• range in
size from 20 nm (10-9 meters) to 250 nm.
• some of
the smallest bacteria - the chlamydia and mycoplasma almost as small as largest viruses, that they too can pass through filters
that retard 99% of the other bacteria.
• early 1900
diseases like foot-mouth-disease in cattle, some cancers (in animals) and yellow fever in humans caused by filterable viruses.
became permanently associated with this life form.
in 1915 & 1917.
however were not "seen" until the electron microscope was developed in the late 1930s.
• in 1935
- viruses could be CRYSTALLIZED like inorganic salts (table salt) and protein molecules.
• REPLICATE their genetic material, like all other life forms,
of nucleic acid polymers.
• UNABLE to grow and reproduce OUTSIDE OF A LIVING CELL.
absolutely dependent upon continued survival of hosts
nature of viruses presents a challenge for investigator who must not only grow virus but also be able to cultivate virus'
• With plant
and bacterial viruses possible to extract sufficient virus from infected host to do analysis.
were mainly COMPOSED OF PROTEIN AND NUCLEIC ACID.
• in 1931
use of fertilized hen's eggs to culture ( "petri dish”) some viruses.
• first use
of artificially cultivated viruses for vaccine production.
• many viruses
still grown on eggs - relatively inexpensive and techniques are well established
"Are you allergic to eggs?"
receiving a viral immunization; means that the virus were grown on eggs and that egg proteins (to which many people are allergic)
are present in the vaccine.
of electron microscope possible to study morphology of viruses.
• it was
quickly realized that the size and shape of an individual virus is a constant and distinguishing characteristic.
a virus's size and shape is always part of its description.
may consist of circles, ovals, long thick or thin rods, flexible or stiff rods and ones with distinctive heads and tail components.
viruses are around 20 nm in diameter and largest around 250 nm.
from all other life forms in that they can contain ONLY ONE FORM OF NUCLEIC ACID.
use RNA as their genetic material and other use DNA, but NEVER both.
acid polymer may either exist as DOUBLE STRANDED (DS) DNA or RNA or as SINGLE STRANDED (SS) DNA or RNA.
• Each of
these characteristics is a constant for a particular virus and is part of it description.
acid polymer may contain as few as 4 to 7 genes for very small viruses to 150 to 200 genes for very large viruses, some viruses
nucleic acid exists in more than one molecule.
• Some contain
a few enzymes,some contain none
• but no
viruses contain the large numbers of enzymes found even in smallest bacteria.
• A NAKED
virus - protein subunits that make up protective covering around viral genome (DNA),
subunits called CAPSOMERES, entire protein coat is called CAPSID.
• An ENVELOPED
virus - have a lipid-based membrane surrounding protein capsid, envelope partly composed
of cell membrane within which the virus replicated, contains proteins and carbohydrates. Proteins- mixture of host cell and virus.
All viruses are covered with a PROTEIN COAT.
coat mainly composed of a FEW TYPES of proteins of which there are many copies per virus;
protein subunits called CAPSOMERES, made so that they spontaneously come together (ASSEMBLE) in a PREDETERMINED way
- produce virus coat called CAPSID.
• All virus
contain important proteins type - ATTACHMENT PROTEIN or docking protein(ATTACH TO ITS TARGET CELL before entering
protein found on outer surface of virus so easy access with RECEPTOR SITES on target host cells.
proteins often called SPIKES, they can extend away from cell so as to better contact with
• in addition,
virus may contain small quantities of carbohydrate (glycoprotein).
• all viruses
- LIMITED HOST RANGE and even within a host they attach to and invade only those cells with the APPROPRIATE RECEPTOR
is result of same BASIC PRINCIPLE that controls all the other specific mechanisms of life: LIGAND/RECEPTOR BINDING SPECIFICITY.
and AIDS viruses only attack man (recently 1995 - first reports of a chimpanzee being infected with HIV reported).
lambda only attacks cells which contain receptor for binding sugar maltose.
virus can live in ducks, chickens, wild birds, pigs and humans.
Basic principle of viral infection of a given cell:
• if a cell's
OUTER SURFACE contains RECEPTOR to which a virus's ATTACHMENT PROTEIN can BIND, virus will be able to
invade and grow in that cell
• only applies
within RELATED SPECIES or to different types of cells within a host.
• For example,
lambda phage will only naturally invade a few species of Gram negative bacteria,
• but if
put a plasmid in a G- cell that contains the gene for the lambda receptor, then lambda can bind to and inject its DNA into
example is COMMON COLD VIRUSES.
are specific for the human UPPER RESPIRATORY TRACK - they contain appropriate AP for binding to receptors on cell membrane
of specialized cells in upper respiratory tract.
• Other viruses
that cause intestinal diseases only bind to certain receptors of cells in the intestine;
bind only to liver cell-receptors and cause hepatitis;
only bind to receptors on and live in nerve cells.
or DOCKING with the host receptor protein.
• Entry or
PENETRATION of the viral nucleic acid into the host cytoplasm.
• BIOSYNTHESIS of the viral components.
(MATURATION) of the viral components into complete viral units.
• RELEASE of the completed virus from the host cell.
• Some bacteriophage
among larger, more complex viruses.
• phage =
head, a tail, a tail plate and tail fibers
of host, long tail fibers WOUND AROUND TAIL, when presence of a suitable host sensed by phage tail fibers UNWIND and
extend out from tail plate, increasing area of potential contact with host
• tip of
tail fiber contains DOCKING PROTEIN. When one or more of these adsorption proteins contacts a RECEPTOR PROTEIN
on host, binds tightly to it, bringing remaining tail fibers quickly into contact with other receptor proteins on host, firmly
ATTACHING VIRUS TAIL to host outer wall.
sets in motion a series of events leading to phage lysozyme lysing hole in cell wall.
• tail fibers
contract forcing tail through into cytoplasm.
• DNA from
the head is injected host cytoplasm.
• in host's
cytoplasm viral DNA take over control.
a special nuclease fragmentation of host's DNA .
• viral DNA
produces enzymes and proteins which use host transcription and translation mechanism
to make new virus.
MANUFACTURE new phage components in large quantities in cytoplasm; proteins formed assist in maturation process.
• Many phage
components SELF ASSEMBLING in made so as to SPONTANEOUSLY assemble into certain PREDETERMINED forms or
shapes, - head, tail, tail fibers etc.
PHAGE completely assembled ready to begin another life cycle, cell is lysed or ruptured
phage released into environment!
TREATMENT/PREVENTION OF VIRAL DISEASES
• Major viral disease treatment factors:
1. No viral disease ever been CURED by medical treatment.
Viruses not susceptible to ANTIBIOTICS.
intracellular parasitic nature of viruses difficult to treat
• viral reproduction
occurs only inside living cells and mostly uses host cell’s own metabolic machinery to generate new virions,
task to find /develop drugs both:
to penetrate cell’s cytoplasmic membrane
selectively damage ONLY viral components.
drugs that disrupt a virus’ protein or nucleic acid synthesis as well as the host’s system an unacceptable option.
• How then
can viral infections be dealt with?
still most effective, weapon against viruses, immunization.
arousing a host’s evolved immunological defense against foreign antigens (e.g. specific viruses), prevents infection.
eliminated smallpox a human disease attempting to eliminate polio and measles.
strategy" works on viruses limited to Homo sapiens.
• Many viruses
survive in non-hominid reservoirs (e.g. influenza &, hantavirus).
• In these
cases strategy depends on reservoir(s), , mechanism(s) of dissemination to humans. The most common strategies used in this
continuous battle are:
1. Immunization of hosts with dead or attenuated
virus (e.g. flu, polio) or with genetically engineered (G.E.) antigens.
2. Immunization of hosts using cloned viral
DNA shot directly into host cells. Transcription and translation
of the viral DNA produces enough viral antigen to immunize the host.
3. Immunization of hosts using foods containing cloned viral genes that produce viral antigen(s). Hosts ingesting
the food/antigen become immune to the virus.
4. Immunization of humans and alternate hosts (e.g. pets and vets against rabies).
5. Minimize contact between humans and the natural reservoir(s) (e.g. Hantavirus & mice).
6. Minimize vector/human contact (e.g. mosquito/yellow fever).
of viral genetics grown with developing molecular biological strategies for dealing with viruses.
• none can
be said to cure an established viral infection, but, by minimizing virus load in infected individual,
or decrease spread of virus to new hosts (e.g. HIV from mother - fetus) and its damage to
• infected host.
Use of analogues that inhibit crucial viral enzymes.
- AZT and acyclovir specifically inhibit replication of genomes of HIV and Herpes
- Protease inhibitors inhibit HIV proteases that are required to form a functional
- Ribavirin blocks genome formation of several viruses.
Use of agents that block infection
- Amantadine blocks influenza penetration and uncoating.
- Monoclonal antibodies bind virus particles in blood which inactivating &
marking for destruction by immune cells.
- G.E. soluble receptors bind virions in blood/serum preventing reaching the
- All viruses require specific receptors, any virus can be treated this way
as long as receptor is known, cloned and produced in large quantities.
Use of agents that stimulate or enhance efficacy of host’s immune system
- Interferons (IL-2) kills viruses and activates T-killer cells.
- Cytokines stimulate killer T-cell production.
- Cytokines stimulate antibody production.
Physicians cautiously talk of a "CURE" for HIV through use of combinations
of above treatments.
idea - if combined attack can lower virion concentration sufficiently body’s
natural immunity can "clean up" remaining virus render host virus free.
Predictions of outcome not totally unreasonable to consider as in 1997.
Some neurological diseases are caused by protein infectious
particles (PRIONS). These include several animal and at least 3 human diseases. One of these diseases, KURU, infects its victims
when they eat the brain tissue of their enemies (a questionable activity at best). The best studied of these diseases is scrapies
in sheep. The disease entity seems to be composed completely of PROTEIN and to entirely lack any nucleic acid. This poses
a major problem given the significant role of DNA and RNA in life. Three theories are currently being considered to explain
1. That prions contain, as yet undetected nucleic acid. Extensive purification and testing using the
most sensitive methods available have failed to demonstrate any nucleic acid in purified, infectious prions.
2. that an unknown bacterium that is hard to cultivate and that passes through filters is responsible.
Again, there is no proof for such an organism.
3. That prions represent a type of protein that is able to convert a "normal" protein into a "prion protein".
This theory is currently the most popular and there is some evidence accumulating to suggest that it is valid. This theory
says that when the prion protein gets into the brain of a victim it binds to a normal or pre-prion protein and somehow converts
it into a prion; the new-prion then proceeds to convert other natural proteins. As the number of prions increase destruction
of the brain occurs, eventually killing the victim.
fall victim to agents composed of NAKED RNA that are only 300 to 400 nucleotides long, called VIROIDS. The evidence is conclusive that viroids cause plant diseases, but the mechanism of pathogenicity is not known. So
far NO HUMAN viroids have been discovered, but it is considered a real possibility that they exist.