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STUDY OF VIRUS
VIRUSES
infectious agents that are too small to be seen with a light microscope
“virus” in Latin means “poison”
WHAT ARE VIRUSES
lack cell nucleus, cell organelles, or cytoplasm
replicate only inside a living host cell
contain either DNA or RNA but not both
herpes = DNA
polio = RNA
virus do not grow or divide
DIVERSITY & CLASSIFICATION
Criteria used to classify viruses:
1) Disease symptoms
2) Physical structure of virus particles
3) Structure & sequence of the virus genome
RNA VIRUSES
comprise70% of all viruses
the high error rate of the enzymes involved in RNA replication results in:
viruses which show much higher mutation rates than do DNA viruses
high mutation rates lead to the continuous generation of virus variants which show great
adaptability to new hosts
VIRAL MULTIPLICATION
viral multiplication requires:
1) that a virus particle infect a cell
2) and program the host cell’s machinery
to synthesize the components required for the assembly of new virus
particles
COMPONENTS OF VIRUSES
core
nucleic acid
capsid
protein coat
envelope
lipid bilayer membrane
not all viruses have an envelope
CORE
“a piece of bad news wrapped up in a protein”
nucleic acid is the “bad news”
viruses use their genetic information to replicate themselves in host cells
disrupts host cell functions
CAPSIDS
accounts for most of the viruses mass
protein coat which protects the nucleic acids
determines the shape of the virus
capsid structure is determined by the enclosed viral nucleic acid
ENVELOPES
acquire their envelope after they are assembled in a host cell as they move through one
or several membrane systems
ER, Golgi apparatus, plasma membrane
combinations of host derived lipids, proteins and carbohydrates
ENVELOPES
spikes may or may not be present
assist the virus in attaching to receptor sites on the host cell membrane
envelopes are made from host cell membranes and the virus is effectively “hidden” from
attack by host’s immune system
enveloped viruses are damaged easily
naked viruses are more resistant to harsh environmental conditions
BUDDING
Some viruses have devised strategies to exit the infected cell without its total
destruction
The viability of the cell depends on the integrity of the cell membrane
Viruses leaving the cell must therefore allow this membrane to remain intact
achieved by budding of the particle through the membrane
during which process the particle becomes coated in a lipid envelope derived
from the host cell membrane & with a similar composition
Not all enveloped viruses bud from the cell surface membrane
may use cytoplasmic membranes
the golgi complex
herpes viruses which replicate in the nucleus may utilize the nuclear membrane
the virus is transported to the cell surface & subsequently released
NAKED VIRUS PARTICLES
those in which the capsid proteins are exposed to the external environment
this strategy has drawbacks
In some circumstances it is wasteful resulting in the premature death of the cell
ENUMERATION OF VIRUSES
enumerated by spreading a suspension on the surface of a lawn of actively growing
cells susceptible to the virus
a virus particle infects, reproduces, and its progeny re-infect surrounding cells
a zone of clearing in the cell layer is produced
The plaque presumably originated from one virus particle
the number of virus in the original suspension is proportional to the number of plaques
obtained
VIRAL FORMS
Viruses can infect all forms of life
bacteria, plants, protozoa, fungi, insects, fish, reptiles, birds, and mammals
VIRAL GENOMES
smaller than bacterial systems
one of the largest viral genomes is 190 kilobases
compared to 590 for the smallest bacterial system
economy is achieved with overlapping genes
some nucleotide sequences are read in more than one reading frame
As genome size increases, virus structure and life cycle become more complicated
REPRODUCTIVE CYCLES
two types of reproductive cycles
1) lytic or virulent infection
new virus particles are made and released (burst) from the host cell
2) transformation or lysogenic infection
virus genome is integrated into that of the host cell
replicated as part of the host as it grows
LYTIC REPRODUCTIVE CYCLE
1) Attachment
2) Penetration
3) Take-over
4) Replication
5) Synthesis
6) Assembly
7) Release
LYTIC REPRODUCTIVE CYCLE
1) Attachment to the surface of the cell
The type of cells a virus can infect is highly specific
A virus protein binds specifically to a cell receptor
Viral Specificity
CD4 on T-cells for HIV
ICAM on upper respiratory epithelial cells - Rhinoviruses (common
cold)
Immunoglobulin-like receptors - polio virus
The association between the virus and its host imposes specific
conditions for pathogenesis
ex: rhinoviruses require a temperature not exceeding 34°C
this restricts growth to only those cells in the cool outer layer
of the nasal mucosa thereby preventing spread to deeper
cells where temperatures are higher
2) Penetration
the cell wall and membrane are breached by enzymatic degradation
injection of the genetic material into the cell
the protein coat does not enter the cell
3)Take-over of host biosynthetic machinery
prevents synthesis of cellular proteins
enables expression of viral genes
4) Replication of nucleic acid
5) Synthesis of coat proteins
6) Assembly of genomes into protein coats
7) Release from the cell
The time-frame for the reproductive cycle can be:
20-30 min in bacteria
8-40 hours in animal cells
HOST CELL PROTECTION STRATEGY
1) have no receptor sites for the virus to bind with
2) produce restriction enzymes
attack the foreign nucleic acid
TRANSFORMATION REPRODUCTIVE CYCLE
virus repress expression of the genes used to initiate lytic infections
viral genes are held in a transformational stage
a switch or signal converts the virus to the lytic growth cycle described earlier
LATENT INFECTIONS
Some viruses have a capacity for latent infections
symptoms only arise under stress
ex: Herpesviruses
has a gene that controls the timing of gene expression
VIRAL INFECTION
some viruses may establish forms of “silent” infection
in most cases their multiplication usually causes cell damage or death
viruses must depend on host survival for their own survival
thus tend to establish mild infections in which death of the host is more an aberration
than a regular outcome
VIRUS INCORPORATION
Viruses use normal human cell reactions to antigens to invade the cell membrane
In this case a virus needs only to come into contact with the cell membrane
VIRAL PATHOGENESIS
vast majority of virus infections are sub-clinical (asymptomatic)
critical stages in replication determine the nature of the disease they produce
1) Entry into the Host
2) Primary Replication
3) Spread Through the Host
4) Host Immune Response
5) Secondary Replication
6) Cell & Tissue Damage
7) Persistence
1) ENTRY INTO THE HOST
the site of entry can influence the disease symptoms produced
Skin (dead cells) cannot support virus replication
Most viruses which infect via the skin require a breach in the physical
integrity of the barrier
some viruses employ vectors
ticks
mosquito's (yellow fever)
bats (rabies)
Respiratory tract
Most common site
possess immune defense mechanisms
ciliated epithelium, mucus secretion, lower temperature
adenoviruses, rhinoviruses, herpesviruses, orthomyxoviruses
Gastrointestinal tract
hostile environment; gastric acid, bile salts
ingestion
enteroviruses, poliovirus, hepatitis A, reoviruses
Genitourinary tract
less hostile than GI tract
usually sexually transmitted
human papillomaviruses, herpes simplex, HIV
Conjunctiva
exposed and relatively unprotected
2) PRIMARY REPLICATION
virus must initiate an infection by entering a susceptible cell
frequently determines whether the infection will remain localized at the site of entry or
spread to become a systemic infection
3) SPREAD THROUGHOUT THE HOST
via direct cell-to-cell contact
via the bloodstream
insects, blood transfusion, I.V. drug abuse
via the nervous system
spread occurs by direct contact with neurons at the primary site of infection
from peripheral nerves the virus can spread to the CNS by axonal transport along
neurons
4) HOST IMMUNE RESPONSE
has a major impact on the outcome of an infection
5) SECONDARY REPLICATION
Occurs in systemic infections when a virus reaches other tissues in which it is capable
of replication
Poliovirus
gut epithelium - neurons in brain & spinal cord
If a virus can be prevented from reaching tissues where secondary replication can
occur, generally no disease results
6) CELL & TISSUE DAMAGE
Viruses may replicate widely throughout the body without any disease symptoms if they
do not cause significant cell damage or death
some viruses may not cause cell death
being released from the cell by budding rather than by cell lysis
causing persistent infections
May be passed vertically to offspring if they infect the germ line
All vertebrate genomes including humans are stuffed with retrovirus genomes which
have been with us for millions of years
Conversely, Picornaviruses cause lysis and death of the cells in which they replicate,
leading to fever and increased mucus secretion
7) PERSISTENCE
Long term persistence of virus results from two main mechanisms:
a) Regulation of lytic potential
b) Evasion of immune surveillance
VIRAL EFFECTS ON CELL
1) cell death
2) little direct effect
3) cell transformation
CELL DEATH
The effect of viruses is seen in the whole body
respiratory viruses destroy respiratory epithelium
polio virus destroys anterior horn cells in spinal column, causing paralysis
LITTLE DIRECT EFFECT
Some viruses produce very little cell death
hepatitis B virus does not cause pathology in the liver
Most of the tissue damage is caused by the host's immune response to the viral
infection
CELL TRANSFORMATION
Viruses can transform cells leading to malignancy
Human papillomaviruses (genital cancers)
Hepatitis B (liver carcinoma)
Epstein Barr virus (EBV) (mononucleosis)
Human T-cell Leukemia Virus
VIRAL STRATEGY
The intracellular location of the virus protects the virus against some of the host's
immune mechanisms
The intracellular location also makes the virus vulnerable because of its dependence on
the host cell's synthetic machinery
host cell metabolism may be altered by subtle changes produced by the viral infection
(inflammation, fever, circulatory alterations, and interferon)
VIRAL CHEMOTHERAPY
Viruses are difficult targets for chemotherapy because they replicate only within host
cells
The similarity of host and virus makes it difficult to find antiviral agents specific enough
to exert effect on viral replication in infected cells but not in host cells
each virus has a few specific steps of replication that may be used as targets for highly
selective chemotherapeutic agents
HOST VIRUS INTERACTIONS
Hit and Run infections
Systemic infections
Persistent infections
HIT AND RUN INFECTIONS
common cold viruses (rhinoviruses)
Short incubation period (36 to 48 hours)
Pathology in the upper respiratory tract and secondary invasion by normal flora of oral
bacteria
Symptoms last for 5-7 days and then eliminated by the host
immune protection is poor since there are >100 serotypes of rhinovirus
orthomyxoviruses (influenza A and B)
immune protection against subsequent infection may be poor
because these viruses can change their antigenic profile of their surface proteins
SYSTEMIC INFECTIONS
measles, chickenpox, mumps, and rubella
Incubation period 14 to 21 days
recovery is mainly due to cell-mediated responses
long term protection from subsequent infection is good
may be due to the fact that there is only one serotype
PERSISTANT VIRAL INFECTIONS
Latent infections
virus does not replicate
may occur in non-dividing cells such as neurons
Chronic infections
active replication of virus
Transformation of virus infected cells may occur after years of persistence
(hepatitis B)
VIRUS EVADE IMMUNE RESPONSE
strategies to evade the immune response
1) Latent infection
Herpes simplex and varicella zoster
infect dorsal root ganglia
In these nerve cells, there is very little expression of viral RNA and protein
host immune response is unaware of virus presence
2) Mutation
alteration of the important proteins recognized by the immune system
HIV and influenza A
3) Inhibition of immune recognition
Inhibition of cell surface expression of molecules on infected cells
Inhibition of antigen processing
4) Target host cytokines
Inhibition of inflammatory cytokines
interleukin
tumor necrosis factor (TNF)
5) Lysis of immune cells
HIV kills helper T- cells
PREVENTION & TREATMENT
Prevention
Vaccination and public health measures
Treatment
Antiviral Vaccines
PREVENTION
1) Public health measures
laws, sanitation practices
2) Vaccination
Most of the damage to cells in virus infections occurs very early before clinical
symptoms of disease appear
makes treatment difficult
VACCINES
following exposure to an antigen, a rapid secondary immune response is generated
leading to the accelerated elimination of the organism and protection from clinical
disease
Success depends on the generation of memory T and B cells and the presence in the
serum of neutralizing antibody
introduction of vaccination has lead to a dramatic downward trend in incidence of viral
diseases
The principle of vaccination is to induce a "primed" state in the vaccinated subject
IMMUNE RESPONSE
vaccines must stimulate as many of the body's defense mechanisms as possible
mimic the disease (without pathogenesis)
1) Humoral Immunity
antibodies & complement
2) Cell Mediated Immunity
T-cells
most important in virus infections
VACCINATION STRATEGIES
Types of vaccine
1) Recombinant Vaccines
2) Sub-cellular fractions
3) Attenuated (Live Virus) Vaccines
4) Heterologous Vaccines
5) Inactivated (Killed) Vaccines
1) RECOMBINANT VACCINES
newest types
completely safe, except for rare adverse reactions
also tend to be the least effective
1) Synthetic Vaccines
2) Recombinant Vaccines
3) Virus Vectors
Following injection into the subject, the recombinant organism will replicate and express
sufficient amounts of the foreign protein
induces a specific immune response to the protein
genetic engineering can be used to introduce a gene for a protein from one organism
into the genome of another
ex: vaccinia virus
Such an organism (expressing a foreign gene) is called a recombinant
2) SUBCELLULAR FRACTIONS
possible to use a vaccine directed against only one or two proteins of a virus
The organism is inactivated and the protein of interest is purified and concentrated from
the culture medium
advantages
safe
few local reactions occur at the injection site
disadvantages
poor immunogenicity
need multiple boosters
3) ATTENUATED VACCINES
Live, attenuated vaccines
virus have been sufficiently weakened, or attenuated, in the laboratory
reduced temperature
results in the selection of mutants which replicate poorly in the human host and are
therefore of reduced virulence
replication of the vaccine strain in the host reproduces features of wild type infection
without causing clinical disease
do infect cells and multiply in the body
stimulate immunity without causing a full-blown infection
measles, mumps and rubella vaccines
oral poliovirus vaccine (OPV)
do not spread from a vaccinated child to another person
Potential drawbacks to these vaccines include
a) danger of reversion to virulence
b) possibility of causing extensive disease in immunocompromised individuals
4) HETEROLOGOUS VACCINES
Closely related organism of lesser virulence
share many antigens with the virulent organism
vaccine strain replicates in the host and induces an immune response that cross reacts
with antigens of the virulent organism
Small pox vaccine
Both cowpox virus and vaccinia virus are closely related to variola virus
causative agent of small pox
Edward Jenner (18th century physician) observed that milkmaids who had
been infected with cowpox virus were immune to smallpox
Wide spread use of vaccinia virus as a vaccine lead to the world wide
eradication of smallpox
5) INACTIVATED (KILLED) VACCINES
exposure to denaturing agent
propiolactone
formaldehyde
results in loss of ineffectivity without loss of antigenicity
Inactivated vaccines and purified protein vaccines do not have any living germs in them
stimulate the immune system without causing any infection
inactivated polio vaccine(IPV)
killed pertussis vaccine
diphtheria, tetanus toxoids, and hepatitis B vaccine
These vaccines are not infectious and are therefore relatively safe
are usually of lower immunogenicity
multiple doses may be needed to induce immunity
More effective than subunit vaccines
expensive to prepare
denaturation may lead to loss of antigenicity (measles)
useful when living vaccines are not available because attenuated strains have not been
developed
reversion to wild type occurs too readily
possible to use an inactivated preparation of the virulent organism to immunize the host
ANTIVIRAL DRUGS
Historically, the discovery of antiviral drugs has met with relatively little success
Any stage of virus replication can be a target for a drug, but drug must be more toxic to virus
than to the host
Principal drugs are:
Acyclovir, Famciclovir, Valaciclovir
herpesvirus infections
Ribavirin
respiratory virus infections
Azidothymidine (AZT), Dideoxyinosine
HIV infection
Rimantidine, Amantadine
influenza virus infections
CHEMOTHERAPUTIC INDEX
Dose of drug which inhibits virus replication / Dose of drug which is toxic to host
The smaller the value of this number the better
several orders of magnitude difference is required for a really safe drug
DIAGNOSIS OF VIRAL INFECTION
Diagnosis can be by detection of :
virus
electron microscopy
viral antigen
immunofluorescence
effect of virus
cytopathic effect on cells
virus nucleic acid
by PCR (polymerase chain reaction)
anti-viral antibody
by ELISA
VIRAL DISEASES
1) Influenza
2) Measles (Rubella)
3) Mumps
4) Herpes Simplex
5) Hepatitis
6) Polio
7) “Common cold”
8) Rabies
9) Small pox
10) HIV
INFLUENZA
RNA virus
Influenza is a disease of the upper respiratory tract
envelope is from the host's plasma membrane
There are three distinct influenza viruses based on the differences of their glycoprotein
in the envelope
Type A is found in horse, swine, birds and humans
cause of most pandemics
Types B and C are found in humans only
Because the RNA segments can be rearranged
the virus can evade previous immunity via changes in composition of the
spikes
MEASLES
RNA virus
Transmission is by respiratory droplet
has an envelope for adsorption to the cell surface
MUMPS
RNA virus
virus enter through the respiratory tract, replicate, then spread to other areas
causing cell necrosis and inflammation
maintain an envelope of lipid membrane to assist in fusion to the host cell
live attenuated vaccine is available for infants after one year and adults who have not
had the disease during childhood
HERPES SIMPLEX
DNA virus
causes cold sores, keratitis, genital and neonatal infections
Herpes has an envelope with spikes from the nuclear membrane of the host
two types of herpes simplex:
Type 1
Found primarily in the oral and facial areas
the most prevalent type and can become latent in sensory root ganglia
Type 2
Found primarily in the genitals and is sexually transmitted
Recurrent infections are common but they are milder than the primary
infection because of partial immunity
Recurrence can be due to stress, hormones, excessive sunlight
causes lesions on the genitals and is associated with cancer of the cervix
neonatal transmission can occur during delivery
because of an undeveloped immune system mortality rate is about 60%
neonatal survivors usually have neurological disorders
HEPATITIS
inflammation of the liver
caused by numerous different viruses
Hepatitis A Virus (HAV)
Hepatitis B Virus (HBV)
Hepatitis C Virus (HCV)
Hepatitis D Virus (HDV)
Hepatitis E Virus (HEV)
HAV and HEV
fecal-oral route is the predominant mode of transmission
HBV, HCV, and HDV
bloodborne viruses and are primarily transmitted by percutaneous and mucosal
exposures
HEPATITIS A
RNA virus
Transmission is by the fecal - oral route
source can be contaminated water, seafood or an infectious food preparer
Antibody to the virus persists in serum so patients become immune to infection
Gamma globulin provides passive immunization
HEPATITIS B
enveloped DNA virus
Humans are the only natural reservoirs for HBV
transmission may be by direct contact, or indirect contact through transfusion,
contaminated needles
Chronic infection is associated with viral replication in liver and lymphoid tissues
HEPATITIS C
RNA virus
primarily transmitted parenterally and is one of the primary causes of post transfusion
hepatitis
No vaccine is available and there is no immunity with infection
HEPATITIS D
RNA virus
transmitted parenterally
HEPATITIS E
RNA virus
spreads by fecal - oral route
In most cases it is waterborne
Mortality is generally low except in infants and pregnant women
No vaccine is available
POLIOVIRUS
cause poliomyelitis (flaccid muscular paralysis)
transmitted by the fecal-oral route
Primary site of infection is lymphoid tissue associated with the oropharynx and gut
following which the virus may infect the CNS
The effectiveness of vaccination for polio is underscored by the fact that the World
Health Organization and the UN Childrens' Fund predict if present trends continue, polio
will join smallpox as the second ever human disease to be eradicated
RHINOVIRUS
Cause of 'the common cold'
but not the only one!
105 serotypes
hence repeated infections
Relatively fragile viruses
Extensive human volunteer studies show no evidence for susceptibility when exposed
to cold/wet conditions (!)
although general immune status is probably important
Symptoms due to damage to ciliated epithelium in upper respiratory tract
predisposes to secondary bacterial infections
a major problem in infants and elderly
a major economic pest worldwide
lost working days
No effective prophylaxis or treatment
little or no cross-protection between serotypes
Protection relies on levels of antibodies
may be relatively short-lived (a few years rather than life-long)
RABIES
Infects neurons of the CNS
rabies virus are disclosed as the yellow-green bodies
HIV (HUMAN IMMUNODEFICIENCY SYNDROME)
Classified as a retrovirus
RNA genome
contains the enzyme reverse trancriptase
envelope of lipoprotein
envelop has spikes
allow HIV to attach to the CD4 receptor on a host cell
The viral RNA becomes integrated into the the chromosomal DNA of the host cell
HIV TRANSMISSION
Transmission of HIV requires transfer of or exposure to infected bodily fluids
HIV virus are located within macrophage cells in fluids
blood
10-1000 infectious particles (IP) per milliliter
semen
10-50 IP/ml
Routes of HIV transmission include
intimate sexual contact
anal receptive intercourse (most dangerous form of sexual contact)
breast milk
blood contaminating needles
organ transplants
artificial insemination
blood transfusions
BLOOD TRANSFUSIONS
transmission by blood is unlikely in developed countries
blood is tested for HIV antibodies
slight risk because blood might be donated during the interval between infection and
appearance of detectable antibodies
Tests for the virus itself are also available, but they have not proved to be superior in
screening blood
There is no risk at all in donating blood
HIV TRANSMISSION
HIV is not transmitted by
insects
hugging
sharing household facilities
drinking glasses
towels
kissing is not known to spread the infection
Saliva usually contains less than 1 IP/ml
STAGES OF HIV
1) A few weeks after primary HIV infection there is a burst of virus replication and high
levels of virus particles
2) Within weeks to months, a humoral and cellular immune response to HIV is detected
levels of culturable virus decrease dramatically
3) Patients then enter a phase of clinical latency
characterized by lack of symptoms
moderately decreased levels of T cells
low levels or absence of culturable virus in the blood
HIV THERAPY
Current strategies aim at:
blocking virus dissemination
decreasing viral burden
available agents are only partially effective in suppressing virus replication
Clear cut but limited benefit is realized when azidothymidine (AZT) is given to a patient
with advanced HIV disease
benefits of early intervention are only temporary and do not result in significant long
term advantages with regard to course of disease and death
HIV
Listeria monocytogenes
a bacterium found in spoiled cheese
has been genetically engineered to produce one of the HIV virus' protein
products
Researchers believe this may prove to be a safe and effective way to help build
immunity to HIV without exposing patients to the HIV virus itself
AIDS
Acquired Immunodeficiency Syndrome
only the end stage of HIV infection
average time from infection to development of AIDS is 10 years
PRIONS
convert normal protein molecules into dangerous ones simply by inducing the benign
molecules to change their shape
Prions are responsible for transmissible and inherited disorders of protein conformation
can also cause sporadic disease
post mortem appearance of the brain shows large vacuoles in the cortex and
cerebellum
KNOWN PRION DISEASES
widespread in animals
all fatal
cause the brain to become riddled with holes
can lie dormant for years (or even for decades in humans)
SCRAPIE
most common form
found in sheep and goats
Afflicted animals lose coordination and eventually become so incapacitated that they
cannot stand
in some cases, an intense itch develops that leads them to scrape off their wool or hair
hence the name "scrapie”
OTHER PRION DISEASE
transmissible mink encephalopathy
chronic wasting disease of mule deer and elk
feline spongiform encephalopathy
bovine spongiform encephalopathy
often called “mad cow disease”
very worrisome
MAD COW DISEASE
identified in 1986
began striking cows in Great Britain
causing them to became uncoordinated and unusually apprehensive
source was traced to a food supplement that included meat and bone meal from dead
sheep
The methods for processing sheep carcasses had been changed in the late 1970s
British government banned the use of animal-derived feed supplements in 1988, and
the epidemic has probably peaked
HUMAN PRION DISEASE
human prion diseases are more obscure
1) Kuru
2) Creutzfeldt-Jakob disease
3) Gerstmann-Strussler-Scheinker disease
4) Fatal Familial Insomnia
KURU
has been seen only among the Fore highlanders of Papua New Guinea
natives call it the "laughing death."
individuals become afflicted with a fatal disease marked by
loss of coordination
dementia
The affected individuals probably acquired kuru through ritual cannibalism
natives reportedly honored the dead by eating their brains
The practice has since stopped and kuru has virtually disappeared
CREUTZFELDT-JAKOB DISEASE
occurs worldwide
becomes evident as dementia
strikes one person in a million
typically around age 60
10 to 15 percent of cases are inherited
a small number of cases has been transmitted by
corneal transplantation
implantation of dura mater
electrodes in the brain
use of contaminated surgical instruments
injection of growth hormone derived from human pituitaries
GERSTMANN-STRUSSLER-SCHEINKER DISEASE
manifest as loss of coordination
signs of damage to the cerebellum
usually inherited
typically appear in midlife
FATAL FAMILIAL INSOMNIA
manifest as
dementia
difficulty sleeping
usually inherited
typically appear in midlife
was discovered only recently
EMERGING INFECTIONS
"new, or drug-resistant infections whose incidence in humans has increased or whose
incidence threatens to increase "
"environmental changes probably account for most emerging diseases”
changes wrought by urbanization
changes wrought by travel
emergence of AIDS
may reflect changes in urbanization and travel that have allowed rapid spread of a
sexually-transmitted infection throughout the world
It can be assumed that other diseases may also emerge in the coming decades
by the year 2025, it is estimated that 65% of the human population will live in cities
Emerging infections are often the result of an initial trans-species transmission event
“Zoonosis”
followed by viral replication and spread in the new host
Most such infections involve RNA viruses
have a higher rate of mutation than DNA viruses
GENE (VIRAL) THERAPY
Viruses can be used to introduce copies of their genetic information into animal cell
genomes
may prove useful to incorporate new genes into animal cells
replace a defective gene that is responsible for a disease condition
with a good copy of that gene
The virus would serve as a vector for the gene therapy
the virus is genetically modified so that it is incapable of replication itself
DNA VACCINES
most recent development in vaccine technology is the use of DNA expression vectors
as vaccines
inject a purified preparation of a DNA vector into which the gene for a protective antigen
has been cloned
DNA molecules are taken up by a few host cells
the DNA is then translated into the antigenic protein
which is then "recognized" by the immune system
experimental DNA vaccines against hepatitis have been shown to be very effective
DNA vaccines are administered by delivery of gold particles coated with the purified
DNA
The particles are physically driven into the skin with a blast of air under high pressure
MANTOUX TEST
a test for tuberculosis (TB)
injection of tuberculin
a protein derived from the tubercle bacillus
or a purified protein derivative of tuberculin
If the patient is (or has been) infected with tuberculosis a positive reaction occurs at the
site of the injection within 48 to 72 hours
tuberculin
being a 'foreign protein' recognized by the body of a person who has experienced TB
evokes a delayed immune response
in the form of a raised, red, itchy swelling
The reaction may also be positive in a person who has previously been immunized
against the disease by a vaccine
A negative response is certain proof that the individual concerned has not had TB and
has no immunity to it
END VIRUS