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Basic Virology > Virus Genomes And Viral Replication Strategies > Flashcards

Virus Genomes And Viral Replication Strategies Flashcards

1
Q

Viral life cycle definitions:

  • susceptible
  • permissive
  • productive infection
A

A cell is:
– susceptible for a virus if the virus can penetrate
– permissive for a virus if viral genome replication is possible
(this does not necessarily mean that the virus can infect this cells under natural conditions)
-Production of infectious virus particels in a cell defines a productive infection

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2
Q

What are the types of virus infections and their characteristics?

A
  • LYTIC: the Host cell dies, Production of viruses can be seen easily
  • PERSISTENT: continuous production of viruses, cells survive infection, limited infection with newly forming cells replacing cells dying from infection, balance between virus and host (long time/lifetime infection)
  • LATENT: few virus-proteins/RNAs are expressed, no infectious virus is produced, well orchestrated molecular controls are necessary to maintain latent status, often specific set of latency genes/RNAs are expressed, external stimuli drive reactivation eg. Herpes-Virus: stimuli can be stress or UV-light
  • TRANSFORMING: as a result of infection with specific DNA/RNA viruses, some cells show increased cell devision rates and change their behaviour, carcinogenic, involved in ca 20% of cancers
  • ABORTIVE: poor virus/infection rate
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3
Q

What is a virus?

A

Very small, infectious, obligate intracellular parasite
Viral genome consists of RNA or DNA
In subtile host cell viral genome is replicated and determines the synthesis through virus own or cellular components
New viruses are generated with newly synthesised components within the host cell
Viruses are vehicles for transmission of viral genome to new host

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4
Q

What are the reasons for the Formationsflug particles?

A

Closed capsid to protect genome during transfer
Allows specific entry to defined host - specific binding to receptors followed by endocytosis of „wrong cargos“
Allows specific genome assembly
Allows budding at specific sites

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5
Q

What is the basic principle of viral replication?

A

Virus entry → uncoating - genome replication and protein synthesis - virus assembly - virus release

The protein synthesis is only executed by the hosts machinery

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6
Q

Amplification scheme of bacteria vs viruses

A

Bacteria:

  • lag-Phase: Adoption to culture condition
  • log-Phase: Amplification by devision
  • stationary Phasen Slow growth/end of devision due to limited nutrients or toxic metabolites

Viruses:

  • Eclipse: infectious particles invade and dissociate
  • burst: release of huge numbers of progeny per cell
  • stationary phase: end of viral replication due to cell death or limited host factors
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7
Q

What is the tropism of viruses and what dose it determine?

A

The tropism of viruses are host and or tissue specificity
Determined by:
-receptors
-cell type-specific promoter-enhancer-elements (DNA viruses)
-host factors for entry, gene expression, assabmly and and transport
-entry rout into organism, kind of inoculation

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8
Q

What are the different courses of viral infections?

A
  1. Acute infection - clearance
  2. acute infection - latency - reactivation of virus (gets out of control with immune disorder eg patients with AIDS)
  3. acute infection - chronic infection (balance host:virus)
  4. slow chronic infection (HIV: kills immune system)
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9
Q

What information is and isn’t contained in the virus genome?

A

Is:

  • particle generation and genome packaging
  • genome replication
  • Regulation Of replication cycle
  • antagonists of cellular defence mechanisms
  • spread to other cells/organisms

Isn’t:

  • protein synthesis machinery
  • enzymes of energy metabolism
  • factors for membrane biogenesis
  • telomeres, centromeres
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10
Q

Why are RNA virus genomes called relicts of „RNA-world“?

A

Theory: RNA primary form of replicating organic material, autocatalytic RNAs (ribozymes)
Essential requirements:
-copy of the genome without loss of information: RdRp or RT, RNA-Elements control replication and transcription in cis, „de Novi“ synthesis of RNA, mechanisms for priming
-Generation of translatable RNA (mRNA): Mechanisms for capping and polyadenilation, cap snatching, IRES elements
-

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11
Q

Criteria for classification of viruses

A

-genome
-enveloped vs non-enveloped
-replication strategies:
Virus genome serves as
→mRNA (positive strand RNA viruses)
→viral RdRp transcribes mRNA (negative strand viruses and dsRNA viruses
→viral RT transcribes genome into dsDNA and cellular DdRp transcribes mRNA(Retroviruses)
→cellular DdRp transcribes mRNA (dsDNA viruses besides poxvirus)
→viral DdRp transcribes mRNA (poxvirus)
→Replication of genomes into dsDNA and transcription by cellular DdRp (ssDNA viruses)
The replication strategy determines the place of replication in the cell.

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12
Q

Polyomavirus -circular dsDNA virus (SV40): initiation of Replication

A
  1. T-Antigen (T-Ag) binds as 2 hexamers in the presence of ATP; strand melting of A/T rich regions.
  2. In the presence of the heterotrimeric “replication protein A” (RPA; binds ssDNA) unwinding of DNA occurs (T-Ag-helicase) under hydrolysis of ATP.
  3. DNA Pol a/primase binds to each single strand and synthesizes short pieces of RNA serving as primers for DNA synthesis. In this process the interaction between Pola/Primase and T-Ag(as chaperon) is important. Pola/Primase are then replaced by replication factor C and “Pold complex”.
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13
Q

SV40 elongation

A

Topo I, II and T-Ag unwind supercoil DNA.
Leading strand is synthesized by a complex of pold, replication factor C (RF-C), and proliferating cell nuclear antigen (PCNA).
Lagging strand: pola/primase synthesizes Okazaki fragments which are completed by pold, RF-C, PCNA. RPA keeps DNA in ss state. RNase H and FenI remove RNA primers, pold fills gaps and DNA ligase I ligates the fragments.

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14
Q

Characteristics of adeno virus

A
  • no lipid envelope
  • protein „primer“ (TP) for genome replication
  • virus encoded replication machinery including DdDp - transcription via cellular DdRp Pol II und III
  • „Splicing“
  • all mRNAs with identical „leader“ sequence
  • temporally and quantitatively controlled gene expression
  • linear, 36-40 kB
  • frequently used in therapy
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15
Q

What are the three main goals of early adeno virus gene expression?

A
  1. to induce the host cell to enter the S phase of the cell cycle. E1A, E1B and E4 (viral) gene products play roles in this
  2. To set up viral system to protect the infected cell from various antiviral defences of the host. The E1, E3 VARNA genes contribute to these defuses (PKR)
  3. To synthesise viral gene products needed for viral DNA replication and synthesis of structural proteins
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16
Q

Describe the functions of the E1, E2, E3, E4 and L genes of adeno virus

A 
E1 functions, E1B
Two forms, generated by different translational start codons (different reading frames). Longer form of E1B binds to and inactivates p53 – initiation of S-phase, transformation of the cell in cooperation with E1A
E2 functions
Three products, generated by alternative splicing. 72 kDa form (E2A) binds to single stranded DNA (AdDBP); 80 kDa form (E2B1) corresponds to pTP that is processed to the 55kDa TP; a 140 kDa form (E2B2) represents the Adenopolymerase.
E3 functions
Diverse small proteins, not essential for life cycle, but modulate Adenovirus infection. E3-gp19K inhibits glycosylation of MHC class I proteins and thus inhibits the presentation of antigenic peptides to CTLs (persistence). Other E3 gene products inhibit TNF-alpha mediated cell-lysis early during infection. E3-11.6K (death protein) induces cell death to release progeny virus.

E4 functions
7 proteins, generated by alternative splicing. The proteins modulate transcription, replication, splicing of L-transcripts. ORF6 is oncogenic by binding to p53.
L functions
The mRNAs of the 11 structural proteins II-XII are spliced from a common pre-mRNA. They form the core, pentons and hexons.

17
Q

Explain the steps of initiation of replication of adeno viruses

A

A complex consisting of pre-TP (pTP=80 kD) and Adenopolymerase (Pol) as well as other transcription factors bind to end of DNA.
Binding of adenoviral ssDNA binding protein DBP leads to strand melting at the origin of the dsDNA.
Template sequence: 3 ́-GTAGTA…-5 ́
DNA synthesis initiates at a serine residue of pTP by synthesis of the tri-nucleotide CAT; template are nucleotides 4-6.
pTP-CAT then sildes back to position 1 on the
template and starts with elongation (= jump of primer). Common mechanism for protein primed DNA synthesis (also observed for phages like φ 29)!
The remaining single strand has self complementary ends, forms a partial ds, which is again target of replication machinery

18
Q

What are the main features of the Herpesvirus?

A

ds DNA: Herpesviruses

  • 126 kB ds DNA, linear
  • Immediate early, early, late genes (differential gene regulation) - ca. 84 ORFs
  • Latency in neurons; reactivation by „stress“
  • Replication in nucleus; concatamers
  • Speciality: a lot of proteins (Tegument) in the virus
19
Q

What are the main features of the parvovirus?

A

Causes Erythema infectiosum or fifth disease (mainly during childhood) German: Ringelröteln
Infects reticulocytes (red blood cell precursors)
Protein
Parvovirus
- Linear genome, 5 kb, + or – strand
with 5 ́ and 3 ́ „hairpins“; the latter serves as „Primer“
- 5 ́ end covalently bound to viral protein (protein is removed for replication)
- some parvoviruses depend on helperviruses e.g. Adeno Associated Virus

20
Q

Describe the replication mechanism of parvovirus

A
  • for,action of hairpin structure at 3‘ and 5‘ ends
  • elongation of 3‘ end
  • unfolding of 5‘ hairpin and elongation
  • cleavage by endonuclease at trs-site (nicking →replication without loss of information)
  • unfolding of hairpin structure, initiation of DNA synthesis at cleavage site and elongation
  • formation of hairpin structures at all ends, seperation of strands and initiation of DNA synthesis
21
Q

What are the features of the circovirus?

A
  • circular genome, 1.7-2.2 kb
  • only 2 ORFs: capsid and replicative protein
  • depend in replication strictly on host
  • disease in swine and birds
22
Q

What are the features of the hepadna virus (HBV)?

A
  • ds DNA genome 3,4 kb
  • very narrow host range
  • partially single stranded (not for Avi-Hepadna),
    part of (+) strand is missing (gap)
  • RT bound to 5 ́end of DNA (-)-strand
  • (+)-strand of DNA contains 18 base RNA
    with Cap at 5 ́end
  • host enzyme completes (+)-strand
    to ccc (covalently closed circular) form - cellular Pol II transcribes mRNAs
  • this is used by HBV RT to synthesize in
    the capsid a partiell ds DNA
23
Q

How does the polarity of the genomic RNA effect mechanism of replication?

A

Positive strand RNA: genome = mRNA (eg polio virus)
Negative strand RNA: antigenome = mRNA (eg influenza virus)
Ambisense: antigenome and genome = m RNA

Basic Virology (10 decks)

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