• Verkeerd document? Gratis ruilen
  • Geschreven door studenten die geslaagd zijn
  • Direct beschikbaar na je betaling
  • Online lezen of als PDF
Verkopen
Kies je studieland
Kies je taal
Document preview thumbnail
Voorbeeld 4 van de 123 pagina's
Samenvatting

Summary Lecture Notes Virology | Introduction | Universiteit Antwerpen | 2024/2025

Document preview thumbnail
Voorbeeld 4 van de 123 pagina's

Full summary Virology, 3rd bachelors BMS, teached by Peter Delputte Grade: 16/20

Voorbeeld van de inhoud

2024-2025 Virology



Virology
Introduction
What is a virus? Where do they originate?
What are viruses?
• Where can we find them? Everywhere
o More viruses in a liter of sea water than people on earth
o Human virome and the global virome
• Most abundant biological entities on the planet
• Major roles in global ecology and evolution of the biosphere
• All organisms on the planet harbor distinctive repertoires of viruses
• We breathe and eat billions of virus particles
• Human DNA consists partly of ancestral viral genetic material
• Obligate intracellular parasites that package their genomes in tiny protein/lipid
particles (when a virus cannot infect a cell, it will go extinct)
o Viruses are found to infect each life form: archaea, bacteria, eukaryotes,
plants and animals
o DNA or RNA, ss or ds, protein coat, +/- lipid envelope

Viruses are small and diverse in structure
• Virion = genome packed into lipid particles (‘like a seed that comes alive when
entering the cell’ = obligate intracellular)
• Viruses are small
o At the edge of what we can see with the LM: better visible with EM
o Mimivirus (400nm) and pandoravirus (1000nm) are unusually large viruses
§ Recently discovered, approach the size of a bacteria
§ They live on amoeba à they were first thought to be bacteria
§ Both dsDNA viruses
§ Pandora has a mouth used to attack the cell and release its genome in
the cell
• Latency = ‘sleeping virus’ à 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 à 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) à many viruses are just
‘passengers’ and don’t cause disease because our immune system has
learned to deal with it = co-evolution.
o Long lasting/ chronic infections = latency
• Viruses provide a gene-pool
o By infecting cells, viruses will insert their genomic material in the genome of
the host, contributing to the human genome (transposable elements are
genes we have acquired from viruses; retrotransposons = from retroviruses)


1

,2024-2025 Virology


• There is variability in the genome of viruses: they have high mutation rates!
o They don’t have a DNA-repair mechanism, nor proofreading
§ Thus, most of the replication have a lot of mutation resulting in a virus
that cannot infect = junk-viruses
o This results in some viruses with high variability (e.g. coronavirus: alpha, beta,
delta, gamma, omicron)
o The variability in virus genome is important to be able to evade immune
system host (= survival of the fittest)!!!
• Viruses are important disease-causing agents, but not all viruses make us sick
o Many viruses are just passengers through our body
o Our IS has learned to deal with (some) viruses
• Viruses diaer in structure, but minimal components (very small viruses don’t fit a big
genome):
o Many particles are spherical = round shapes à can package a lot of material
in a round shape, other structures are more complex = bullet shape,
philomentous and more complex structures (variola and pox)
o Genome: DNA/RNA and ss/ds and (+) stranded /(-) stranded
o Capsid protein = capsid around genome of virus
o Capsid + genome = nucleocapsid = virion
o All viruses have capsid proteins, but not all of this form a very stable crystal-
like capsid structure!!!
o Virion + things that come to expression when a virus infects a cell = virus
à all viruses need to ‘become/make’ mRNA to make proteins; they are all
parasites of the host protein synthesis machinery
• Some viruses also have a lipid envelope
o Lipid envelope is not encoded in genome
o Lipid envelope ‘stolen’ from eukaryotic cell (membrane of cell/ ER/ GA)
o Viruses do not only rely on the host cell for their lipid envelope, but on a lot of
things: energy production, protein synthesis, reproduction
• !!! Bacteria replicate exponentially while viruses don’t!
o First viruses do Brownian movement à (bacteria
has flagella and goes in a specific direction)
o By chance the virus binds to receptor of cells
o Virus is 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)
• Are viruses dead/alive à dead
o They cannot produce their own energy (no carbon metabolism)
o They cannot reproduce/ evolve by themselves (obligate intracellular)
o There are no ancestral viral lineages: no single gene has been identified that is
shared by all viruses
o 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



2

,2024-2025 Virology


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
o Escaped genes hypothesis: some genes where present in ancestor cells/
bacteria and just escaped from cells, they were the products of degeneration
of ancestral cells that lost their autonomy (this theory become 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
o Probably a combination of these three!

Di3erent kinds of genome in viruses
• dsDNA à use the DNA-polymerase of cells to replicate à proofreading à less
mutations à less variability à less chance to infect another species because of this
low mutation rate (Herpes is a dsDNA virus, thus Herpes of your cat will probably not
infect you)
• RNA-virus à uses RNA-dependent-RNA-polymerase to replicate à it is not from the
human cells since it does not exist here, so the virus encodes for it à no
proofreading à more mutations à more variability à more chance to cross
species-barrier (SARS-COV-2 is an RNA virus and thus crosses species barriers and
can cause pandemics)
o RNA viruses can be linear/circular or segmented (diaerent RNA-strands next
to each other)
o RNA-viruses don’t need a nucleus to replicate and can stay in cytoplasm
(most of them will still go in nucleus tho)
o + stranded ssRNA will be in cytoplasm (for translation) and – stranded RNA in
cytoplasm or nucleus
o Viruses don’t care about +/- stranded, they mostly are ambisense: you can
read the genome from both sides
• Genome of virus always consists of 2 core modules:
o Encodes for genome replication = non-structural proteins
§ This is used to group diaerent virus families:
• RNA-viruses
o RNA-dependent-RNA-polymerase (RdRp)
o Reverse transcriptase
• DNA-viruses
o Protein primed family B DNAP
o Rolling circle replication endonucleases
o Superfamily 3 helicase
§ The replication machinery might have arisen from the primordial pool
of genetic elements




3

, 2024-2025 Virology

§ Five hallmark viral replication genes
• Viruses don’t have specific genes that classifies them as
viruses (unlike mammalians/humans)
• No close homologues in cellular life, but shared by diverse
viruses
• Links viruses with diaerent nucleic acid types & non-viral
mobile genetic elements
• RdRp (RNA-dependent RNA polymerase) universally conserved
across all RNA viruses à needed for replicationand translation
o RNA recognition motif (RRM) = 1 of the most common
RNA-binding domains à occurs in all forms of cellular
life à structurally related domains are widespread in
many viruses & mobile genetic elements
• DNA viruses have diaerent DNA-dependent DNA polymerases
• Retroviruses have reverse transcriptase
o Encodes for structural proteins (capsid)
§ Often: virus makes polyproteïns that are cut by proteases into smaller
proteins
§ Capsids have limited diversity and have the same structural backbone
in every virus = 60% of viruses have an icosahedral structure (looks like
a cristal). Other common capsid structures are rod-
shaped/filamentous or helical
§ Capsid can consist of lipid parts or proteins
§ Every virus had genes that encode for capsid. Some viruses have
genes encoding for receptor-binding proteïns (but sometimes, the
receptor binding proteins van be found on capsid proteïns)
§ The structural proteins may have been acquired from hosts at diaerent
stages of evolution à sequence and structure comparison indicate
that many capsid proteins evolved from ancestral cellular
carbohydrate-binding or nucleic acid-binding capacity and genome
protection
o Viruses can also have other genes than only these 2 core modules:
§ Regulation and timing of replication cycle
§ Modulation of host defense mechanism (this is not immune invasion
because it is not absolute: it will just block the immune response long
enough for virus to replicate)
• Genes that are not encoded in the viral genome
o The genome of viruses does not have telomeres/ centromeres like in
chromosomes
o The viral genome does not have genes encoding protein synthesis machinery
(ribosomes, tRNA)
o The viral genome does not have genes encoding for the membrane synthesis
• Chimeric origin of viruses
o The structural proteins may have been acquired from hosts at diaerent stages
of evolution
o The replication machinery might have arisen from the primordial pool of
genetic elements


4

Documentinformatie

Geüpload op
7 oktober 2026
Aantal pagina's
123
Geschreven in
2024/2025
Type
Samenvatting
€9,99

Verkeerd document? Gratis ruilen Binnen 14 dagen na aankoop en voor het downloaden kan je een ander document kiezen. Je kan het bedrag gewoon opnieuw besteden.
Geschreven door studenten die geslaagd zijn
Direct beschikbaar na je betaling
Online lezen of als PDF

Verkocht
7
Volgers
0
Items
16
Laatst verkocht
5 dagen geleden



Waarom studenten kiezen voor Stuvia

Gemaakt door medestudenten, geverifieerd door reviews

Kwaliteit die je kunt vertrouwen: geschreven door studenten die slaagden en beoordeeld door anderen die dit document gebruikten.

Niet tevreden? Kies een ander document

Geen zorgen! Je kunt voor hetzelfde geld direct een ander document kiezen dat beter past bij wat je zoekt.

Betaal zoals je wilt, start meteen met leren

Geen abonnement, geen verplichtingen. Betaal zoals je gewend bent via Bancontact, iDeal of creditcard en download je PDF-document meteen.

Student with book image

“Gekocht, gedownload en geslaagd. Zo eenvoudig kan het zijn.”

Alisha Student

Bezig met je bronvermelding?

Maak nauwkeurige citaten in APA, MLA en Harvard met onze gratis bronnengenerator.

Bezig met je bronvermelding?

Veelgestelde vragen