Summary samenvatting human infecious diseases

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Summary - samenvatting human infecious diseases

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  • What are the routes of virus transmission?
    • Air
      • influenza, SARS
    • Water
      • polio, diarrhea 
    • Contact
      • HIV, Ebola, Herpes
    • Food
      • Norovirus 
    • Vertical (offspring), germ line 
      • plant virus 
    • Mosquito vectors 
      • Zika
    • Bats as virus host 
  • What is a virus?
    The smallest genetic entities. 
    A piece of genetic information with a protein coat that hijacks' the host cells and replicates itself
  • What are the 3 main characteristics of viruses?
    1. Infectivity 
      • penetrate and multiply in host cell 
    2. Obligate intracellular parasite 
      • cannot replicate by itself, no protein synthesizing machinery or energy producing machinery 
    3. property to survive outside a living cell in an extracellular state 
      • in an inert state or via carrier, depends on environment 
  • A virus is composed of
    • Nucleic acid 
      • RNA or DNA 
      • SS or DS 
      • segmented or non segmented 
    • protein shell 
      • assembled form smaller subunits: coat proteins 
    • lipid membrane / viral envelope 
      • some viruses
      • made from host cell 
  • All viral RNA genomes are __1__ (linear/circular) except for __2__
    1 = Linear
    2 = viroids
  • Viroids 
    • circular single strand RNA 
    • no coding capacity 
    • occurs in plants 
    • very small genome 
    • can only replicate with help of host (polymerase) 
  • The properties of the viral genetic material depends on
    The family to which the virus belongs
  • The minimal virus needs the 2 genes:
    1. DNA/RNA-polymerase
      • multiplication of RNA or DNA genome 
    2. coat protein
      • protection and host interaction 
  • The viral genomes varies between (nucleotideS)
    2,000 - 1,000,000
  • What is mutation rate
    The number of necleotides per 1000 nt of genome length that mutate per year
  • What affects the mutation rate?
    • The nature of the genetic material 
      • RNA viruses mutate quicker than DNA viruses
    • number of generation per year 
  • Why do RNA viruses mutate quicker than DNA viruses
    DNA polymerase has proofreading whereas RNA polymerase doesn't
  • What is taxonomy
    The theoretical concept that helps to understand evolutionary relationships in biology
  • The official virus families end on "viridae"
    names of genera end on "virus"
  • What are the main coat proteins
    VP1, VP2, VP3
  • Nearly all negative stranded RNA viruses lack a
    Clear protein coat 
    --> have an evelope that surrounds and protects the genome
  • What are structural proteins
    The viral-encoded proteins that are present in the virus particle (virion)
  • What are examples of structural proteins
    Coat proteins, nucleoproteins, glycoproteins
  • What are non-structural (Ns) proteins
    Proteins that are not present in the virus particle (virion) but produced after the virus has entered a host cell
  • What is the role of non-structural proteins (ns) in the virus replication cycle?
    • Enzymatic activities
      • viral polymerase, protease, helicase 
    • affect the host's immune system 
      • interferon antagonists, anti apoptotic proteins 
  • The viral envelope (lipid membrane) contains the glycoproteins
    Haemagglutinin (HA)
    Neuraminidase (NA)
  • Interface
    The outer layer of a virus (protein coat/viral envelope) between the virus particle and host cell surface
  • What are the functions of the protein coat?
    1. Protection of genetic material during extracellular state 
    2. recognition and penetration of host cell 
      • host range 
      • tissue tropism 
    3. escape from the immune/defense system 
  • How do viruses avoid recognition and inactivation by the immune system?
    1.  Minimize anti-genetic determinants/variation at surface
    2.  pursuing maximal symmetry of protein coat/lipid envelope (=minimal energy) 
  • What is a capsid
    The protective layer of proteins that cover the nucleic acid genome in virions. 
    capsid is made up of capsomeres
  • The viral coat is built up from individuals protein subunit - coat proteins 
    • protein's tertiary structure is never symmetrical 
    • the required symmetry is realized by regular arrangement of smaller, non-symmetrical components 
    • viral coat proteins are encoded by small open reading frames to achieve this   
  • Why is the viral coat built up of small subunits?
    1. Save space on the genome 
    2. increase genetic stability
      (small open reading frames -> less risk of mutation)
    3. possibly to self-assembly 
    4. achieve symmetric from asymmetric proteins 
  • Which virus shapes achieve maximal symmetry and minimal surface variation?
    Viruses with a protein coat 
    • rod shaped, spherical or complex 
  • Structure of Rod-shaped virus 
    • asymmetrical but identical coat proteins in a circle (disc) 
      • growing spiral (helical symmetry) in which all subunits are placed in equivalent positions relative to each other  
    • viral genome encapsulated as a spiral or helix 
    • size of rod can vary with size of genome to be encapsulated 
  • Which virus is more symmetrical - spherical or rod-shaped virus?
  • Structure of spherical virion 
    • icosahedral symmetry 
    • an icosahedron has 2-, 3- and 5-fold symmetry axes 
      • without 5-fold -> no perfect globe 
      • composed of 20 equilateral triangles 
    • minimal energy 
      • maximal symmetry 
      • protects nucleic acid 
  • The surface of an icosahedron has 60 protein molecules that can be rearranged in equivalent positions (3 proteins per triangle * 20)

    the basic virion is composed of 12 pentamers of coat proteins
  • What is triangulation
    The original 20 equilateral triangles of the icosahedron are subdivided into smaller triangles to allow more symmetrical positions for coat proteins   
  • What does queasy equivalency mean?
    Because there are pentamers and hexamers the position between the subunits is different 
    • some have 5 neighbors and some 6     
  • How do you calculate the number of hexamers?
    Hexamers = 10 * (T - 1)

    there are ALWAYS 12 pentamers and the rest are hexamers 

    the number of hexamers increases when T increases 

  • How do you calculate the triangulation (T) number?
    T = (Number of coat proteins)/ 60
  • What is the eight-stranded anti parrel beta-barrel?
    The coat proteins of icosahedral viruses have a similar tertiary structure that is rich in beta-sheets -> large hydrophobic core
  • The primary structure (amino acid sequence) varies a lot between virus families
  • Why is the atomic structure of proteins important?
    It helps to understand which parts of the protein coat can interact with receptors 

    - epitopes
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What is CPE?
Cytopathic effect 
  • a change in the structure of the cell due to antiviral infection 
    • detachment in experiment B   
How are ISGs made?
  • Sensing viruses via TLRs or RIG-I like receptors 
  • IFN-beta produced and secreted by cells
  • binding of IFN-beta to the IFNAR receptor 
  • induction of the JAK/STAT pathway 
  • induction of the expression of interferon stimulated genes (ISGs)
    • antiviral activity 
What is suramin? What is it used for?
  • An antiviral
    • treat  human sleeping sickness caused by trypanosomes (parasite) 
    • counteract infection of several viruses 
      • interfere with RNA-nucleocapsid protein interactions 
To which immune system does IFN-beta belong to?
The innate immune system
How come can the polyhedron gene and p10 gene be replaced?
Because baculovirus can replicate without these genes
Is Baculovirus pathogenic for humans?
How is SHUVA replicated?
In the cytoplasm
  1. virus attaches to host receptors through Gn-Gc polyprotein
  2. virus is endocytosed into vesicles in the host
  3. fusion of virus membrane with vesicle membrane
  4. ribonucleocapsid segments are released in the cytoplasm 
  5. transcription
  6. viral mRNA are capped in the cytoplasm
  7. replication starts when enough nuceloprotein is present to encapsidate neo-synthesized antigenones and genomes 
  8. the ribonucleocapsids buds at glogi apparatus releasing the virion by exocytosis 
How is SHUVE transcribed?
  1. Rdrp (L) binding to promotor on each encapsicated segment
  2. terminated by a strong hairpin sequence at the end of each gene 
  3. mRNA are capped by L protein during synthesis using cap snatching but are not polyadenylated 
What are characteristics of the SHUVA virus?
  • Anthropod-borne virus
  • negative ssRNA
  • 3 segmented genomes
    • S segment 
      • encodes for Nss protein by leaky scanning
    • M segment 
      • encodes for polyprotein > cleaved into Gn, Nsm, Gc proteins 
    • L segment 
      • encodes for polymerase
  • zoonotic virus
    • spread to animals and humans by mosquitos and midges
  • Gc protein forms trimeric spike at surface
Occlusion derived virus
Occlusion derived virus