CLASS: 10:00 – 11:00
DATE: October 29, 2010
PROFESSOR: Dokland
I.
II.
III.
IV.
DNA Viruses
Scribe: Adam Baird
Proof:
Page 1 of 7
INTRODUCTION TO DNA VIRUSES [S1]
a. Today’s lecture is on DNA viruses. This will be the only lecture on DNA viruses, so this lecture will provide a
general overview of viruses with DNA genomes, particularly those that have relation to or include human
pathogens.
b. Today’s lecture should provide an understanding of the specific challenges (and advantages) that viruses
with DNA genomes have (as opposed to RNA genome). Today’s lecture will also introduce the solutions that
the viruses have found to these specific challenges.
c. Ultimately, today’s lecture will show how these solutions and mechanism affect the mechanisms of the
viruses.
THE FAMILIES OF DNA VIRUSES [S2]
a. This chart is (more or less) an exhaustive list of the recognized families of viruses with DNA genomes.
b. Notice the division into three groups.
1. The largest group is those with double-stranded DNA genomes.
2. The smaller group is those with single-stranded DNA genomes.
3. The “special” group is those with DNA-RNA hybrid genomes. These replicate by a unique
mechanism involving reverse transcription. (This won’t be discussed any further though.)
c. Notice the families that are highlighted in red. These are the families that include members that infect
humans. There are some important human pathogens; there are adenoviruses, herpes viruses, etc.
d. Most of these families include viruses that do not infect humans though. Most of families include viruses that
infect bacteriophages.
e. The first group, the caudovirales, includes the most abundant biological entities on the planet with an
estimated 1031 individual viruses. If you were to take just a milliliter of seawater from anywhere on the planet,
you’ll find about 1 – 10 million of these viruses.
f. DNA viruses are the most abundant “organisms” on the planet (if you include viruses as organisms).
g. Some of these families include viruses that only infect insects.
h. Notice the families that are bold. These are the families that infect mammals, but not humans. It’s not too far
of a stretch to imagine that in the future, human pathogens may arise out of these families as well.
DNA VIRUSES [S3]
a. DNA viruses come in a range of size and complexity.
1. One end of the scale is the circovirus, which are about as simple as a virus can get. They have
single-stranded DNA genome with only 1.7 kb encoding for just 2 genes. One of these genes, of
course, must be the capsid protein. It’s important to note that each virus encodes at least one gene
for a capsid protein (a structure protein); that’s what makes it a virus (as opposed to a plasmid). They
are only 17 nm in capsid diameter – about as small as virus can get.
2. A more typical DNA virus is the adenovirus. It has 30 – 38 kbp encoding for 30 – 40 genes. It is
about 90 – 100 nm in capsid diameter. Compare this to the largest RNA virus, coronavirus, which is
smaller than the adenovirus. On average, the RNA viruses are smaller than DNA viruses; size is
related to the properties of the genomes itself.
3. The other end of the scale is the mimivirus. This virus has a genome of 1.2 Mbp encoding for 911
genes. They are 600 nm in capsid diameter. Compare this to the simplest cell, mycoplasma, which
has genomes that are only half as large as the mimivirus. So the mimivirus actually rivals and even
surpasses the size and complexity of many cells. Of course, like all viruses, the mimivirus does
depend on a host cell for its replication (since it lacks the ability to do it on its own).
DNA VS. RNA VIRUSES [S4]
a. DNA usually forms a double helix, which is rigid and chemically very stable. RNA is usually single-stranded,
although it tends to also form secondary structures with regions of double-stranded RNA. RNA is quite
flexible and is chemically less stable than DNA.
b. Importantly, RNA replication is very error-prone. DNA replication is very accurate. This is one of the main
reasons why DNA viruses can generate much larger genomes. RNA genomes would start accumulating too
many errors to effectively replicate; but this is also a strength to the RNA virus, as it provides variation that
allows it to respond to the environment or the immune system over time.
c. Another important consideration is that viral DNA (any other DNA) is not recognized as foreign by the cell,
and is in fact protected by the cell. RNA (particularly double-stranded RNA) is recognized by the cell as
foreign and is actively degraded by the cell. Double-stranded RNA is an intermediate in all replication of RNA
viruses. This means that RNA viruses must protect their genome at all times from being attacked by the cell.
RNA viruses have elaborate mechanisms to evade the cell’s degradation methods.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: October 29, 2010
Proof:
PROFESSOR: Dokland
DNA Viruses
Page 2 of 7
d. All of these properties have a bearing on the life cycle of the virus. Viral DNA is generally always packaged
into pre-formed virus capsid. It will make a capsid and then put the DNA in side. RNA viruses usually coassemble their genome together with a capsid protein.
V.
TYPICAL DNA VIRUS LIFE CYCLE [S5]
a. Here is the general overview of a typical DNA life cycle.
1. The virus enters the cell by some mechanism (like endocytosis, direct fusion, or some other
mechanism to cross the cell membrane).
2. Once the DNA is inside the cell, it then has to get into the nucleus (because that’s where replication
and transcription machinery is found).
3. Once in the nucleus, the genome will get replicated and transcribed. Proteins are always produced in
the cytoplasm, so this involves the typical cellular process of exporting the RNA, making the protein,
and then importing the proteins back into the nucleus.
4. Usually, most groups of DNA viruses will then assemble their capsid inside the nucleus.
5. The final step is getting out of the cell. The simplest way to do that is simply to lyse the cell. Other
viruses are exported through some other mechanism (like budding from the surface, secretion by
other cellular mechanisms, etc.)
VI.
DNA VIRUS LIFE CYCLES [S6]
a. The cell protects the DNA. Once you have the DNA in the cell, it’s not a problem; it can get transported into
the nucleus by the cellular machinery.
b. One important thing to note: since DNA is the normal genetic material of the cell, the DNA viruses can use
the regular replication and transcription machinery already found in the cell. However, since the cell does not
typically replicate RNA, all RNA viruses have to code an RNA polymerase for its replication. DNA viruses do
not need that (although some DNA viruses produce their own DNA polymerase anyway
c. Most DNA viruses replicate in the nucleus, although there is an exception to that, which will be discussed
later.
VII.
SPECIFIC CHALLENGES FOR DNA VIRUSES [S7]
a. Having a DNA genome has its advantages, but it certainly has its challenges as well.
1. DNA viruses may require infection of actively growing cells.
a. Most cells do not actively replicate their genome all the time; they only replicate in DNA in the
S Phase of the cell cycle. Many cells are frozen in the G1 Phase of the cell cycle (which is
before DNA replication). That means that the cells are not producing the proteins required for
DNA replication; if no replication occurs, then the virus cannot replicate either. There are few
solutions to that challenge. Some viruses, the simpler viruses, have to infect cells that are
already actively replicating (like blood cells, epithelial cells, etc.). Other viruses will produce
proteins that will actively promote the transition of the cell into the S Phase. For that very
reason, certain viruses will bring their own proteins.
2. Another strategy that DNA viruses use is viral latency. This means that they will stay quiescent in the
host cell for a long period of time (sometimes years) as a plasmid in the nucleus (as in the case of
herpes viruses) or as a integration into the genome (as in the case of papilomavirus) that will
possibly be reactived when the cell transitions into the S Phase.
VIII.
GETTING ACCESS TO THE CELLULAR DNA REPLICATION MACHINERY [S8]
a. In most cases, these viruses need to get into the nucleus. The nucleus has its own machinery for
importing/exporting proteins and nucleic acids. They have nuclear pore complexes, which most viruses will
utilize these to get their genomes into the nucleus. There are few possible strategies here.
1. In some cases, the whole virus can enter intact into the nucleus. Only for the smallest viruses
(maybe less than 50 nm in size) can do this though.
2. Otherwise, the virus will disassemble in the cytoplasm and then use the cellular import machinery to
import the DNA or DNA-protein complex into the nucleus.
3. Other viruses will actually dock at the nuclear envelope and actively inject their DNA into the nucleus
(with a mechanism very similar to bacteriophages infecting bacterial cells). See the picture in the
bottom right-hand corner.
4. The final strategy is to not go into the nucleus at all, which is used by some viruses.
IX.
DNA REPLICATION [S9]
a. Let’s have a brief review of DNA replication.
b. DNA replication requirements:
1. A template - The DNA that will be replicated. In this case, the template would be viral DNA.
2. DNA polymerase – The protein that carries out replication.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: October 29, 2010
Proof:
PROFESSOR: Dokland
DNA Viruses
Page 3 of 7
3. A primer – DNA polymerase is unable to start copying DNA on a naked single-strand of DNA; they
need a primer. So the cell makes a small piece of RNA and then continues DNA replication from that
primer. Then the primer is subsequently removed.
4. Accessory proteins – Like helicase, RNA nuclease, primase, single-stranded binding protein.
c. It’s important to note that DNA replication is unidirectional. It will only go from 5’ to 3’. When you have
replication at the replication fork (like the picture on the top right-hand side), one strand can be continuously
copied in a straight line (called the “leading strand”) and one strand has to be copied in small, discontinuous
steps (called the “lagging strand”). On the lagging strand, new primers must keep being made, and then new
fragments must be made, and finally the primers must then be removed and joined together afterwards.
d. Viruses may use the exactly the same mechanism. They may have leading strand synthesis and lagging
strand synthesis and they may use RNA primers. Some viruses, however, may not use RNA primers and may
use their own DNA hairpin structures or terminal proteins attached to the genome as a primer instead.
e. If you have a linear genome (like the picture on the bottom right-hand side), and you replicate the genome,
you would be left with a primer at each end. When you remove that primer, you have a piece of singlestranded DNA at the end, which cannot be replicated (because there is no way that a primer can be placed
with it). The single-stranded DNA, then, may get degraded. Unless this complication is fixed, the DNA
genome will continually get shorter and you will eventually run out of genome, especially for a virus.
1. Eukaryotic cells (which do have linear chromosomes) encode telomerase, which fill in the ends of the
strand, keeping it intact.
2. Prokaryotic cells have circular genomes, so there is no end (and they don’t have to worry about this
complication).
3. Many viruses also have circular genomes, but other viruses use different strategies than the
prokaryotic cells. Some viruses have a special protein attached to the end, which serves as the
primer, so there is no single-stranded left behind at the end.
X.
SMALL, ssDNA VIRUSES: PARVOVIRIDAE [S10]
a. We’ll now talk about a few different groups of viruses.
b. The parvoviridae, or the parvoviruses, are single-stranded DNA viruses with a genome of about 5,000
nucleotides that code for only a few proteins (and one of those proteins being the capsid protein, which are
very small). There are 60 copies of capsid protein. It’s about as simple as a virus can be.
c. The bottom pictures show what the virus look like (in a reconstruction and in a micrograph).
d. There are many species of parvoviruses that infect various animals (like dogs, cats, etc.). The feline
parvovirus is a common problem.
e. There is only one important pathogen in humans, with is the B19 erythorovirus, which causes the “fifth
disease”, a traditional childhood disease.
f. The genome of the parvovirus has a unique structure with hairpins at the end. (See the top picture.) By
having this hairpin, the parvovirus can prime its own replication.
XI.
ERTHEMA INFECTIOSUM (FIFTH DISEASE) [S11]
a. This is a picture of erythema infectiosum, or “fifth disease”. It’s basically a rash. It generally causes a fever. It
clears in 1 – 2 weeks.
b. The rash is cause by the immune response (unlike chicken pox, for example, where the rash is actually the
virus being produce in the skin).
c. In children, it’s not typically a problem. In adults, it can lead to a more severe disease because adults have a
more robust immune response.
d. B19, like other parvovirus, is very simple. It has to replicate in actively growing cells, and in this case,
replication occurs in erythroid precursor cells (bone marrow).
XII.
PARVOVIRUS LIFE CYCLE [S12]
a. This is the life cycle of parvovirus. It is very simple.
1. Enter the cell via endocytosis.
2. Get into the nucleus.
3. Replicate the genome.
4. Assemble the capsids.
5. Exit the cell (via lysis of the cell).
XIII.
PARVOVIRUS REPLICATION [S13]
a. The genome replication is an interesting and unique mechanism. The genome has complementary ends that
can form hairpin structures at both ends of the genome. So, a hairpin structure will then serve as a primer,
eventually leading to replication in the 5’ to 3’ direction all the way to the other hairpin structure to the end.
Then, a viral protein (one of the three proteins) will form a nick on the other side, which will then serve as the
primer for the replication of the other end. Ultimately, the whole structure is “resolved”, and a copy of the
genome is made.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: October 29, 2010
Proof:
PROFESSOR: Dokland
DNA Viruses
Page 4 of 7
XIV.
PAPOVAVIRUSES: POLYOMA AND PAPILLOMAVIRIDAE [S14]
a. Other important groups of viruses (grouped together under papovaviruses) are polyomaviruses and
papillomaviruses.
b. These are relatively small, naked (non-enveloped) viruses formed by 72 pentamers (forming a structure seen
in the pictures).
c. Both families have similar genomes. They both have circular, double-stranded DNA. Although, the
papillomaviruses are somewhat larger and more complex.
d. Polyomaviruses:
1. VP1 is the capsid protein.
2. Encodes a couple of other proteins that are very important. The Large T antigen, specifically, is a
regulatory protein that has the ability to transform cells (promote their growth and potentially turn it
into a cancerous phenotype, although it doesn’t usually do this in humans).
e. Papillomavirus:
1. One of the few viruses that are commonly involved in human cancers (particularly cervical cancer).
2. It has much of the same structure as polyomaviruses though. It has a few more proteins though,
many of which are involved in promoting the oncogenic phenotype.
XV.
POLYOMAVIRUS REPLICATION [S15]
a. Replication of the polyomavrius basically follows the same replication as most other DNA.
b. It has a circular DNA.
c. It will proceed through 2 replication forks using RNA primers, DNA polymerase (from the cell), leading strand
synthesis and lagging strand synthesis. It is finally copied it in both directions, resulting in two copies of the
genome.
XVI.
LIFE CYCLE OF POLYOMAVIRUS [S16]
a. The important thing to note is that the Large T antigen has two main roles:
1. Recruitment of DNA polymerase to the replication origin. The fate of a polyomavirus actually
depends on the Large T antigen, which is specific to the cell type being infected. Depending on the
cell type, the polyomavirus may enter into one of two possible cycles: the “productive cycle”, where
viruses are produced, and the “transforming cycle”. Which cycle it enters depends on the Large T
antigen. (Very important note: In order for the virus to replicate, the cell has to be in the S Phase.)
a. If the virus infects a permissive cell (as in permissive for growth), it will produce great
amounts of the Large T antigen, the DNA polyemerase will then be recruited to the origin, the
DNA will be replicated, more of the virus will be produced, and the cell lyses – hopefully the
immune system will take care of it.
b. However, if it enters into a cell that is non-permissive (as in non-permissive for growth), the
production of Large T antigen will promote the transition of the cell into S Phase, thus
promoting the replication of the virus. The production of Large T antigen is not high enough to
directly promote the transition into S Phase, so in some cases, the virus integrates into host
cell genome. So it will be sitting there constantly producing low amount of Large T antigen,
which ultimately may lead the transformation of the cell into a cancerous phenotype. That
doesn’t normally happen for polyomaviruses in human cells (although there are examples of
this in other cell types).
XVII. PAPILLOMAVIRUS INFECTION [S17]
a. Papillomaviruses have a similar mechanism to the polyomaviruses, although it is a little more complex.
b. Papillomaviruses can infect the skin (can lead to warts). It is normally cleared by the immune system over
time, although it may take quite a long while.
c. The virus will settle in the granular layer. The stimulation of cell growth here is what causes warts.
d. If this virus integrates into the genome and sets up a continuous production of E6 and E7 oncogenes, they
will inactivate tumor suppression genes, which may lead to transformation of the cell (a common cause of
cervical cancer).
XVIII. ADENOVIRUSES [S18]
a. We’re now looking at increasingly complex viruses now.
b. Adenoviruses are probably the largest non-enveloped viruses that infect humans. The pictures show what it
looks like.
c. It is about 90 nm in diameter. It has a genome of 30 – 38 kbp.
d. It is a linear genome. It has a terminal protein that is covalently attached to the 5’ end of the genome (which is
important for its replication).
e. It also encodes it own DNA-dependent DNA polymerase. (It does not use the host’s DNA polymerase.)
XIX.
ADENOVIRUS DISEASE [S19]
a. Adenoviruses are relatively common in humans.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: October 29, 2010
Proof:
PROFESSOR: Dokland
DNA Viruses
Page 5 of 7
1. 5 – 10% of respiratory disease in children
2. Worldwide and non-seasonal (can occur any time of the year)
3. Variety of strains, some of which cause different disease.
a. Acute Respiratory Disease (ARD) is a common problem in military settings due to crowded
quarters.
b. Conjunctivitis (also known as “shipyard eye”) is another common disease.
c. Other strains may lead to gastroenteritis.
4. Symptoms include high fever, sore throat, aches, conjunctivitis, etc.
b. The virus enters in through the epithelia, respiratory tract, gastrointestinal tract, urinary tract, etc. and sets up
an infection, possibly spreading to lymphoid tissues and persists there for a long time (meaning that it will
continually produce the virus over that time).
c. It may be transmitted through respiratory or oral route. Because it is a non-enveloped virus, it is a resistant
virus. If you put some adenovirus on a doorknob, for example, it may survive there for a very long time. It is
resistant to inactivation by acid (like in the stomach), dehydration, and detergents.
d. Military recruits used a vaccine against adenovirus, but it was discontinued in 1996 (which actually led to a
spike of adenovirus in the military).
XX.
ADENOVIRL CONJUNCTIVITIS [S20]
a. Picture showing adenoviral conjunctivitis.
b. A risk factor is irritation of the eye.
XXI.
ADENO NUCLEAR ENTRY [S21]
a. “This isn’t important. Let’s skip it.”
XXII. ADENOVIRUSES USE A 5’ TERMINAL PROTEIN TO PRIME DNA REPLICATION [S22]
a. Adenoviruses replicate in a unique way, called “displacement synthesis”.
b. Here is picture of it.
c. It gets around the problem of having the single-stranded ends that cannot be replicated at the end of the
replication cycle.
d. The DNA polymerase is recruited to the end of the genome. It will start on the terminal protein (as shown in
yellow on the picture) and will start replicating from 5’ to 3’. This will displace the other strand. The singlestrand will be protected by a DNA-binding protein (produced by the virus).
XXIII. HERPESVIRUSES [S23]
a. Among the most complex viruses that infect humans
b. They are quite large, 120 – 230 kbp coding for at least 70 – 150 genes.
c. They have a icosahedral nucelocapsid core surrounded by tegument. On the outside of the tegument is the
envelope, which contains a number envelope glycoproteins.
XXIV. HERPESVIRUS DISEASE [S24]
a. There are a variety of human pathogens, commonly divided into alpha-, beta-, and gammaherpesviruses.
b. Alphaherpesviruses
1. Include herpes simplex viruses (probably the most well-recognized of these viruses).
2. Include varicella-zoster virus, which causes chickenpox in children and shingles in adults.
3. The viruses infect mucosalepithelia and cause apoptosis, lysis of the cell, fusion of the cell, etc.
4. It may move into the neurons too, where it enters a latent stage (which is very typical of herpes
viruses).
c. Betaherpesviruses
1. Cytomegalovirus is a very important virus. It is common cause of birth defects.
d. Gammaherpesviruse
1. Epstien-Barr virus infects cells of the immune system and may undergo latency in those cells as well.
XXV. HERPESVIRUS LIFE CYCLE [S25]
a. The herpesvirus life cycle is a complex, multi-stage process.
b. It can typically be divided into three phases.
1. Step 1 (Immediate Early)
a. After infection, the nuclear capsid goes to the nuclear envelope and injects the DNA into the
nucleus, which starts Step 1.
b. The protein expressed here are transcription factors, which are involved in the promotion and
expression of additional viral proteins, which leads into Step 2.
2. Step 2 (Early)
a. The early genes include DNA polymerase and other genes and proteins involved in DNA
replication.
b. The virus will set up a “nuclear factory”, which is where it will carry out all of the DNA
replication and assembly.
CLASS: 10:00 – 11:00
DATE: October 29, 2010
PROFESSOR: Dokland
XXVI.
XXVII.
XXVIII.
XXIX.
XXX.
XXXI.
XXXII.
XXXIII.
XXXIV.
XXXV.
Scribe: Adam Baird
Proof:
Page 6 of 7
DNA Viruses
c. The replication of the genome leads to the Step 3.
3. Step 3 (Late)
a. Synthesis of structural genes (the ones that will be used to form the variant itself).
b. Assembly occurs in this stage; very complex and not even fully understood. It involves
assembly of the nuclear capsid. The DNA is packaged into the nuclear capsid. The nuclear
capsid buds through the nuclear envelope, entering the cytoplasm, heads toward the
assembly site, where it will acquire it integuments and envelope. Eventually it buds and is
released into the cell.
c. One common problem with herpesviruses is that it can spread directly from cell to cell,
avoiding the immune system (the B Cells can’t clear the virus). T Cell-mediated mechanisms
are required to clear it.
ASSEMBLY & DNA PACKAGING IN HERPESVIRUSES RESEMBLE TAILED dsDNA BACTEROPHAGES
[S26]
a. The replication of the herpesvirus genome follows the “rolling circle mechanism”. So the genome itself is
circular. When it’s time to replicate, it will form a nick on the leading strand (left picture) and will then
synthesize the lagging strand (right picture). It will then roll out a continuous string of linear DNA that contains
20 – 40 genomes all stuck together, which will then form the template for DNA packaging. It will dock at the
nucleus, get packaged in, sent of by terminase, and then packaged into a new capsid. This mechanism is
actually very similar to the mechanism in bacteriophages. In many ways then, herpesviruses can be
considered a DNA bacteriophage.
VIRAL LATENCY [S27]
a. Remember that latency is not persistence.
b. Latency means that no virus is produced. In the case of herpesvirus, after productive infection, the virus will
enter into a stage of latency (like the alphaherpesviruses). It will go into the nucleus and leave its DNA there
in the form of plasmid that will remain there for a long time. But because it’s in a latent stage, there will be no
virus production.
c. Persistence means that there is a constant production of virus from some remote site.
d. The viral genome may remain latent for a long time, until the immune system of the host compromised, and
then it will spread back out to its peripheral sites and begin a new productive cycle. This is what shingles (in
adults) does.
CYTOPLASMIC DNA VIRUSES: THE EXCEPTION TO THE RULE [S28]
a. Remember: most DNA replicates in the nucleus. But there are some viruses that replicate in the cytoplasm.
We can lump them together as cytoplasmic DNA viruses. The most important one (from the human
perspective) is poxviridae, which causes smallpox.
b. Since these viruses replicate in the cytoplasm, where there is no DNA polymerase or RNA polymerase, it
must be able to be self-replicating. Because of this, these viruses are usually large and complex.
c. The will set up a “viral factory” in the cytoplasm to do this.
d. These viruses are very specific to their host cells. Many of these other poxviruses usually infect only their
main hosts. Some can infect humans, but fortunately it cannot spread, so all the virus will cause is localized
lesions.
THE POXVIRUSES [S29]
a. Poxviruses are the most familiar to most people. Vaccinia virus (cowpox) is a unique brick-shaped variance
with multiple envelope layers. It has a circular genome with up to a few hundred thousand base pairs in size
with structural hairpins at the end.
POXVIRIDAE PHYLOGENY [S30]
SMALLPOX (VIRIOLA) [S31]
a. Smallpox is also pretty familiar. This was eradicated in the 1970s.
ORF (SHEEP AND GOAT POX) [S32]
REPLICATIN CYCLE OF VACCINIA VIRUS [S33]
a. Here is an overview of the replication cycle. It is very complex.
b. There are steps of uncoating to get the genome out. Everything takes place in the cytoplasm. The viral
factory where the viruses are assembled.
NO TITLE [S34]
a. This is a cell micrograph. The replication complex (viral factory) is shown. DNA is produced here.
b. The dark spots shown are the immature viruses being assembled. It starts off crescent-shaped, and then turn
into a round virus and will eventually acquired the cell envelopes, turning into the classic brick-shaped
variants.
DNA VIRUSES: THINGS TO CONSIDER [S35]
a. Summary.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: October 29, 2010
Proof:
PROFESSOR: Dokland
DNA Viruses
Page 7 of 7
b. Important! Study this.
c. What are the properties of DNA vs. RNA? How will those properties impact the replication process of the
virus?
d. How does it get into the cell? How does it get into the nucleus?
e. What does the virus need to replicate itself? (DNA viruses can use the replication machinery of the cell. RNA
viruses must bring their own polymerase.)
f. Cells only replicate their DNA during S Phase. What does the virus do about that? How does it deal with this?
Does it act like parvo? Does it act like polyoma?
XXXVI. LITERATURE AND RESOURCES [S36]
a. Some additional websites and literature that might be helpful.
[End 49:12 mins]