Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Welcome to Principles of Biology. Thisbook was written by the Open Alternative Textbook
Initiative at Kansas State University and isbeing released as a podcast and distributed under
the terms of the Creative Commons AttributionLicense. Today's episode is chapter twenty eight
point three Viruses. All hyperlinks,images and sources can be found at the
(00:21):
link to the book. In thedescription that's the salubrious thing about zoonotic diseases,
they remind us, as Saint Francisdid, that we humans are inseparable
from the natural world. In fact, there is no natural world. It's
a bad and artificial phrase. Thereis only the world. Humankind is part
(00:42):
of that world, as are theebolaviruses, as are the influenzas and the
hivs. As are marburg and NAIPAand tsars, As are chimpanzees and palm
civets and Egyptian fruit bats. Asis the next murderous virus, the one
we haven't yet discovered, David quamminspilover animal infections and the next human pandemic.
Twenty twelve ina an electron micrograph showsthe tobacco mosaic virus, which is
(01:04):
shaped like a long thin rectangle photobeechshows an orchid leaf in varying states of
decay. Initial symptoms are yellow andbrown spots. Eventually the entire leaf turns
yellow with brown blotches, then completelybrown. A. The tobacco mosaic virus
seen by transmission electron microscopy, wasthe first virus to be discovered. B.
(01:30):
The leaves of an infected plant areshown credit A scale bar data from
Matt Russell. Credit Bee modification ofwork by USDA Department of Plant Pathology Archive,
North Carolina State University. No oneknows exactly when viruses emerged or from
where they came. Since viruses donot leave physical evidence in the form of
fossils. Modern viruses are thought tobe a mosaic of bits and pieces of
(01:53):
nucleic acids picked up from various sourcesalong their respective evolutionary pats. Viruses are
a cellular parasitic entities that are notclassified within any of the three domains because
they are not exactly alive, butthey do parasitize, evolve, reproduce,
and co evolve with other organisms.They inhabit a shadowy world that may not
(02:13):
be alive but is very close toit. They have no plasma, membrane,
internal organelles, or metabolic processes,and they do not divide. Instead,
they infect a host cell and usethe host's replication processes to produce progeny
virus particles. Viruses infect all formsof organisms, including bacteria, archea,
(02:34):
fungi, plants, and animals.Viruses are diverse. They vary in their
structure, their replication methods, andin their target hosts or even host cells.
They infect every type of organism known, from archea to bacteria to eukaryotes,
and are found in every environment.They are also remarkably abundant. It
(02:54):
is estimated that each millilead of seawater contains one hundred and seven virus both
DNA and RNA varieties. They aremajor players in the evolution of the life
forms on this planet. Genes derivedfrom viruses allab mammals to develop a placenta,
for example, how viruses replicate.Viruses were first discovered after the development
(03:16):
of a porcelain filter called the Chamberlainpast filter, which could remove all bacteria
visible under the microscope from any liquidsample. In eighteen eighty six, Adolph
Meyer demonstrated that a disease of tobaccoplants, Tobacco mosaic disease could be transferred
from a diseased plant to a healthyone through liquid plant extracts. In eighteen
(03:37):
ninety two, Dmitri Ivanowski showed thatthis disease could be transmitted in this way
even after the Chamberlain pastor of filterhad removed all viable bacteria from the extract.
Still, it was many years beforeit was proven that these filterable infectious
agents were not simply very small bacteria, but were a new type of tiny
disease causing particle virions. Single virusparticles are very small, about twenty to
(04:00):
two hundred and fifty nanimeters. Onenanometer equals one slash one zero zero zero
zero zero zero amm, although therecent discovery of entities called panderoviruses approximate one
micrometer or one slash one zero zerozero mm in diameter has shaken that paradigm
somewhat. Individual virus particles are theinfectious form of a virus outside the host
(04:21):
cell, unlike bacteria, which areabout one hundred times larger. We cannot
see most viruses with a light microscope, with the exception of the pandoraviruses and
some large vireons of the pox virusfamily. Figure. Relative sizes on a
logarithmic scale from zero point one nanometersto one m are shown. Objects are
(04:43):
shown from smallest to largest. Thesmallest object shown, an atom, is
about point one mm in size.A C sixty molecule or bucky ball is
one nanometer. The next largest objectsshown are lipids and proteins. These molecules
are between one and ten nanimeters.The influence of virus is about one hundred
(05:04):
nanimeters. Bacteria and mitochondria are aboutone m. Human red blood cells are
about seven m. Plant and animalcells are both between ten and one hundred
m. Pollen from a morning gloryflower and a human egg are between one
hundred m and one millimeter. Afrog egg is about one millimeter. The
size of a virus is very smallrelative to the size of cells and organelles.
(05:28):
It was not until the development ofthe electron microscope in the nineteen forties
that scientists get their first good viewof the structure of the tobacco mosaic virus
figure and others. The surface structureof virions can be observed by both scanning
and transmission electron microscopy, whereas theinternal structures of the virus can only be
observed in images from a transmission electronmicroscope. Figure two photos of the ebolavirus
(05:53):
are shown. PHOTOA is a scanningelectron micrograph. There are many three dimensional,
long, round ended viruses shown.PHOTOBE is a color enhanced transmission electron
micrograph. The viruses are the samesize and shape as in PHOTOA, but
here some internal structure can be seen. In longitudinal cross section. The Bola
(06:15):
virus is shown here as visualized throughA a scanning electron micrograph and B a
transmission electron micrograph. Credit A modificationof work by Cynthia Goldsmith CDC. Credit
B modification of work by Thomas W. Geisbert Boston University School of Medicine.
Scale bar data from Matt Russell.The use of this technology has allowed for
(06:38):
the discovery of many viruses of alltypes of living organisms. They were initially
grouped by shared morphology, meaning theirsize, shape, and distinguishing structures.
Later, groups of viruses were classifiedby the type of newclaic acid they contained
DNA or RNA, and whether theirnuclaic acid was single or double stranded.
(06:59):
More recently, molecular analysis of viralreplication cycles has further refined their classification.
Currently, virus classification begins at thelevel of order and proceeds to species level
taxonomy using the scheme. The termsin parentheses are the taxon suffixes for that
taxonomic level virus classification order virals,family, viridy, subfamily, verny,
(07:26):
genus, virus species usually xxx actsdisease virus, example, tobacco mosaic virus.
A virion consists of a nucleic acidcore, an outer protein coating,
and sometimes an outer envelope made ofprotein and phospholipids derived from the host cell.
The most visible difference between members ofviral families is their morphology, which
(07:47):
is quite diverse. An interesting featureof viral complexity is that the complexity of
the host does not correlate to thecomplexity of the vireon. Some of the
most complex virion structure are observed inbacteriophages, viruses that infect the simplest living
organisms. Bacteria. Viruses come inmany shapes and sizes, but these are
(08:09):
consistent and distinct for each viral family. Figure. All virions have a nucleic
acid genome covered by a protective layerof protein called the capsid. The capsid
is made of protein subunits called capsimaers. Some viral capsids are simple polyhedral spheres,
whereas others are quite complex in structure. The outer structure surrounding the capsid
(08:31):
of some viruses is called the viralenvelope. All viruses use some sort of
glycoprotein to attach to their host cellsat molecules on the cell called viral receptors.
The virus exploits these cell surface molecules, which the cell uses for some
other purpose, as a way torecognize and infect specific cell types. The
(08:52):
T four bacteriophage, which infects theColi bacterium, is among the most complex
virions known. Tephoor has a proteintail structure that the virus uses to attach
to the host cell and a headstructure that houses its DNA. Adenovirus,
a non enveloped animal virus that causesrespiratory illnesses in humans, uses protein spikes
protruding from its capsimirs to attach tothe host cell. Non Enveloped viruses also
(09:16):
include those that cause polio, poliovirus, plantar wortz, papillomavirus, and hepatitis
A hepatitis A virus. Non Envelopedviruses tend to be more robust and more
likely to survive under harsh conditions,such as the gut. Enveloped virions like
HIV, human immuno deficiency virus thecausative agent, and AIDS acquired immune deficiency
(09:39):
syndrome consist of nucleic acid RNA inthe case of HIV, and capsid proteins
surrounded by a phospholippid bilayer envelope andits associated proteins figure Chicken pox, influenza,
and mumps are examples of diseases causedby viruses with envelopes. Because of
the fragility of the envelope, nonenveloped viruses are more resistant to changes in
(10:01):
temperature, pH and some disinfectants thanenveloped viruses. Overall, the shape of
the vireon and the presence or absenceof an envelope tells us little about what
diseases the viruses may cause or whatspecies they might infect, but it is
still a useful means to begin viralclassification. An illustration shows bacteriophage T four,
(10:22):
which houses its DNA genome in ahexagonal head, a long straight tail
extends from the bottom of the head. Tail fibers attached to the base of
the tail or bent like spider legs. An adenovirus houses its DNA genome in
a round capsid made from many smallcapsimir subunits. Glycoproteins extend from the capsimir
(10:45):
like pins from a pincushion. TheHIV retrovirus houses its RNA genome and an
enzyme called reverse transcript tase in abullet shaped capsid. A spherical viral envelope
lined with matrix proteins surrounds the capsid. Glycoproteins extend from the viral envelope.
Viruses can be complex in shape orrelatively simple. This figure shows three relatively
(11:09):
complex virions, the bacteriophah T fourwith its DNA containing head group and tail
fibers that attach to host cells,adenovirus, which uses spikes from its capsid
to bind to the host cells,an HIV, which uses glycoproteins embedded in
its envelope to do so. Noticethat HIV has proteins called matrix proteins internal
(11:30):
to the envelope, which helps stabilizevirion shape. HIV is a retrovirus,
which means it reverse transcribes its RNAgenome into DNA, which is then spliced
into the host's DNA. Credit bacteriophageadenovirus modification of work by NCBI NIH credit
HIV retrovirus modification of work by NIIDNIH. Unlike all living organisms that use
(11:54):
DNA as their genetic material, virusesmay use either DNA or RNA as theirs.
The virus core contains the genome ortotal genetic content of the virus.
Viral genomes tend to be small comparedto bacteria or eukaryotes, containing only those
genes that code for proteins the viruscannot get from the host cell. This
(12:15):
genetic material may be single stranded ordouble stranded. It may also be linear
or circular. While most viruses containa single segment of nucleic acid, others
have genomes that consist of several segments. All of these features are used to
help classify viruses into orders, families, et cetera. DNA viruses have a
(12:37):
DNA core. The viral DNA directsthe host cell's replication proteins to synthesize new
copies of the viral genome and totranscribe and translate that genome into viral proteins.
DNA viruses cause human diseases such aschicken pox, hepatitis B, and
some venereal diseases like herpes and genitalwartz. RNA viruses contain only RNA in
(13:00):
their course to replicate their genomes inthe host cell. The genomes of RNA
viruses and code enzymes not found inhost cells. RNA polymerase enzymes are not
as stable as DNA polymerases and oftenmake mistakes during transcription. For this reason,
mutations changes in the nucleotide sequence inRNA viruses occur more frequently than in
(13:22):
DNA viruses. This leads to morerapid evolution and change in RNA viruses.
For example, the fact that influenzais an RNA virus is one reason a
new flu vaccine is needed every year. Rapid evolution results in new flu strains
being produced constantly in various parts ofthe world. Human diseases caused by RNA
(13:43):
viruses include hapatitis, measles, HIV, common cold virus, ebola, and
rabes. Steps of virus infections.Viruses are specialized parasites, usually only infecting
one type of cell or one typeof organism. A virus must take over
a cell to replicate. The viralreplication cycle can produce dramatic biochemical and structural
(14:05):
changes in the host cell, whichmay cause cell damage. These changes,
called cytopathic effects, can change cellfunctions or even destroy the cell. Some
infected cells, such as those infectedby the common cold virus rhinovirus, diethru
lysis bursting or apoptosis, programmed celldeath, or cell suicide, releasing all
(14:26):
the progeny virions at once. Thesymptoms of these viral diseases result from the
immune response to the virus, whichattempts to control and eliminate the virus from
the body, and from cell damagecaused by the virus. Many animal viruses,
such as HIV human immino deficiency virusleave the infected cells of the immune
system by a process known as budding, where virions leave the cell individually.
(14:50):
During the budding process, the celldoes non undergolysis and is not immediately killed.
However, the damage to the cellsthat HIV in may make it impossible
for the cells to function as mediatorsof immunity, even though the cells remain
alive for a period of time.Most productive viral infections follow similar steps in
the virus replication cycle. Attachment,penetration, encoding, replication, assembly,
(15:16):
and release. A virus attaches toa specific receptor site on the host plasma
membrane through attachment proteins and the capsidor proteins embedded in its envelope. The
attachment is specific, and typically avirus will only attach to cells of one
or a few species, and onlycertain cell types within those species with the
appropriate receptors. The nucleic acid ofbacteriophages is injected directly into the host cell,
(15:41):
leaving the capsid outside the cell.Plant and animal viruses can enter their
cells through endocytosis, in which theplasma membrane surrounds and engulfs the entire virus.
Some enveloped viruses enter the cell whenthe viral envelope fuses directly with the
plasma membrane. Once inside the cell, the viral capsid is degraded and the
(16:03):
viral nucleic acid is released, whichthen becomes available for replication and transcription.
Obviously, the naked DNA of abacteriophage is already available for transcription and replication
immediately after being injected. Into thebacterial cell. The replication mechanism depends on
the viral genome DNA or RNA.DNA viruses usually use host cell proteins and
(16:26):
enzymes to make additional DNA that isthen used to copy the genome or be
transcribed to messenger rona mRNA. ThemRNA is then used in protein synthesis.
RNA viruses, such as the influenzavirus, usually use the rona as a
template for synthesis of viral genomic RNAand mRNA. The viral mRNA is translated
(16:48):
into viral enzymes and capsid proteins toassemble new virions. Figure. The last
stage of viral replication is the releaseof the new virions into the host organism,
where they are able to infect adjacentcells and repeat the replication cycle.
Some viruses are released when the hostcell dyes, and other viruses can leave
infected cells by budding through the membranewithout directly killing the cell. The illustration
(17:12):
shows the steps of an influenza virusinfection. In step one, influenza virus
becomes attached to a receptor on atarget epithelial cell. In step two,
the cell engulfs the virus by endocytosisand the virus becomes encased in the cell's
plasma membrane. In step three,the membrane dissolves and the viral contents are
(17:33):
released into the cytoplasm. Viral morranaenters the nucleus, where it is replicated
by viral RNA polymerase. In stepfour, viral mRNA exits to the cytoplasm,
where it is used to make viralproteins. In step five, new
viral particles are released into the extracellularfluid. The cell, which is not
(17:56):
killed in the process, continues tomake new virus. In influence of virus
infection, glycoproteins attached to a hostepithelial cell. As a result, the
virus is engulfed. Ronan in proteinsare made and assembled into new virions lydic
in lysogenic pathways. Cell death maybe immediate or delayed after attachment and penetration
(18:19):
by the virus, for example,bacteriophages. Viruses that infect bacteria may or
may not kill their host immediately.There are two viral replication strategies. When
the virus kills the host cell itis called the lytic cycle, and when
the virus does not kill the host, but replicates when the host replicates.
It is called the lysogenic cycle.Figure. Viral replication strategies. The two
(18:44):
viral reproductive strategies, the lydic cycleand the lysogenic cycle lydic cycle. The
lytic cycle causes death of the hostcell, and the term refers to the
last stage of the infection, whenthe cell lyces, breaks open and releases
new virions that were produced within thecell. These new virions can infect healthy
cells and the cycle is repeated.Figure. So why haven't all the bacteria
(19:07):
in the world been destroyed by bacteriophages? The answer is natural selection of defense
mechanisms by bacteria. Mutations of bacterialsurface proteins that are not recognized by a
particular phage allow the bacteria to surviveby preventing attachment. Without going into detail,
bacteria have internal defenses that allow themto cut up viral DNA before it
(19:30):
can infect the cell. Then onemight ask why hasn't all the bacteriophages in
the world gone extinct by not beingable to reproduce Once again, the answer
is natural selection. Viruses mutate tobypass the defense mechanisms of the bacteria.
This illustrates that the parasite host relationshipis in a constant evolutionary duel. Similar
(19:52):
coevolutionary strategies characterize the interactions of virusesand animals or viruses and plants lysogenic cycle.
There is another reason why bacteria arenot extinct because of bacteriophages. Many
bacteriophages do not kill their host,but coexist within their host, and when
this occurs it is called the lysogeniccycle. After penetration, the viral DNA
(20:17):
or RNA can either be incorporated intothe host DNA, or the viral genome
can be a self replicating entity.Once this occurs, the viral genome is
replicated along with the host cell's DNA, but the virus does not destroy the
cell as it does in the lydiccycle figure. However, at some point,
the viral genes are turned on andcan trigger the virus to enter the
(20:37):
lydic cycle and kill the host cell. Figure. Cell starvation or cell damage
e g. From radiation may triggera lysogenic infection to turn into a lydic
infection, thereby killing the host cell. The next generation of viruses, depending
on the host cell condition, canease either of the viral replication strategies lysogenic
(20:57):
or lydic on the next hope.Most viruses and disease viruses cause a variety
of diseases in animals, including humans, ranging from the common cold to potentially
fatal illnesses like meningitis. Figure Thesediseases can be treated by antiviral drugs or
by vaccines, but some viruses,such as HIV, are capable of avoiding
(21:18):
the immune response and mutating so asto become resistant to antiviral drugs. The
illustration shows an overview of human viraldiseases. Viruses that cause encephalitis or meningitis
or inflammation of the brain and surroundingtissues include measles, arbivirus, rabes,
jc virus, and lcym virus.The common cold is caused by rhinovirus,
(21:42):
par influenzovirus and respiratori sin sitio virusI. Infections are caused by herpes virus,
adenovirus, and cytomegalovirus. Pharyngitis orinflammation of the pharynx, is caused
by adenovirus, exstein barvirus and cytomegalovirus. Paratitis or inflammation of the parotid glands
(22:03):
is caused by mumps virus. Gingevostomatitisor inflammation of the oral mucosa, is
caused by herpes simplex typeivirus. Pneumoniais caused by influenza virus TYPESA and B,
parinfluenza virus, respiratory sensitial virus,adinovirus, and SARS coronavirus. Cardiovascular
(22:23):
problems are caused by Coxackie B virus. Hepatitis is caused by hepatitis virus TYPESA,
B, C, D. NEmyelitis is caused by poliovirus an HLTV
one. Skin infections are caused byvirus allozostravirus, human herpes virus six,
smallpox molluscum, kintagiosum, human papillomavirus, parvovirus B nineteen, rubella measles,
(22:47):
and coxackieavirus. Gasterrenteritis or digestive diseaseis caused by adinovirus, rhodavirus, norovirus,
astrovirus and coronavirus. Sexually transmitted diseasesare caused by Herpie's simplex type two,
human papillomavirus and HIV. Pancreatitis Bis caused by Coxsackie B virus viruses
(23:11):
are the cause of dozens of ailmentsin humans, ranging from mild illnesses to
serious diseases. Credit modification of workby Michael Hackstrom. This podcast will be
released episodically and follow the sections ofthe textbook in the description. For a
deeper understanding, we encourage you reviewthe text version of this work voice by
(23:33):
voicemaker dot Ian. This was producedby Brandon Casturo as a creative Common Sense production.