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97 Cards in this Set

  • Front
  • Back
characteristic sturcture of enveloped viruses
coated with a lipoprotein membrane (w/ lipid derived from host cell membrane, and often spike-like projections of glycoprotein on
what destoys the infectivity of enveloped viruses
treatment wtih ether, does not harm polio or any other simple nucleocapsid viruses
characterize the stability of enveloped viruses
generally unstable, transmission requires close contact
characterize assembly pattern of enveloped viruses
more complicated than that of unenveloped viruses
-few cell-associated virions at any time
-continuous release of virions w/o gross cellular damage (cell may ultimately die)
-use of a modified cellular membrane
-viral envelope acquired from hotel cell membrane as virus exits cell via "budding" process
characterize the cell membrane of enveloped virus
contains viral glycoprotein spikes
antigens for neutralizing antibody on enveloped viruses
envelope glycoproteins
antigens for neutralizing antibody on
unenveloped viruses
nucleocapsid protein
what kind of viruses are sensitive to ether?
enveloped viruses
how are unenveloped viruses released from infected cells?
how are enveloped viruses released from infected cells?
orthomyxoviruses- (nucleocapsid structure)
enveloped (composed of lipid as well as viral glycoproteins)
8 helical nucleocapsids
orthomyxoviruses- (virion nucleic acid)
8 segments of single (-) stranded RNA

(each RNA segment has genetic info to encode at least one unique viral protein product)
what type of RNA viruses have RNA polymerase in their virion
(-) stranded RNA viruses

double-stranded RNA viruses
viral antigens of orthomyxoviruses
virion envelope membrane antigens = viral gylcoproteins

Hemagglutinin (H)
Neuramidase (N)
Hemagglutinin (H)
H glycoprotein
-fxns early in the infection of a cell
-required for absorption of virions to host cells
- primary target for neutralizing antibody
Neuraminidase (N)
N-antigen/ N-glycoprotein

-enzyme that fxns late in the infection of the host cell

-enzyme fxn to release newly formed virions from infected cell surface by cleaving sialic acid bonds

-cleavage allows newly formed virus to:
infect new cells
be sneezed or coughed to infect a new host and initiate a new infection
Ab to hemagglutinin
neutralize orthomyxovirus virions

most important in controlling orthomyxovirus infection
Ab to neuramiinidase
does NOT nuetralize orthomyxovirus virions

however, it does:
- slow down the release of newly formed virions
-slows down infection in the infected individual
-reduces the severity of the disease
-reduces the likelihodd that the infection will spread to a new individual

HOWEVER Ab TO HEMAGGLUTININ IS MORE IMPORTANT (can neutralize virions and block infection of new cells)
Mechanism of orthomyxoviruses
agglutinate red cells (HEMAGGLUTINATION)
agglutination of red cells
how is relative concentration of orthomyxovirus virion measured in a clincial sample?
hemagglutination can be used

(does not require that virions be infectious, only that hemagglutinin (H), the H-antigen, be present and functional in the envelope of virions.
inhibition of hemagglutination

can be used to titrate the relative concentration of antiviral Ab in serum samples
Why can't RBCs support a productive virus infection?
they do not synthesize RNA or proteins
How do RBCs interact with orthomyxoviruses
RBCs possess the surface receptor that bind the H-antigen

explains basis for hemagglutination
PANDEMIC of 1918-19
world-wide epidemic of Influenza
30-50 million deaths
How are minor epidemics detected
calculated of excess mortality (above expected for influenza-pneumonia)
Types of Human Influenza
influenza A
influenza B
influenza C
different influenza strains within each type of influenza are based on:
antigenic differences in the hemagglutinin and neuraminidase

as well as genetic variation in polymerase genes and other genes encoded by the influenza virus
annual influenza vaccine usually includes:
2 different influenza A strains that are anticipated to represent the predominant H-antigen and N-antigen types of the current flu-season

and one influenza B strain
Influenza A
minor epidemics every..
major epidemics (pandemics) every..
minor, 2-3 years

major 10-30 years
influenza is an example of what type of virus?
what causes minor epidemics?
ANTIGENIC DRIFT: minor variation by mutation within existing RNA segments yield a minor epidemic

a different minor antigenic varient of the H-antigen is responsible for each epidemic wave.

exisiting antibody in the human population from previous epidemics confers partial immunity.
Minor antigenic variation

caused by mutations in the gene for the H-antigen
what causes major pandemics?
when existing Ab in the human population from previous epidemics fails to confer any immunity.

all pandemics result from ANTIGENIC SHIFT (major antigenic variation of the H-antigen)
what is always shifted in pandemic strains of influenza A?
H glycoprotein antigen is always antigenically shifted

N glycoprotein is sometimes shifted as well (usually makes pandemic worse, bc patients lack both the neutralizing Abs to the H antigen) as well as the severeity reduction effects of Ab specific for the N-antigen.
major change in H-antigen
results in pandemic

1) GENETIC RECOMBINATION bt human and animal influenza A viruses

minor mutation in H-antigen

causes minor epidemic, due to partial immunity
requirements for genetic recombination between two closely related viruses
two viruses must:
infect the SAME CELL
at more or less the SAME TIME
why is viral recombination rare in polio virus?

when 2 parental viruses infect the same cell, each RNA molecule replicates separately

progeny RNA molecules are then randomly assembled into virions

Recombination is rare or absent because it REQUIRES BREAKAGE and REUNION of the viral RNA molecules (like xing over in classical genetics)
how is viral recombination detected?
using genetic markers
why is viral recombination more prevalent in influenza viruses?

Two parental viruses infect the same cell

Each nucleic acid molecule replicates independently

The progeny RNA molecules are then randomly assembled into virions

In this case (if there are 2 nucleic acid molecules/ parental virion) about 1/2 the progeny virions are recombinant

HIGH RECOMBINATION is due to random REASSORTMENT (rather than crossing over required in single molecule recombination)
one of 2 mechanisms of genetic recombination in viruses. (e.g. the recombination of RNA molecules from different Influenza A viruses infecting the same cell, resulting in a new Influenza A virus strain)
what contributes to recombination of viruses?
-2 similar viruses infect same cell around same time
-viral genome composed of multiple segments of RNA (reassortment = recombination)
examples of viruses with high level of recombination
those with segmented genomes, eg:
rotaviruses (mult. segments, double stranded RNA)
orthomyxoviruses (8 segments (-) stranded RNA)
non-genetic interaction, whereby virions are assembled from randomly chosen components (of DIFFERENT closely related viruses)

e.g. Polio type I and type 2

cell infected by both viruses
potential virions assembled with Type I RNA:
a) All type 1 capsomers, Type I RNA
b) All type 2 capsomers, Type I RNA
c) A mixture of type I and type 2 capsomers, Type I RNA

b&c phenotype of virion does not correspond to genotype of the RNA, but only transient because progeny will have only Type I capsomers and type I RNA
lab diagnosis of influenza
virus isolation in:
embryonated eggs or tissue cultures

or comparision of acute and convalescent sera, looking for a rise in antihemagglutinin (anti H) Ab by the hemagglutination inhibition assay.

rapid diagnosis, uses fluorescent Ab on a throat swab specimen
influenza virus transmission
person-to-person by coughts and sneezes

droplets initially infect the upper respiratory tract and the infection often extends to the lower respiratory tract
symptoms characteristic of influenza
fever, chills and aches
pathogenesis of influenza
virus directly enters the respiratory tract (mucosal surface)

infects cells and and launches infection at the sight of virion entry causing:

destruction of ciliated epithelium in the respiratory tract

toxic components released from the sites of local growth in the respiratory tract cause systemic symptoms (headache, muscle pains)

viremia is NOT common , does NOT play role in pathogenesis
most common complication of influenza
pneumonia, sometimes with secondary bacterial infection:
- pneumococcus (most common)
- staphylococcus (most of the fatal cases)

bacterial pneumonia due to destruction of ciliated epithelium and malfunctioning infected alveolar macrophages
why is pneumonia a common complication of influenza infection?
influenza results in the destruction of ciliated epithelium in the respiratory tract

the absence of this innate immune mechanism and the malfunctioning of infected alveolar macrophages leads to increased susceptibility for pneumococcus infection.
influenza is most fatal in what population(s)?
elderly (65+)
as well as infant population
what underlies most influenza caused death?
respiratory insufficiency (COPT, etc..)
Influenza (Immune response)
no obligatory viremia, therefore short incubation period (days)

bc infection attacks the respiratory tract, immunity is largely dependent upon secreted IgA

immunity is less effective than immunity in viremic diseases and may be short-lived (3-10 years)

disease caused by re-infection is generally milder than the primary infection
most important factor in immunity to (and in recovery from acute) Influenza infection
Influenza Vaccines
polyvalent formaldehyde killed injected vaccine

(typically: Two H-antigen variants of type A influenza and one type B strain)

*new virus isolates added each year to update the vaccine

~70% effective
efficacy of killed Flu Vaccine
problems with killed flu vaccine
will not efficiently induce secreted IgA
induces an IgG response and IgG Abs that are sub-optimal for protection
who gets killed influenza vaccine?
special risk groups
everyone over age 50
medical personnel (esp. those caring for elderly population)
young pediatric age group
(can be used in all age groups)
polyvalent (several A and B strains) live-attenuated influenza vaccine

administered by intra-nasal spray

selected for optimal growth at low temperature, grows poorly at body temperature

efficacy ~ same as killed vaccine

Treatment for Influenza
Influenza A infections (ONLY A) can be prevented or treated with drugs:

Drugs active against both A & B:
oseltamivir (Tamiflu) and
zanamivir (Relenza)
**both inhibit neuraminidase activity,
drug used to prevent/treat influenza A

tricyclic amine, probably blocks late phase of the absorption-penetration-uncoating process

more effecitve if given before infection
not markedly toxic to patients (human's don't have biochem fxn analogous to penetration-uncoding step of influenza A growth)
Tamilflu and Relenza
drugs active against influenza A and influenza B

if given w/in 48 hours of infection...
inhibit neuraminidase activity:
slows down the release of virus from infected cells, slows cell-to-cell spread of virus, reduce symptomatic period
Paramyzoviruses (virion characteristics)
1 molecule
single (-) stranded RNA
helical nucleocapsid
Similarities between paramyxo and orthomyxo virions
minus-stranded RNA (complementary to mRNA)

RNA polymerase present in the virion
Examples of paramyxoviruses of humans
mumps and measles (cause systemic infections with viremia)

non-systemic respiratory disease:
parainfluenza virus (4 types)
Respiratory Syncytial Virus (RSV)
Characteristics of non-systemic paramyxoviruses (4 types of parainfluenza virus and RSV)
a) no major shifts in antigenicity
(1 molecule of RNA, vs. major shifts in viruses with multi-segmented genomes)

b) many subclinical infections

c) severe, febrile, lower respiratory infection only on initial (childhood) infection. Infection does NOT result in life-long immunity. Thus, adult infections are relatively common, but generally less severe

d) virions agglutinate red cells and the hemagglutination tests are useful
(acute laryngo-tracheo-bronchitis)
characterized by dyspnea and stridor (high pitched, noisy inspiration)
Croup (population affected)
primarily a disease of the first 3 years of life, with a peak incidence at age 2
Croup (most common cause/ virus type)
Parainfluenza viruses, which are Paramyxoviruses
Croup (treatment)
gluccocorticoids can be used to treat severe cases
Respiratory Syncytial Virus (virus type)
paramyxovirus (non-systemic)
Respiratory Syncytial Virus (population affected)
most frequent cause of severe lower respiratory infection in infants

recently recognized as significant infection of the elderly population

(IgA doesn't provide good long-term immunity)
Respiratory Syncytial Virus (treatment)
chemotherapy with aerosolized ribavirin, uncertain efficacy

used with high-risk patients and in severe infections

passive immunization of high risk infants (premature, pulmonary displasia, etc.) with high doses of monoclonal Ab against RSV (palivizumab) is effective in preventing severe RSV pneumonia

no vaccines are available
SARS (caused by what type of virus?)
SARS-associated coronavirus
SARS (disease characteristics)
serious lower respiratory tract infection,
dry cough and dyspnea
SARS (nucleocapsid struture)
single molecule (+) stranded RNA
helical nucleocapsid
SARS (transmission)
transmitted by respiratory droplets (maybe other pathways)
SARS (incubation period)
incubation period 2-10 days
SARS (population affected)
nearly all cases in adults,
severity increasing with age
SARS (case-fatality rate)
SARS (origin, epidemiology)
first appeared in China
rapidly spread world-wide by international air travel
effective case-finding, isolation or quarantine may have halted this epidemic
protein classes involved in the interferon system
virus inhibitory proteins
function of the interferon system
suppresses viral growth
proteins, newly synthesized and secreted into EC fluid by:
- virus-infected cells (secrete alpha and beta interferons) and
- antigen-stimulated T cells (secrete gamma interferon)
when are interferon and virus inhibitory proteins synthesized?
AFTER viral infection
virus inhibitory proteins (+ important examples)
proteins synthesized by UNINFECTED CELLS when their plasma membrane interferon receptors bind interferon molecules

- 2-5-A synthase
- a specific protein kinase
How does a cell "know" that it is infected by a virus and thus should produce interferon that will protect other cells in the body?
what do virus-inhibitory proteins do?
block protein synthesis

w/o protein synthesis, an infected cell cannot produce progeny virions
2-5-A Synthase
an enzyme that synthesizes 2-5-A (a short polynucleotide)

2-5-A activates a ribonuclease that DESTROYS mRNA, thus inhibiting protein synthesis
A specific protein kinase
one of the virus inhibitory proteins:

inhibits protein synthesis by:
specifically phosphorylating initiation factor 2, which is essential to start the process of protein synthesis

phosphorylated initiation factor is not active, thus protein synthesis is inhibited
toxicitiy of interferon to uninfected cells
relatively non-toxic because:
both virus inhibitory proteins are inactive, until the interferon-treated cell becomes infected
what kind of affect do different viruses have on interferon production
interferon is a CELLULAR PRODUCT

interferon is unrelated to the virus that induces its synthesis

the same interferon is produced by a cell infected with a vairety of viruses

specificity of interferon protection
interferon shows species specificity in protection

it will protect cells only from the same species that produced it (bc interferon receptor binds only interferons of its own species)

interferon DOES NOT show viral specificity: a variety of viruses (DNA or RNA) are inhibited, although their sensitivity to interferon may vary
(cells protected by it)
(viruses affected by it)
(mechanism of action)
cells protected: only the species that produced it and related species

viruses affected: any virus

mechanism: blocks protein synthesis in infected cells by via induction of synthesis of virus inhibitory proteins
(cells protected by it)
(viruses affected by it)
(mechanism of action)
cells protected: any species

viruses affected: only the virus that induced it

mechanism: neutralizes extracellular virions by blocking adsorption and penetration
compare timeframes of interferon and Ab production
interferon production: TRANSIENT (appears several days after infection, peaks ~ day 14, gone a few days after that

neutralizing IgG: made for life

neutralizing IgM: declines in a few months