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Virology > Viriods, Virophages, and Prions > Flashcards

Viriods, Virophages, and Prions Flashcards

1
Q

What is a Viroid

A

•Viriodsare very tiny particles with covalently closed, single stranded circular RNA.

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2
Q

do viroids have a capsid

A

•The RNA of viriodsare not protected by a protein coat (capsid

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3
Q

Viroid nomenclature

A
  • The name viriodswas coined from their similarity with viruses;•Viriods= Vir(Virus) + iod(like
  • Thus, viriodsare regarded as subviruse
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4
Q

Viroid genome

introduction

A

•Viriodgenome do not encode proteins, but are capable of independent replication in hosts leading to disease conditions.

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5
Q

What do viroids infect

A

•Viriodsare so far known to infect mainly plants, but one species have been found to cause Hepatitis D in humans

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6
Q

Viroid RNA length

A

•The length of the viriodRNA varies between 246 -434 nucleotide

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7
Q

Discovery of viroids

A

first discovered by theodor Diener from infected potatos in 1976

thought to be a virus, bout would not pellet after centrigation

the virus-like agent was found to be sensitive to RNA, but insensitie to DNA, chloroform, ethanol and phenol

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8
Q

Viroids as the potential origin of life

A
  • Recently, a group of scientist proposed that viriods may have been the simpliest life form since they exist as RNA without a protein coat (Moelling and Broecker 2021).
  • They are the smallest of life forms capable of replication which have undergone Darwinian evolution.
  • Thus, since early life forms existed as simple forms, viriods are likely the first form of life on earth since they aresimple both in structure and function and do not code for protein
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9
Q

What are the two families of viroids

A
  1. Pospiviriodae

2. Avsunvirioda

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10
Q

Pospiviriodae

A

Pospiviriodae:

Viroid

The members of this group are named after the potato spindle tuber viriod.

Members have rod-like shape, a small single stranded region and a central conserved region.

They replicate in the nucleus, where their RNA is replicated by plant RNA polymerase II.

The ends of the synthesized RNA are ligated to form a circular RNA

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11
Q
  1. Avsunviriodae
A

•2. Avsunviriodae:

Viroid

Members are rod-like and named after the avocado sunblotchviriod.

  • Members replicate their RNA in the chloroplast as theylack a conserved region.
  • ViriodRNA are transported to the chloroplast where concatemericRNAs are synthesized using the chloroplast-dependent RNA polymersase.
  • Cleavage of the synthesized viriodRNA is achieved by the viriodencoded ribozymes
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12
Q

Viroids as plant pathogens

A
  • Generally, viriodsare pathogen of plants with great economic importance in agriculture industry.
  • More than 30 viriodshave been identified; 28 were found to infect the dicotyledons(plants with two seed leaf), while 2 infect the monocotyledons (plants with one seedleaf).
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13
Q

examples of viroids as plant pathogens

A
  • Coconut cadang-cadangviriod: causes a deadly infection in coconut trees
  • Apple scar skin viriod: Infections in apple trees results in unappealing fruits.
  • Avocado sunblotchviriod(ASBV): Infects avocado plants
  • Chrysanthemum stunt viriod(CSV): causes chrysanthemum stu
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14
Q

Viriodattachment and entry

A

•Viriodattachment and entry is mediated by viriodbinding proteins (Virp1

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15
Q

viroid RNA and proteins

A

•viriodRNA isn’t known to encode any protein: the AUG initiation codon is absent in some specie

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16
Q

Viroid enzymes (for replication)

A

•Enzymes involved in viriodreplication are; RNA polymerase, RNA cleavage and RNA ligase

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17
Q

Viroid autonomous replication

A

•Viriodsundergo autonomous replication in host cells, involving RNA polymerase II, an enzyme which play a role in transcription into mRNA in most cellular organisms.

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18
Q

Viroid RNA replication

A

•RNA replication mechanism involves a “rolling circle”, resulting in the synthesis of a concatemeric, linear (+) strand RNA

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19
Q

Viroid production of progeny RNA

A

•Progeny RNA is produced through cleavage into unit length monomers that are ligated into circle

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20
Q

Transmission fo viriods

A

. Cell to cell transmission of progeny viriodin plant cells occur through;

I) Plasmodesmata(channel between two adjacent cells through the cell wall).

II) Phloem: Progeny viriodscan be transported through the phloem to infect new cells.

From these cells, viriodspenetrate the pollen, ovule and seed. Young plant arising from an infected seed becomes infected with the viriod.

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21
Q

New infection mechanisms of Viroids

A

New infection can occur through:

Viriodcontaminated seeds, cutting and tubers

Viriodcontaminated equipment and implements

Insect vectors (aphids

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22
Q

Signs of plants infected with viroids

A
  • The most common symptoms of viriod infected plants are:
  • stunted growth,
  • deformation of leaves and fruits,
  • stem necrosis,
  • death of plant (final resort)
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23
Q

Prevention and Control of Viriods

A
  • Use of chemical disinfectants in the field to spray infected plants such as:
  • 1 -5% sodium hypochloride
  • 2% formaldehyde
  • 6% hydrogen peroxide
  • Also, these chemicals can inactivated viriods. Thus, can be used to disinfect farm equipment and implements to avoid contaminating plan
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24
Q

Introduction to virophages

A
  • Virophagesare viruses capable of infecting other larger (giant) viruses-infecting host for the derivation of some its needed replication machinery as well as parasitizes the helper virus.
  • Thus, virophagesare obligate parasites.
  • Similar to satellite viruses, but virophagesmostly are parasitic to the helper virus (large virus) resulting in death in most case
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25
Q

Virophages are not subviral agents

A

According to ICTV, Virophagesare viruses with functional genome which encodes structural proteins and those required for DNA replication.

Virophagespossess the full complement of a virus in having a capsid, nucleic acid which can self-assemble into a nucleocapsidand uses the cell ribosome-encoding machinery for replication

Also, viriophageshave been regarded as a small-bonifideviruses infecting other viruses.

In contrast, satellite viruses are subviralagents,lacking genes that can code for all functions needed for replication and are dependent on co-infection of the host by a second virus (helper virus).

E.g., the satellite RNAs do not encode capsid protein, but depend on protein from the helper virus for packaging its genom

26
Q

Virophages vs Satellite Viruses

Genomes

A

•So far, virophagesare known to be DNA viruses while satellite viruses are known to possess genomes that are either DNA or RNA

27
Q

Virophages vs Satellite Viruses

replication

A
  • Virophagessuppress the replication capacity of its viral host by its parasitic mode of life thereby enhancing replication of host cells and limiting pathology, while satellite viruses may not hinder the replication of its helper virus.
  • Replication in virophagesoccur almost entirely in the giant virus by hijacking the replication machinery of the virus host to replicate its own genome. Conversely, replication in satellite viruses involves the utilization of host cell machinery to initiate expression and replication of its genome in the nucleus. Thereafter, transported to the cell cytoplasm to hijack the gene replication machinery of the helper virus to replicate the genome of its progeny.
  • E.g., the helper virus (tobacco necrosis virus) encodes an RNA polymerase utilized by the satellite virus (satellite tobacco necrosis virus) for replicating its genome.
  • Thus, the initial classification of virophagesinto dsDNAsatellite viruses is now placed in a divergent family of dsDNAsatellite viruses infecting protiststhat are not subviralagent
28
Q

Virophage classification

What are the two Genuses

A
  • Virophageshave been classified into the virus family-Lavidaviridae.
  • The lavidaviridaefamily is a divergent family from the dsDNAsatellite viruses infecting protiststhat are not subviralagents.
  • Two genera have been carved out from the family:
  • Genus: Sputnikvirus
  • Genus Maviru
29
Q

Large/Giant viruses

A
  • Giant viruses are the most complex of all viruses (genetically and structurally) whose genome was isolated in 2003.
  • They serve as host for virophages.
  • They replicate their genome inside the host cell cytoplasm and encode a large number of genes similar to some bacteria.
  • The first identified giant virus was the AcanthamoebapolyphagaMimivirus(APMV)
30
Q

AcanthamoebapolyphagaMimivirus(APMV)

A

the first giant virus to be identified

  • AMPV has a capsid size of 500 nm, with a dense fibrilelayer of about 140 nm in length.
  • The genome of AMPV is dsDNA, and quite unique in having a huge size of 1.2 Mbp(megabasepairs), encoding about 979 putative proteins.
  • These unique characteristics led to the creation of the virus family mimiviridaein 2005
31
Q

Virophagesas parasites to the megaviruses

A
  • Giant viruses were found to be host to viriophagesby a team of researchers in 2008.
  • Virophagesare the first true parasites of viruses, thought to share similarity with the satellite viruses.
  • Virophageshijack the replication machinery of the prey (giant viruses) for the replication of its own genome.
  • Further, the parasitic activity of virophagesinduce partial inhibition of the giant viruses in the host cell resulting in the synthesis of defective particles which are harmless to the host.
  • Molecular sequencing have shown evolutionary relationship between virophages, giant viruses and host cells as sequences of the former have been demonstrated in genome of the giant viruses and host cel
32
Q

Virophage entry into viral hosts and cellular host cells

A

•Virophageshave been observed to exhibit two major modes of entry depending of species.

  1. Attachment to giant viral host:

Virophagestrain such as sputnik infect cells of cellular organisms simultaneously with the giant virus host using the capsid fibrils for attachment. The proposed mechanism of attachment involved interaction of the muchroom-like fibers that surround the virophagecapsidand peptidoglycan-like structure surrounding the mimivirusfibrils.

  1. Host cell entry through clathrinmediated endocytosis:

Research using electron microscopy have shown that Maviruscan enter cells of cellular organisms independently of the giant virus using the clathrin-mediated endocytosi

33
Q

Virophage genome release upon entry (Sputnik)

A
  • Upon cell entry, virophage such as sputnik releases its genome into host cell. It was hypothesized that this occurs after a loss of one or several pentameric capsomers, induced by stress owing to reduction in pH.
  • All but one of the virophage genes encode ready-to-use transcripts which are packaged into mRNA.
  • Although the roles of virophage mRNA is still under investigation, it has been proposed to trigger parasitic mode of life in the giant vir
34
Q

Virophagereplication machinery

A
  • As parasites of viruses, virophagesdepends entirely on the transcription and DNA replication machinery of its giant virus host, instead of those of cellular organisms.
  • The genome may or may not encode polymerase enzy
35
Q

The Mavirus(virophage

replication

A

•The Mavirus(virophage) have been observed to encode DNA polymerase, thus, it was hypothesized that the virophagegenome replication is controlled by the virus-encoded replication machinery

36
Q

sputnik (virophage replication)

A

no DNA or RNA polymerase genes have been found in the sputnik virophage. Thus, it was hypothesized that its gene expression is catalyzed by the transcription-replication complex of its giant virus based on evidences from electron microscopy

37
Q

Replication products of virophages (4x)

A

•Replication products includes four virophageencoded proteins such as

major capsid protein (MCP),
minor capsid protein (mCP),
cysteine protease
ATPase.

These proteins are thought to play roles in virophageassembly and maturation

38
Q

Introduction to prions

A
  • Prions are infectious protein agents arising from inside a host cell, thought to be lacking a nucleic acid as found in viruses.
  • The name was coined by Stanley Prusinerfrom the phrase; Infectious protein= Prion
  • Diseases caused by prions have extremely long incubation periods which could last for years.
  • Symptoms of prion diseases are dementia and loss of coordination; leading to gradual depreciation of the host and deat
39
Q

Discovery of prions

A
  • Prions ignited the interest of researcher towards the end of the 20thCentury with the outbreak in the UK of a disease called bovine spongiform encephalopathy (BSE).
  • BSE is popularly known as the ‘’mad cow disease’’ and the transmission of a variant to humans causes the Creutzfeldt-Jakob disease (vCJD)
40
Q

Transmissible Spongiform Encephalopathy

A

•Transmissible Spongiform Encephalopathy (TSE): refers to diseases caused by prions.

TSE was coined as follows:

Transmissible: The infectious agents are transmissible to host of the same species or different species

Spongiform: formation of holes in the brain similar to the appearance of a sponge.

Encephalopathy: means disease of the bra

41
Q

Characteristics of prions TSEs

What causes them

What is PRNP

Cell Types

A
  • Causative agent: TSEs are thought to be caused by misfoldingforms of normal cell proteins, without the evidence of nucleic acids in them.
  • Versions of the normal protein have been observed in some vertebrates such as mammals, birds, fish and reptiles.
  • In humans, the gene encoding the normal protein is PRNP.
  • The function of the protein remains unknown, but observed to revolve between endosomes and cell surface where it is positioned in the plasma membrane by a glycosylphosphatidyl-inositol anchorat its C terminus.
  • The protein is found in different cell types, but mainly that of the central nervous system (CN
42
Q

Prion protein

A
  • The molecule of a prion protein contains a loop due to disulfide bond.
  • The loop has two asparagine residues, either or both can be N-glycosylated.
  • Thus, the prion protein can exist in three glycoforms; •unglycosylated, •monoglycosylatedand •diglycosylated.
  • Sugar molecules attached to the prion protein may be of different type
43
Q

Figure 2: Normal Proteins vs misfoldedprions

A

a & b are normal forms, while ‘c’ is the misfoldedform.Much of the conformation of the normal protein is a α helix.In misfoldedproteins, there is decrease in α helix and an increase in β sheet.This conformational change is followed by a change in protein properties such as resistance to digestion by proteinase K. Note that the normal protein is completely digested by this enzym

44
Q

Proteins in prion-infected tissues

A
  • Protein molecules in prion-infected tissues may aggregate as rods, fibrils or other forms depending on the prion strain and host.
  • The normal forms of the protein have been designated as PrPc(prion protein cell), while the misfoldedprotein has been designated as PrPsc(Sc= scrapie) or PrPres(resistance to proteinase)
45
Q

Prion proteins and disease outcomes

homo/heterozygous a.a.

A
  • Disease outcomes due to prions can be affected by the presence of certain amino acids at specific sites in the prion protein such as disease susceptibility and incubation period.
  • E.g., the PRNP gene encoding either methionine or valineat codon 129 may show varying disease outcome depending whether the person is homozygous(valine/valineor methionine/methionine) or heterozygous (methionine/valine).
  • So far, all cases of human variant Creutzfeldt-Jakob Disease (vCJD) have been homozygous for methionine at codon 12
46
Q

The Protein-only hypothesis

A
  • The hypothesis states that: Prions are misfoldedinfectious proteins without a nucleic acid.
  • If true, introduction of misfoldedproteins into a host have capacity to trigger a misfoldingof normal proteins.
  • Implication is that the new misfoldedprion retains the amino acid sequence of host prion and not that of the donor.
  • Also, the hypothesis suggests that the prions (disease agent) have an internal origin/source from self body proteins through inheritance.
  • Explanation is that host infection is initiated by inheriting a prion gene encoding a protein with an amino acid sequence having a high possibility of misfolding
47
Q

Replication in prions

A
  • The mechanism of prion replication is still under investigation.
  • Explanation have so far been based on the ‘’Protein-only Hypothesis’’
  • However, several mechanisms of replication have been proposed:
  • Molecules of misfoldedproteins have capacity to initiated a misfoldingof normal protein
  • It is quite difficult to understand how infectious proteins are able to replicate without any nucleic acid as none is yet to be detected for these proteins.
  • However, scientific evidence using mice suggests that prions are disease agents capable of infecting the brain, and can be transmitted to other mice through an infected brain
48
Q

3 ways prion “seeds” may occur

A

•Initiation of replication requires a ‘seed’ (an aggregate of misfoldedproteins) which can occur in three way

  1. The ‘seed’ could be introduced into the body
  2. It could arise from a rare conformational change in a normal protein molecule
  3. It could arise from the result of expression of a mutant prion gene
49
Q

Prion Strains

A
  • Strains can be differentiated based on phenotypic characteristics that are consistently transmitted from one generation to another. E.g. strains of scrapiedisease have been observed to induce varying clinical syndromes in goats.
  • Misfoldingof proteins into different conformations may result in different strains.
  • Level of glycosylation of prion protein: strains may vary in having different ratios of the three glycoforms(unglycosylated, monoglycosylated, diglycosylated)
50
Q

Transmission of Prions

A
  • Infective prions have been observed in milk, faeces, urine, placenta and nasal secretion of infected host.
  • Transmission can occur through:
  1. Direct contact with infected host
  2. Indirectly by acquiring prions from the external environment (ingestion, inhalation).
  3. Tissue contamination / transpla
51
Q

Prion transmission efficiency

A
  • Route of infection and dose: Brain infection with prions is more efficient that ingestion. Also, the larger the prion dose, the more efficiency of transmission.
  • Species barrier: Infection of prions from a host species to a different one may fail or require a high than minimum dose
52
Q

Prion diseases could arise in three ways

A
  1. Spontaneously
  2. By inheritance
  3. Entry of TSE agent into the body: Transported through the digestive tract to the lymphoreticularsystem (lymph nodes, spleen, Peyer’spatches) for amplification, and then to the CN
53
Q

Prion accumulation

A
  • Prion replication is slow, but it accumulates as the misfoldedproteins are not completely degraded by proteinase K, forming insoluble aggregates referred to as plaques.
  • Accumulation of plaques block the neurons of the CNS causing dysfunction and death of cells leading to holes in the brain.
  • Death in neuronal cells could culminate in death of the host
54
Q

1.Scrapie

A

1.Scrapie:

It infects sheep and goats.Infected animals scrape against hard objects like fence posts, many grind their teeth, stumble and eventually die.

Scrapiecan be transmitted among sheep through injection of brain tissue.

Sheep are more susceptible to scrapieif the prion gene has a valineinstead of an alanine at codon 13

55
Q
  1. Atypicalscrapie
A
  1. Atypicalscrapie: a new distinct TSE identified in sheep
56
Q
  1. Chronic wasting disease
A
  1. Chronic wasting disease: Discovered in the 1980’s in wild mule deer, moose, white tailed deer and elk under captivity.

It’s the only TSE so far reported to occur in free-ranging animals

57
Q
  1. Bovine Spongiform Encephalitis (BSE)
A
  1. Bovine Spongiform Encephalitis (BSE): was first observed in UK in 1986 during an outbreak amongst cattle, but has spread to many parts of the world.

BSE have been reported in other animals such as domestic cats, tiger, and herbivores (bison and eland)

Transmission is by feeding meat and bone meal to cattle as food supplement

58
Q

Prion diseases in humans

A

can be grouped into three

spontaneous

Inherited

Aquired

59
Q

Spontaneous prions

A

poradic CJD

60
Q

Inherited Prions

A

Familial CJD

Fatal familial CJD

61
Q

Aquired Prions

A

Kuru

vCJD

62
Q

Preventing prion infectivity

A
  • Treatment applied for preventing activation of prion infectivity are;
  • Exposure to 5% sodium hypochloridesolution
  • Treatment with 1 M sodium hydroxide (NaOH) for 1 to 2 hours.
  • Note that inactivation of prion infectivity is resistant to heat, while some are resistant to autoclaving and irradiation with some chemicals that usually inactivate virus infectivity

Virology (20 decks)

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