VIROLOGY
INTRODUCTION
WHAT IS A VIRUS?
• Obligate intracellular parasites => viruses always need living cells to survive (energy
production, protein synthesis and reproduction)
• Virion = genome packed into lipid particles (‘like a seeds that comes alive when entering
the cell’ = obligate intracellular)
• Latency = ‘sleeping virus’ (herpes) => survival strategy. There are 2 possibilities for a
virus to be able to survive when it cannot directly infect another host:
o Be resistant (stay infectious for a very long time => not many viruses do this)
o Continuously infecting hosts with subclinical infections (you don’t even notice
you are infected so you will spread the virus) => many viruses are just
‘passengers’ and don’t cause disease because our immune system has learned
to deal with it (bell pepper, you excrete the viruses that are one it) = co-
evolution.
o Long lasting/chronic infections so when you are tired, stress, cold, sun
exposure,… you get the desease (herpes simplex) = latency
• Viruses provide a gene-pool
o By infecting cells, retroviruses copy their genome to double stranded DNA and
will insert their genomic material in the genome of the host, contributing to the
human genome. When they died virus not go one unless infection in germline
cells (transposable elements are genes we have acquired from viruses;
retrotransposons = from retroviruses)
o In population it is good because it creates variation (survival of the fittest = more
variation in genetic pool, some variation better adapted to a problem)
• There is variability in the genome of viruses
o They don’t have a DNA-repair mechanism, thus most of the replication have a lot
of mutation resulting in a virus that cannot infect = junk-viruses.
o The variability in virus genome is important to be able to evade immune system
host (= survival of the fittest) !!!
• Viruses are very small 50-100 nm
1
, o Electron microscopy
• Viruses differ in structure, but minimal components: (very small viruses don’t fit a big
genome: only codes for capsid protein, so they rely on the host genome for the rest) (all
viruses must ‘make’ mRNA to make proteins they used host ribosomes)
o Genome: can be dsDNA/ ssDNA/ dsRNA/ ssRNA (ds = double stranded, ss = single
stranded) => + stranded RNA/ - stranded RNA
o Capsid protein = capsid/ shell around genome of virus for protection genetic
material and bind receptor on a living cell (misusing that receptor by the virus)
o Capsid + genome = nucleocapsid = virion
▪ Additional structure can be envelope = membrane stolen from the
infected cell
o All viruses have capsid proteins, but not all of these form a very stable crystal like
capsid structure!!!
o Virion + things that come to expression when a virus infects a cell = virus
• Some viruses also have a lipid envelope
o Lipid envelope is not encoded in genome
o Lipid envelope/membrane ‘stolen’ from eukaryotic cell (membrane of cell/ ER/
GA)
o Viruses don’t only rely on host cell for lipid envelope but on a lot of things: energy
production, protein synthesis, reproduction
• !!! Bacteria replicate exponentially (they divide) while viruses don’t!
2
, o First viruses do Brownian movement. (bacteria has flagella and goes in a specific
direction), viruses move randomly
o Different phases of virus replication: starting with inoculation = inoculate virus to
a cell culture/human and viruses have capacity to bind to cells and enter it
(entery: genome released) and this can result in infection
o By chance the virus binds to receptor of cells
o Virus in internalized in the cell and degraded in a controlled manner so the
genome can be released. With replication and translation, new virus particles can
be produced.
o New virus particles are released (gradually or in a burst)
• All RNA viruses high mutation rate because no proofreading
• DNA viruses use enzym of infected cell to proofread (polymerase)
•
o RNA virus (They have smaller genome) many errors has 2 consequences
▪ If genome is to big they cannot replicate correctly
▪ Create a variety of viruses by the mistakes => most of them not functional
but some do and are than dangerous and infect other species
▪ Quasispecies = when mutation rate is so high that you can’t see what the
original was
o DsDNA stable not much variance
o Strategy to escape immune system: to most easy way to do is like RNA viruses is
to change a lot
• Are viruses dead or alive?
3
, o => dead: they cannot produce their own energy (no carbon metabolism) & they
cannot reproduce/ evolve by themselves (obligate intracellular) & there are no
ancestral viral lineages: no single gene has been identified that is shared by all
viruses & viruses don’t have a structure derived from a common ancestor (like
cells are all derived from a common ancestor cell because there is ‘membrane
heridity’: during cell division, cells obtain membranes from other cells.)
ORIGIN OF VIRUSES
• There are 3 scenarios for the origin of viruses:
o Primordial virus world/ virus early hypothesis: the whole world started with DNA
floating around that could replicate
▪ Viruses are direct descendants of the first replicons that existed during
the pre-cellular stage of the evolution of life. Cells (protocells) did not
exist yet, replicate system was able to make copies. Not with formal
structure that contained these processes
o Escaped genes hypothesis: some genes where present in ancestor cells/ bacteria
and just escaped from cells.
▪ Viruses are the ultimate products of degeneration of ancestral cells that
lost their autonomy and transitioned to obligate intracellular parasitism
(e.g. giant viruses). During the early cell life, some split of as viruses. This
theory became a thing again when large viruses were found.
o Reductive virus origin/ regression hypothesis: viruses are remnants of a degraded
cell: it needed another cell to replicate.
4
INTRODUCTION
WHAT IS A VIRUS?
• Obligate intracellular parasites => viruses always need living cells to survive (energy
production, protein synthesis and reproduction)
• Virion = genome packed into lipid particles (‘like a seeds that comes alive when entering
the cell’ = obligate intracellular)
• Latency = ‘sleeping virus’ (herpes) => survival strategy. There are 2 possibilities for a
virus to be able to survive when it cannot directly infect another host:
o Be resistant (stay infectious for a very long time => not many viruses do this)
o Continuously infecting hosts with subclinical infections (you don’t even notice
you are infected so you will spread the virus) => many viruses are just
‘passengers’ and don’t cause disease because our immune system has learned
to deal with it (bell pepper, you excrete the viruses that are one it) = co-
evolution.
o Long lasting/chronic infections so when you are tired, stress, cold, sun
exposure,… you get the desease (herpes simplex) = latency
• Viruses provide a gene-pool
o By infecting cells, retroviruses copy their genome to double stranded DNA and
will insert their genomic material in the genome of the host, contributing to the
human genome. When they died virus not go one unless infection in germline
cells (transposable elements are genes we have acquired from viruses;
retrotransposons = from retroviruses)
o In population it is good because it creates variation (survival of the fittest = more
variation in genetic pool, some variation better adapted to a problem)
• There is variability in the genome of viruses
o They don’t have a DNA-repair mechanism, thus most of the replication have a lot
of mutation resulting in a virus that cannot infect = junk-viruses.
o The variability in virus genome is important to be able to evade immune system
host (= survival of the fittest) !!!
• Viruses are very small 50-100 nm
1
, o Electron microscopy
• Viruses differ in structure, but minimal components: (very small viruses don’t fit a big
genome: only codes for capsid protein, so they rely on the host genome for the rest) (all
viruses must ‘make’ mRNA to make proteins they used host ribosomes)
o Genome: can be dsDNA/ ssDNA/ dsRNA/ ssRNA (ds = double stranded, ss = single
stranded) => + stranded RNA/ - stranded RNA
o Capsid protein = capsid/ shell around genome of virus for protection genetic
material and bind receptor on a living cell (misusing that receptor by the virus)
o Capsid + genome = nucleocapsid = virion
▪ Additional structure can be envelope = membrane stolen from the
infected cell
o All viruses have capsid proteins, but not all of these form a very stable crystal like
capsid structure!!!
o Virion + things that come to expression when a virus infects a cell = virus
• Some viruses also have a lipid envelope
o Lipid envelope is not encoded in genome
o Lipid envelope/membrane ‘stolen’ from eukaryotic cell (membrane of cell/ ER/
GA)
o Viruses don’t only rely on host cell for lipid envelope but on a lot of things: energy
production, protein synthesis, reproduction
• !!! Bacteria replicate exponentially (they divide) while viruses don’t!
2
, o First viruses do Brownian movement. (bacteria has flagella and goes in a specific
direction), viruses move randomly
o Different phases of virus replication: starting with inoculation = inoculate virus to
a cell culture/human and viruses have capacity to bind to cells and enter it
(entery: genome released) and this can result in infection
o By chance the virus binds to receptor of cells
o Virus in internalized in the cell and degraded in a controlled manner so the
genome can be released. With replication and translation, new virus particles can
be produced.
o New virus particles are released (gradually or in a burst)
• All RNA viruses high mutation rate because no proofreading
• DNA viruses use enzym of infected cell to proofread (polymerase)
•
o RNA virus (They have smaller genome) many errors has 2 consequences
▪ If genome is to big they cannot replicate correctly
▪ Create a variety of viruses by the mistakes => most of them not functional
but some do and are than dangerous and infect other species
▪ Quasispecies = when mutation rate is so high that you can’t see what the
original was
o DsDNA stable not much variance
o Strategy to escape immune system: to most easy way to do is like RNA viruses is
to change a lot
• Are viruses dead or alive?
3
, o => dead: they cannot produce their own energy (no carbon metabolism) & they
cannot reproduce/ evolve by themselves (obligate intracellular) & there are no
ancestral viral lineages: no single gene has been identified that is shared by all
viruses & viruses don’t have a structure derived from a common ancestor (like
cells are all derived from a common ancestor cell because there is ‘membrane
heridity’: during cell division, cells obtain membranes from other cells.)
ORIGIN OF VIRUSES
• There are 3 scenarios for the origin of viruses:
o Primordial virus world/ virus early hypothesis: the whole world started with DNA
floating around that could replicate
▪ Viruses are direct descendants of the first replicons that existed during
the pre-cellular stage of the evolution of life. Cells (protocells) did not
exist yet, replicate system was able to make copies. Not with formal
structure that contained these processes
o Escaped genes hypothesis: some genes where present in ancestor cells/ bacteria
and just escaped from cells.
▪ Viruses are the ultimate products of degeneration of ancestral cells that
lost their autonomy and transitioned to obligate intracellular parasitism
(e.g. giant viruses). During the early cell life, some split of as viruses. This
theory became a thing again when large viruses were found.
o Reductive virus origin/ regression hypothesis: viruses are remnants of a degraded
cell: it needed another cell to replicate.
4
