff neck, fever, increased leukocytes in spinal fluid)

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SPINAL POLIO

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class of paralytic poliomyelitis:

destruction of motor neurons

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BULBAR POLIO:

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class of paralytic poliomyelitis:

attack on the respiratory centers in the medulla and cranial nerves

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SEROTYPES

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really antigenic types (called serotypes because distinction was originally made serologically w/ specific antibodies)

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INACTIVATED (KILLED) VACCINES

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prepared by chemical (usually formaldehyde) treatment

formaldehyde reacts with amino groups

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LIVE-ATTENUATED VACCINES

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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