virus Flashcards

(33 cards)

1
Q

why are viruses living and non living

A

viruses are able to replicate using their genome, but are unable to metabolise e.g. undergo respiration. They also lack cellular organelles and are unable to replicate without a host cell

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2
Q

virus organelles

A

genome, capsid coat, envelope consisting of phospholipid bilayer and glycoproteins,

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3
Q

genome structure

A

single/ segmented/ linear/ circular
RNA or DNA ss or ds

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4
Q

genome function

A

code for viral component synthesis and ezymes that facilitate assemby and genome replication

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5
Q

capsid structure and function

A

consists of capsomeres which are individual protein units, serves to protect, attatch and introduce genome into host cell (capsid + nucleic acid is called nucleocapsid)

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6
Q

envelope structure

A

phospholipids for a bilayer and has glycoproteins, formed after budding from host cell. (glycoproteins are virus manufactured proteins)

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7
Q

how does virus recognise host cell?

A

glycoproteins

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8
Q

4 shapes of virus

A

icosahedral, helical, enveloped, complex

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9
Q

virus infiltration (2 ways)

A

either by injecting genome or entire virus enters and disassembles inside host

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10
Q

how does virus replicate

A

using the host DNA polymerase or RNA polymerase, then use RNA polymerase for transcription and for translation, using host cells ATP

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11
Q

2 kinds of bacteriophage?
explain why they are call that way

A

lytic and temperate
lytic replicate through the lytic life cycle, temperate bacteriophages are capable of the lysogenic life cycle, where they can either undergo cell lysis or they can incorporate their DNA into host cell DNA, becoming a prophage

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11
Q

how does virus exit cell

A

exocytosis, budding or cell lysis

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12
Q

T4 bacteriophage cell structure

A

icosahedral capsid head, contractile sheath - both have protein coat
genome - ds DNA
tail fibers
collar core
base plate and tail pins

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13
Q

replication lytic cycle

A

bacteriophage DNA is immediately transcribed to for mRNA using host RNA polymerase, host cell DNA is degraded into neucleotides which are used to synthesise viral DNA, biosynthesis of viral proteins use host metabolic machinery such as ribosomes. There is an ECLIPSE PERIOD, where phages not yet formed, but only proteins and DNA.

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13
Q

lytic cycle penetration process

A

bacteriophage releases a lysozyme through its tail, digesting the cell wall, releasing molecules which trigger a change in the base plate of the bacteriophage, which then contracts its contractile sheath, holow core penetrate cell wall and when reach the plasma, release DNA. (capsid remains ouside)

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14
Q

lytic cycle attachment bacteriophage

A

attatchment sites on the tail fibres recognise receptor sites on bacteria, showing viral specificity

15
Q

maturation lytic cycle

A

DNA and capsid are assembles into a DNA filled head, other components are assembled independently and joined together.

16
Q

release lytic cycle

A

lysozymes are synthesised, causing the becterial walls to break down

16
Q

explain the lysogenic cycle

A
  1. attatchment is when the tail fiber recognizes complementary bacteria receptor
  2. penetration is when the tail releases enzyme and contractile sheath contracts, injecting viral DNA
  3. replication linear phage DNA forms a circle and integrase forms a integrase pritein complex with viral DNA and Bacteria DNA, catalysing bond breaking and formation (rejoining), integrating the viral DNA into the Bacteria DNA, becoming a prophage. (or also can lytic cycle) when the bacteria undergoes mitosis, the prophage is also replicated, remaining latent
  4. spontaneous induction, where UV light may trigger repressor genes to be destroyed, cell enters lytic cycle. (prophage excised)
    5,6. maturation and release same as T4, which is the assembly using host cell machinery and released through cell lysis by synthesis of lysozymes.
17
Q

envelope of influenza

A

has neuraminidase (enzyme) and haemagglutinin (glycoprotein), phospholipid bilayer from host

17
Q

influenza attachment

A

protruding glycoprotein haemagglutinin complementary binds to sialic acid receptor on host cell

18
Q

penetration and uncoating of influenza

A

endocytosis, host plasma membrane invaginates and pinches off, forming a vesicle (endocytic vesicle) within the cell. Then it binds to a lysosome, which drops the pH levels, which acts as a signal to influenza envelope to fuse with the phospholipid bilayer of the vesicle membrane, nucleocaspid released into cell cytoplasm. The caspid is then degraded by enzymes and Viral Rna enter the nucleus.

18
Q

influenza virus genome

A

genome consists of 8 segments of ssRNA
RNA genome is negative strand (opposite of its mRNA)
packaged with protein to form helical nucleoprotein structure.
3 segments of RNA code for polymerase which form enzyme complex, RNA dependent RNA polymerase and RNA replicase for replication and transcription
other 5 RNA segments code for haemagglutinin, neuraminidase, nucleoprotein, matrix protein M1 and non structural proteins

19
Q

replication of influenza

A

the negative strand DNA is used as a template to form positive strand RNA, catalysed by RNA dependent RNA polymerase. then this positive strand RNA is used as a template for the replication of many negative stand RNA (viral genome)
mRNA strands that are synthesised exit the nucleus into the cytosol and RER where they are translated into proteins

20
HIV retrovirus genome
two copies of ssRNA, both POSITIVE strands, unlike influenza (same sequence as viral mRNA) mRNA tightly bound to nucleocapsid proteins
20
maturation of influenza
glycoproteins transported by vesicles to fuse with the plasma membrane, capsid proteins assosciate with glycoproteins viral genome then associates with nucleoproteins forming helical nucleoprotein when nucleoprotein interacts with the capsid protein, release by budding, which is also evagination (release is facilitated by neuraminidase)
21
HIV capsid
conical shaped, made up of diff proteins from the nucleocapsid proteins in the capsid exists 2 enzyme reverse transcriptase which transcribes the viral RNA into DNA, other 2 enzymes prsent are integrase and protease capsid and genome forms the core
22
HiV retrovirus envelope
phospholipid bilayer from host cell, glycoproteins gp120 and gp41 (gp120 interacts with the CD4 receptor on host cell) host cell is T helper cell
23
HIV attahchment, penetration
1. the glycoprotein gp120 on the virus envelope recognizes and complementary binds to the CD4 receptor on the T helper cell with the help of a coreceptor 2. gp41 facilitates the HIV to fuse with the phospholipid bilayer of T helper cell membrane, capsid is and nucleocapsid proteins are both degraded by enzymes, releasing viral enzymes and RNA
23
replication of HIV
reverse transcriptase catalyses the transcription of the +RNA genome into DNA (cytosol) - first catalyse DNA strand complementary to template viral RNA strand (DNA RNA complex) - RNA is degraded and a second DNA strand is synthesised to form dsDNA then DNA enters the nucleus where integrase catalyses the DNA integration into host cell genome, now considered a provirus (latent stage) activation - DNA is transcripted back into RNA (mRNA) mRNA exits the nucleus and uses the host cell ribosomes to synthesise polyproteins, e.g. gp120 gp41 transported to host cell membrane by vesicles
24
HIV maturation and release
polyproteins and HIV genome RNA assemble at inner surface of plasma membrane, HIV then buds off and evagination, viral envelope has host cell membrane with gp120 and gp41 polyproteins are cleaved by protease to become functional proteins (structural proteins and enzymes)
25
antigenic shift how it occurs and what is it
major change on the surface antigens of a virus, resulting in the virus receptors binding to different species occurs when two or more strains of the virus combine to form a new subtype of the virus, is a case of genetic reassortment - for influenza, when 2 diff strains of influenza infect same cell at the same time, host cell combines their antigens
25
antigenic drift why it occurs in influenza and what is it
mutations involving the the surface glycoproteins of a virus, changing the conformation of the surface glycoproteins, that cannot be recognised by antibodies occurs due to lack of proof reading ability of the RNA dependent RNA polymerase, high rate of replication