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Exam 3 > Ziegler-Viral Structure, Classification and Replication > Flashcards

Ziegler-Viral Structure, Classification and Replication Flashcards

1
Q

How are human viral pathogens classified?

A

They are classified on the basis of:

  1. Virion structure
  2. Nucleic acid
  3. Replication strategy

VNR

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2
Q

What is the infectious virus particle called?

A

A viron

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3
Q

What are virons composed of?

A
  1. Nucleic acid genetic material
  2. Surrounded by a protein coat (capsid)
  3. SOME viruses also have a lipid/glycoprotein envelope
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4
Q

Are viral genomes RNA or DNA? Ss or Ds?

A
  1. Viral genomes can be EITHER DNA or RNA, and Ss OR Ds, Linear or Circular
  2. Ss RNA can have same + or complimentary - polarity as viral mRNA
  3. Viral genomes are HAPLOID except for retroviruses (diploid)
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5
Q

What is a nucleocapsid? What is a capsid?

A
  1. Nucleocapsid: Capsid and enclosed viral genome –Package the nucleic acid in viral assembly, protects nucleic acid
  2. Viral capsid
    a. Composed of capsomers–aggregates of viral specific poly peptides
    b. SHAPE: Cylindrical shape (helical form) or a cubic shape (icosahedron form)
    c. Site of receptors necessary for naked viruses to initiate infections–Capsids of naked viruses contain VIRAL ATTACHMENT PROTEINS (VAP)

**Identical to virion but for naked viruses

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6
Q

What is the viral envelope?

A
  1. Surrounds the nucleocapsid of enveloped viruses
  2. Composed of host cell derived lipids, proteins and viral specific glycoproteins
  3. Specific glycoproteins act as VAPs for enveloped virus
  4. Acquired from viral modified cellular membranes when virus leaves host cell
  5. Disrupted in non-moist environments or by heat, acid and lipid solvents
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7
Q

What is a peplomer?

A

A glycoprotein spike on a viral capsid or viral envelope.

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8
Q

What are the three categories on which viral classification is based?

A
  1. Nucleic acid
  2. Virion structure
  3. Replication strategy
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9
Q

How many families are there of human pathogens and how many contain DNA?

A

21 families, 7 contain DNA

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10
Q

What does the family have to do with the type of disease a virus will produce?

A

NOTHING.
Viruses in the SAME family can produce DIVERSE DISEASES.
Viruses in DIFFERENT families can produce the SAME disease.

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11
Q

What type of parasites are viruses?

A

OIP—Obligate intracellular parasites

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12
Q

What determines a host for a virus?

A

If the virus can:

  1. ENTER a cell
  2. FIND the appropriate cell machinery
  3. EXIT the cell
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13
Q

What are productive viral infections?

A

Virus infections that yield NEW infectious viruses

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14
Q

What are non-productive viral infections?

A

Viral infections that occur when the viral genetic material persists in a cell (latent state) but NO infectious virus is formed

**Some non-productive infections can lead to oncogenic transformation of cells

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15
Q

What are the phases of viral multiplication?

A

A Patient Unich was PAR for the course

  1. Attachment
  2. Penetration
  3. Uncoating
  4. Protein synthesis
  5. Assembly
  6. Release
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16
Q

What are Cytopathic Effects (CPE)?

A
  1. Morphological CHANGES to the host cell caused by the synthesis of viral proteins/effects on host macromolecular synthesis
    ex. cell rounding, cell fusion
  2. CPE can be used to identify a causative agent
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17
Q

What is the general virus multiplication cycle?

A
  1. ATTACHMENT–Viral outer proteins or glycoproteins (VAPS on envelope viruses), bind to chemical groups/receptors on host cell
  2. UPTAKE–by pincocytosis or fusion of viral envelope iwth cytoplasmic membrane
  3. UNCOATING—Virus enters the cell–(non-enveloped gets taken into the vacuole, uncoated, virus is released)
  4. EARLY mRNA and protein (shut off host synthesis and make needed enzymes)
  5. DUPLICATION of nucleic acid
  6. LATE mRNA and protein
  7. ASSEMBLY and intracellular virus accumulation
  8. RELEASE by lysis or by budding out of cell membrane (if enveloped)
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18
Q

What are viroporins?

A
  1. Small, hydrophobic virus encoded proteins that oligomerize at host cell membranes where they are involved in enveloped virus budding and non-enveloped virus cellular lysis.
  2. Have cytopathogenic effects on cell–help to form hydrophillic pores and alter calcium and H gradients
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19
Q

What happens during the maturation and budding of an enveloped viron?

A
  1. Virus assembled in nucleocapsid migrates to membrane where proteins are, buds out and is released (Viral specified proteins on cytoplasmic membrane of infected cell)
  2. Free infectious virion is released into the cell
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20
Q

What happens during the viral life cycle?

A
  1. Capsid penetrates cell
  2. Capsid is uncoated
  3. Host functions replicate genetic material
  4. New virions are assembled and released
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21
Q

What is the one step growth cycle? (virons per cell)

A
  1. Virus is absorbed into the cell, period of time there is no infectious virus
  2. Eclipse period: time it takes before you start to see viruses being made
  3. Latent period: amount of time it takes before the release of the infectious virus
  4. Burst size: the number of viruses you get out, is different for every virus/cell
  5. A virus in an ACTIVELY REPLICATING cell has a shorter/faster explipse period, than a dormant cell (plays a role in the amount of time you have to inactivate virus)
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22
Q

What is the one step growth cycle? (molecules per cell)

A
  1. Virus goes in and gets uncoated
  2. mRNA is synthesized
  3. Series of “early” viral proteins–involved in replication of nucleic acid
  4. Late proteins are the structural proteins of virus (envelope or nucleic capsid)
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23
Q

Where do RNA viruses replicate?

A

Cytoplasm of the cell except for orthomyxoviruses (influenze and retroviruses)

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24
Q

What are other characteristics of RNA virus replication?

A
  1. SS
  2. Classified positive, negative or ambisense depending on ability of virion RNA to asct as messenger RNA
  3. Enveloped
  4. Helical capsids–except for picornavirus, reoviruses and togaviruses
  5. Cells lack cytoplasmic RNA polymerase, so RNA viruses must produce own replicase/transcriptase
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25
Q

What are the characteristics of viral GENOME replication?

A
  1. Negative Sense RNA have replicase/transcriptase associated with RNA in the virion
  2. All ss RNA viruses (except retroviruses) replicate via a double-stranded RNA intermediate.
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26
Q

How are retroviruses different from normal RNA virus replication?

A

Retroviruses use a host cell, DNA dependent RNA polymerase. They also use a reverse transcriptase in their nuclear phase.

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27
Q

Is the spontaneous mutation frequency higher in DNA or RNA viruses?

A

RNA viruses is higher than the DNA viruses because their RNA polymerase is not as accurate in duplication

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28
Q

Where does the transcription of orthomyxoviruses and retrovirus mRNA occur?

A

In the nucleus

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29
Q

Why have RNA viruses had to use unique mechanisms to express their genomes? What are examples of some of these?

A

RNA viruses have unique mechanism to produce individual polypeptides from polycistronic RNA since this is not a property of eukaryotic cells.

  1. Picornavirus synthesizes polypeptides that are then cleaved by viral proteases
  2. Individual initiation and termination signals appear throughout RNA of rabies virus (ssRNA initiation,term throughout)
  3. All transcription begins on 3’ end, but polymerase slides over various size intervening sequences to yield transcript of various compositions and lengths
  4. Orthomyxoviruses and reoviruses have segmented genomes
  5. Retroviruses have spliced transcripts

**Some RNA viruses use a combination of strategies

(HIV and POLIO use these mechanisms)

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30
Q

Where does replication of viral DNA occur?

A

In the NUCLEUS except for POXYVIRUSES which replicates in the cytoplasm.

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31
Q

What is needed for viral DNA replication?

A
  1. Host functions expressed during S phase
  2. Availability of host cell DNA binding proteins for transcription to help determine tissue trophism and host range of virus
  • *Some DNA viruses cause non-productive infections
  • **all dna viruses except paroviruses can transform cells
32
Q

How do Pox viruses replicate and where?

A
  1. Cytoplasm!
  2. Provide their own mRNA and DNA synthetic machinery
  3. Code for viral DNA dependent RNA polymerase and mRNA modifying enzymes for processes like capping and methylation
  4. Poxviruses synthesize their own envelope
33
Q

What viruses have a double stranded DNA genome?

A

HAP

  1. herpesviruses
  2. adenoviruses
  3. papovaviruses
34
Q

What viruses have a partially double stranded DNA genome?

A
  1. Hepadnaviruses
  2. Replicate their DNA in the nucleus via a RNA intermediate using an RNA-dependent DNA polymerase (reverse transcriptase) in their replication
  3. Can transform cells
  4. HBV–acute/chronic hepatitis
35
Q

What type of genome do parvoviruses have? How do they replicate?

A

SS, DNA

Replication steps:

  1. Enters nucleus through nuclear pores
  2. Single-stranded DNA forms hairpin structure which self primes cellular DNA polymerase to synthesize complimentary strand
  3. Double-strand DNA uses cellular DNA polymerase and viral specific endonucleases to form genome DNA
  4. Some strains need a helper virus to replicate (e.g., adeno-associated virus)
36
Q

What is cellular transformation in infected cells?

A

When RNA and DNA viruses cause a stable, inheritable change that results in poor or no control of cellular division

37
Q

What do DNA tumor viruses do to permissive and non-permissive cells?

A
  1. Permissive cells: DNA tumor viruses LYSE, RNA tumor viruses TRANSFORM (some carry oncogenes responsible for transformation)
  2. Non-permissive cells: Dna tumor viruses TRNASFORM
38
Q

What is carcinogenesis and what are the general features of cellular transformation?

A

Carcinogenesis (making cancer) is a multistep process involving multiple genetic changes

Cellular transformation:

  1. Stable, heritable change resulting in poor or no control of cellular growth
  2. Alters morphology, growth control and cellular and biochemical properties
  3. All tumor viruses are DNA viruses or generate a DNA provirus (Retrovirus)
  4. Certain DNA and RNA viruses are associated or implicated in human cancers
39
Q

In what family is the human papilomavirus and what human cancers is it associated with?

A
  1. Papovaviridae
  2. Genital tumors (cervical, vulvar, penile cancers), Squamous cell carcinoma
  3. No envelope
  4. DS circular
40
Q

In what family is the EBV virus and what human cancers are associated with it?

A
  1. Herpesviridae
  2. Nasopharyngeal carcinoima, African Burkitt’s lymphoma, B cell lymphoma (NAB)

DS, Linear, has envelope

41
Q

What family is the Herpes simplex type 2 virus in and what human cancers is it associated with?

A
  1. Herpesviridae

2. Cervical carcinoma

42
Q

What family is the Hepatitis B virus in and what human cancers is it associated with?

A
  1. Hepadnaviridae

2. Hepatocellular carcinoma

43
Q

What family is the HTL virus in and what human cancers is it associated with?

A
  1. Tetroviridae

2. Adult T cell leukemia

44
Q

What are cellular oncogenes?

A
  1. Mutated forms of normal cellular genes
  2. Code for a heterogeneous group of proteins that are involved in normal cell division or differentiation pathways
  3. Abnormal regulation leads to cellular transformation/cancerous growth
45
Q

What are proto-oncogenes?

A

A normal gene that can become an oncogene due to mutations or increased expression. Proto-oncogenes code for proteins that help to regulate cell growth and differentiation.

46
Q

What are viral oncogenes?

A
  1. Copies of cellular oncogenes that have been acquired by certain viruses during replication
  2. Present in the viral genome
  3. Resonsible for cellular transforming activity of viruses which contain them
47
Q

What are tumor suppressor genes?

A
  1. Negative regulators of cellular growth (sometimes called anti-oncogenes or growth suppressor genes)
  2. Cause cellular transformation if the functional activity of both alleles is lost
  3. Exemplified by the retinoblastoma (Rb) gene and the p53 gene
48
Q

What is the difference between DNA and RNA tumor viruses?

A
  1. DNA tumor viruses TRANSFORM non-permissive cells; they KILL permissive cells–rarely produce tumors in the natural host (human DNA tumor viruses are the exception)
  2. RNA tumor viruses TRANSFORM both permissive and nonpermissive cells and do produce tumors in the natural host
49
Q

What are the characteristics of DNA tumor viruses?

A
  1. TRANSFORM only non-permissive cells (infected cells that don’t support total virus replication)
  2. Specific viral proteins interact with products of tumor suppressor genes leads to/contributes to the transformation process
  3. EBV, HBV, HSV, and HPV are associated with human cancers
50
Q

What is the oncogenic potential of adenoviruses? What are the types that are highly oncogenic?

A
  1. Vary in their oncogenic potential from high to not at all

2. types 12, 18 and 31 are highly oncogenic

51
Q

What are the transformation characteristics of adenoviruses?

A
  1. Transform rodent cells b/c can cause productive infection

2. No association with human neoplasms

52
Q

What are the transforming proteins associated with adenoviruses?

A
  1. E1a–binds to 110 (represses cell proliferation)
  2. E1b–binds to p53 (represses cell proliferation)
  3. TP’s can bind, but normal process goes on and cells lyses.
53
Q

What are the types of papiilomaviruses?

A
  1. 60 different types have been described

2. Types 16 and 18 have a strong association with cervical intraepithelial neoplasia (CIN)

54
Q

What are the transformation characteristics of papilomaviruses?

A

DDITCH

  1. HPV DNA- majority of cervical, penile and vulvular cancers contain HPV DNA
  2. Cofactors: include tobacco smoke and coinfection with HSV
  3. Differentiating keratinocytes-where virus multiplies
  4. Type 16 transforms rodent cells
  5. Viral DNA is episomal in normal tissue, but integrated in cancers and CIN
55
Q

What are the transforming proteins associated with Papillomaviruses?

A
  1. E6 – binds to p53

2. E7 – binds to p110Rb

56
Q

What are the types of Polyomaviruses?

A
  1. BK Virus (renal transplant patient)
    JC (PML patient)
  2. SV-40 replicates in monkey cells, transforms rodent cells and induces tumors/transform cells in newborn hamsters
57
Q

What are the transforming proteins associated with polyomaviruses?

A
  1. SV-40 – large tumor (T) antigen has domains that bind to p110Rb and p53
  2. One or two of the three polyoma virus T antigens have transforming activity
58
Q

How is EBV linked to herpesviruses?

A
  1. Some herpesviruses are linked to human cancer, the data is most convincing for EBV
59
Q

What is EBV?

A
  1. Linked to Burkitt’s lymphoma and nasopharyngeal carcinoma
  2. EBV DNA in Burkitt’s cells–> virus is there!
  3. Viral genome is mostly multiple episomes, but some is integrated (most sits out side as episome–an extra chromosomal piece of DNA)
  4. Important viral proteins involved in transformation include: EBNA-2 (transcriptional transactivator), LMP 1 and LMP 2a and b (tyrosine kinases) (if they are not there/mutated don’t get transformation)
  5. Possible cofactors involved are malaria and c-myc proto-oncogene translocation (chromosome 8 to 14)
60
Q

What is HSV-2?

A
  1. Implicated in cervical cancer and CIN

2. DNA fragments, including those containing ribonucleotide reductase, can transform cells

61
Q

What is CMV?

A
  1. Implicated in cervical cancer and CIN

2. Some DNA segments can transform cells

62
Q

What is HHV-8 (KSHV; Kaposi’s sarcoma-associated herpes virus)?

A
  1. Cause of Kaposi’s sarcoma
  2. Implicated in multiple myeloma
  3. Contains 16 cellular genes including C-cyclin and cytokines
63
Q

What are pox viruses?

A
  1. No human viruses cause tumors, although molluscum contagiosum virus produce benign growth of cells
  2. Rabbit Shope fibroma virus and Yuba monkey tumor virus cause fibromas and benign tumors in their hosts
64
Q

What are hepadnaviruses?

A
  1. 75-85% of primary human hepatocellular carcinoma cells carry human hepatitis B virus (HBV) genes
  2. Impaired immunity and alcohol-associated hepatic cirrhosis are co-factors
  3. X protein interacts with p53
  4. Latency period between infection and primary hepatocellular carcinoma ranges from 9-35 years
64
Q

What are hepadnaviruses?

A
  1. 75-85% of primary human hepatocellular carcinoma cells carry human hepatitis B virus (HBV) genes
  2. Impaired immunity and alcohol-associated hepatic cirrhosis are co-factors
  3. X protein interacts with p53
  4. Latency period between infection and primary hepatocellular carcinoma ranges from 9-35 years
65
Q

Which subfamily of oncoviruses has oncogenic potential?

A

Oncovirus subfamily of the retroviruses have oncogenic potential for certain permissive cells

67
Q

What are the three mechanisms by which oncoviruses can cause transformation?

A

IIT

  1. Introduce oncogenes
  2. Insertional activation or promoter insertion
  3. Transcriptional activation
68
Q

What are the important aspects of retroviruses?

A
  1. Enveloped virus with an icosahedral capsid that contains a helical nucleoprotein
  2. Undergoes reverse transcription
  3. Genome (as DNA) integrated into host DNA
  4. Cause tumors
  5. Some members carry oncogenes
    HIV-1, the cause of AIDS
68
Q

What are the morphological type of most oncoviruses?

A

Type C

69
Q

What are the subfamilies of retroviruses?

A

LOS

  1. Lentiviruses
    HIV – man
    Visna – sheep
  2. Spuma viruses
    Foamyvirus
  3. Onco viruses–the only ones that transform cells
    Types B, C, and D
70
Q

What are exogenous type C viruses?

A
  1. Spread horizontally; behave as infectious agents
  2. When oncogenic, mainly cause tumors of reticuloendothelial system and hematopoietic systems (leukemia, lymphomas) or connective tissue (sarcomas)
72
Q

What are endogenous type C retroviruses?

A
  1. Found in all cells of all individuals of a species–part of our genetic make up
  2. Viral information can be activated by radiation, chemical carcinogens or metabolic inhibitors, part of our genetic constitution; not pathogenic for host unless activated
73
Q

What are virogenes and how are the related to retroviruses?

A

PEG

The viral genes involved in replication e.g., gag, pol and env

74
Q

What are the replication patterns of oncoviruses?

A
  1. Viral oncogenes:Viral copies of cellular oncogenes involved in cellular division or differentiation pathways (Include v-ras, v-sis, v-src, v-myc, etc.)
  2. Non-defective viruses: Have all their virogenes and can replicate themselves. Have high oncogenic potential if they also contain an oncogene (Most leukemia viruses and Rous sarcoma virus, an acute tumor virus, contains virogenes and an oncogene)
  3. Defective viruses: Have lost part or an entire virogene which has been replaced by an oncogene. Require a helper virus for replication. Have high oncogenic potential
75
Q

How does retrovirus replication occur?

A
  1. Reverse transcription: creating a DNA copy of RNA
  2. Stuck into host cell chromosome by integrase
  3. mRNA and positive sense full length (will become genome RNA) from it
  4. Goes into cytoplasm and uses our cellular machinery to make proteins from mRNA
  5. Create more virions that leave cell, and every time cel replicates has viral DNA
75
Q

What is the mechanism of oncogenic cells?

A
  1. Mechanism of acute transforming viruses:
    Used by both nondefective viruses (e.g., Rous sarcoma virus) and defective viruses (e.g., many sarcoma and acute leukemia viruses, like Abelson murine leukemia virus) to transform cells
    **Oncogene is integrated into host cell DNA and used to create cancer
  2. Insertional activation or promoter insertion (e.g., chronic leukemia viruses and mouse mammary tumor virus): Involves viral promoters and transcriptional enhancer in LTR’s in activation of cellular oncogenes. A mechanism of transformation by CHRONIC transforming viruses, takes a while to progress

**Virus sits on on oncogene of host cell that promotes cell division in host cell and causes good cell to over replicate

  1. Transcriptional activation (e.g., HTLV-1 and 2):
    Involves transactivator proteins to activate cellular oncogenes
    The tax protein of HTLV-1 enhances transcription of viral genes and cellular genes like IL-2, IL-3, GMCSF and IL-2 receptor (always activated in cells that are ready to divide

**Virus gets into cell, activates promoter region and causes replication, increases transcription of both DNA of host cell AND DNA of virus

Exam 3 (12 decks)

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