Viral classification, structure and replication of DNA Viruses: Adenoviridae, Poxviridae Flashcards

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1
Q

What are viral particals called?

A

Virions

This is considered the mature, infectious virus particle

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2
Q

What is a capsid?

A

This is a protein shell that encloses and protects the viral nucleic acid.

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3
Q

What is the nucleocapsid?

A

This is the internal part of the virus.

Consists of the nucleic acid and other associated proteins.

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4
Q

What is the enevlope?

A

This is the viral membrane

Consists of a lipid bilayer, proteins, and glycoproteins

Originally belonged to the host cell

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5
Q

What are the characteristics of animal viruses?

A

Small size, 0.03 um to 0.3 um

DNA or RNA is the genetic material

Amount of genetic material varies by virus type / species

Some viruses have segmented genomes and others have a single piece of nucleic acid

Usually only have one type of genetic material, DNA or RNA. Exception is the Mimivirus.

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6
Q

What is the Baltimore Classification of viruses?

A

The Baltimore Classification was named after David Baltimore

Class I - dsDNA

Class II - ssDNA

Class III - dsDNA

Class IV - ssRNA + strand

Class V - ssRNA - strand

Class VI - RNA viruses requiring a DNA intermediate for replication

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7
Q

What are the characteristics of the viral capsid?

A

Made up of protein subunits called capsomers

It protects the viral nucleic acid

Complex: Poxvirus

Icosahedral: Solid w/ 20 triangular faces, 12 verticies, 2,3,5 fold symmetry

Helical: Helical morphology

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8
Q

What are the characteristics of the viral envelope?

A

It surrounds the nucleocapsid

Formed from modified host cell membrane

Contains host-derived phospholipid bilayer

Contains virus-derived proteins and glycoproteins for attachment and viral fusion

Matrix proteins (M proteins) are often found associated with the inner layer of the envelope. Aid in viral structure.

Fusion proteins (F proteins) are found on the envelope surface. They cause viral membranes to fuse with cellular membranes.

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9
Q

How many families of human viruses are there and how are they classified?

A

There are six DNA virus families

13 RNA virus families

These viruses are classified based on their:

Nucleic acid

Symmetry of the nucleocapsid

Presence of an envelope

Dimensions of the virion and capsid

Nucleic acid sequence similarities

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10
Q

How are RNA viral families classified?

A

Symmetry of capsid - Icoshedreal or Helical

Envelope - Naked or eneveloped

Genome structure - SS, DS, + or - sense

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11
Q

How are DNA viruses classified?

A

Shape of capsid - Icosahederal, Helical, or Complex

Envelope - Naked or enveloped

Genome structure - SS, DS, linear, + or - sense, or circular

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12
Q

What are the steps of viral infection of a host cell?

A

Attachment to host cell

Entry of the virus into the host cell

Synthesis of viral proteins and genome

Assembly and release of mature virions

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13
Q

What is needed for a virus to attach to a host cell?

A

Viral receptors. These help determine host specificity.

Viruses tend to be very host specific and can be tissue specific.

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14
Q

What is the receptor for HIV-1?

A

CD4

Present on Macrophages and T cells

CD4 normally binds to MHC Class II in order to mediate T cell responses

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15
Q

What are the co-receptors for HIV 1?

A

Cxcr4 and Ccr5

Normally, these are chemokine receptors

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16
Q

True or false; The mode of entry into a cell depends on the viral family.

A

True

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17
Q

How do non-enveloped viruses enter cells?

A

1) Rearrangement of their capsid protein
2) Virus engulfed via receptor mediated endocytosis
3) Partial break up of capsid in vacuole followed by migration into the cytoplasm for further uncoating

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18
Q

How do enveloped viruses enter the host cell?

A

1) Fusion of viral membrane and cell membrane mediated by viral F protein
2) Phagocytosis and fusion of viral membrane with membrane of phagosome. Mediated by viral F protein.

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19
Q

Describe the F protein.

A

The F protein has a hydrophobic domain that can insert into the host cell membrane

The virus and host cell are brought close together and they are ready to fuse

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20
Q

How does HIV-1 binding take place?

A

SU binds CD4

Binding sites for Cxcr4 & Ccr5 are exposed

SU binds Cxcr4 or Ccr5 and induces a conformational change

Peptide is inserted into membrane

Individuals that are homozygous for deletions in Ccr5 are resistant to HIV-1 infection

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21
Q

What is the eclipse period?

A

This is the time from when nucleic acid is uncoated from its capsid

No infectious particles are present

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22
Q

What is the latent period?

A

No extracellular virus can be detected

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23
Q

What are the two mechanisms of virus release from a cell?

A

Disintegration of the infected cell (Burst) - Esp. in case of naked nucleocapsid virus

Slow release - Virus buds off of host cell membrane and acquires membrane in this way

24
Q

What does viral assembly refer to?

A

This is the ‘putting together’ of the virion protein shells

Can be done from individual polypeptides, a polyprotein precursor and/or chaperone-mediated

25
Q

What are the laboratory methods of confirming a viral diagnosis?

A

Isolation and growth of the virus

Cytopathic studies on cells in culture

Electron microscopy

Detection of viral components (Proteins, enzymes, nucleic acids)

Evaluation of patients immune response (Serology)

26
Q

What are the consequences of viral infection?

A

Depends on the virus:

Cell death and lysis

Transformation of host cell into cancerous phenotype

Fusion of membranes of adjacent cells (synctia) - Feature of cells that have been infected with virus that have F protein

Development of inclusion bodies in cells - HSV causes Cowdry type A and Rabies causes negri bodies

27
Q

How would one determine the infectious units of a virus?

A

Live cultivation

Use serial dilution end point method to determine:

Plaque formation (Viral lysis of cells in culture)

Focal Cytopathic changes in tissue culture

Focal proliferation of cells in tissue culture

Pock formation in membranes of chicken embryonated egg

Infection in experimental animals

28
Q

What are other laboratory procedures to investigate viruses?

A

Electron microscopy

Hemagglutinin

Immunological testing via Complement fixation or direct fluorescent antibody

Western Blot

ELISA

PCR

29
Q

How would one measure antibodies produced in response to a viral infection?

A

Complement fixation

Hemagglutination inhibition

Latex agglutination

ELISA

Indirect fluorescent antibody

Western immunoblot

30
Q

What are important immunological responses to viral infection?

A

Viral neutralization by antibodies

Cell-mediated immunity

Interferon production - Interferons inhibit viral multiplication and may provide temporary, localized protection for nearby cells

NK cells - Kill virally infected cells

31
Q

What do cytotoxic T cells do in response to viral infection?

A

Virally-infected cells process endogenously produced viral antigens and present them to cytotoxic T cells

Cytotoxic T cells are activated and are then produce cytotoxic substances

32
Q

How do antibodies prevent viral infection?

A

Antibodies bind to virus (Opsonize)

Endocytosis / phagocytosis is blocked

Uncoating is blocked via capsid stabilization and fusion interference

Virus is destroyed

33
Q

What are the most important cytokines in antiviral immune responses?

A

Type 1 interferons (alpha and beta)

The synthesis of the Type I interferons is induced in a cell by viral infection

This induction may be induced by active and inactivated virus, by ds RNA and other compounds

Interferons are host specific but not virus specific

34
Q

How do Type I interferons work?

A

After Type I interferons are released from a cell, they bind to other cells

A protein transcription factor is activated inside the cell that then turns on a set of genes

The products o f these genes inhibit viral protein synthesis, degrade viral mRNA, and promote apoptosis in virally infected cells

35
Q

What is the pattern of viral activity during an infection?

A

Localized infections: Viral multiplication and cell damage localized near the site of entry

Disseminated infection: Local multiplication at the site of entry, spread through the lymphatics to blood stream and circulation, multiplication at secondary sites, secondary viremia, infection of the target organ

36
Q

What does the incubation period refer to?

A

This is an asymptomatic period where infection is not apperant.

37
Q

How does varicella zoster virus infect and replicate?

A

Day 0: Infection via eye conjunctiva and/or upper respiratory tract

Replication in primary lymph nodes

Day 4-6: Primary viremia; replication in liver, spleen, and other organs

Day 14: Secondary viremia; infection of skin. Appearance of a rash. Infection of sensory ganglia and establishment of latent infection.

38
Q

What is an inapparant infection?

A

These are asymptomatic viral infections

Very common; may result from infection by attenuated virus or from effective host defense mechanisms

These are important medically because they represent an often unrecognized source for the dissemination of a virus. This may confer immunity on a host.

39
Q

What is an acute infection?

A

The virus infects the host and shortly after, disease ensues.

After a defined but short period of time, the host recovers.

The virus may be totally eliminated from the body or it can hide within the body and will result in a latent infection.

40
Q

What are the categories of persistent infections?

A

Latent Infections

Chronic Infections

41
Q

What is a latent infection?

A

Viral particles are not detectable but they will reappear during recurrences of the disease.

Viral nucleic acids are detectable between recurrences.

Herpesvirus infections are the best example of this.

42
Q

What are chronic infections?

A

The virus is always detectable and often shed.

Infected cells produce and release virus but cellular metobolism is little affected and the infected cells can grow and divide.

43
Q

How might viral diseases be controlled?

A

Prevention of transmission

Public health surveillance

Education

Isolation of disease cases

Passive immunization

Active immunization - Live attenuated, inactivated, or subunit vaccines

44
Q

How are most virus vaccines prepared?

A

Live tissue culture

Some genetically engineered vaccines are now being used

Viral DNA vaccines are an active area of research. DNA is engulfed by dendritic cells and protein antigen is presented to T cells. This elicits cell mediated immunity.

45
Q

What are the characteristics of a live, attenuated vaccine?

A

Offer many years of immunity

IgA and IgG antibodies are produced

Stimulates good cell-mediated response

Vaccine rarely reverts to virulence

46
Q

What are the characteristics of an i nactivated vaccine?

A

Immunity does not last a lifetime

IgG antibody produced

Poor cell-mediated response elicited

No reversion to virulence

47
Q

What is required to eliminate a virus from a population?

A

No animal reservoir

Good vaccine

Few or no subclinical cases (Latent infections ensure that virus will survive in population)

One antigenic type or only a few (No antigenic switching)

48
Q

How would on treat a viral disease?

A

Person must be symptomatic

Immune serum is best if given early in infection, before exposure or during incubation period

A limited number of drugs are available for treatment of viral diseases

49
Q

What are the characteristics of Poxviridae?

A

Large, brick-shaped complex particles

Replication of DNA much like that for cellular DNA but uses mainly virus-coded enzymes

Propensity to infect epidermal cells

Viral DNA replicates in cytoplasm of infected cells

50
Q

What are some of the characteristics of Variola (Small pox) virus?

A

Large DNA virus

Dumbbell shaped core

Has a complex membrane

Humans are the only known host in nature

Major health issue until immunization became wide-spread (vaccinia-live virus vaccine)

No naturally occuring cases since 1977 and declared extinct on Friday, Oct. 28, 1979

51
Q

How does smallpox cause disease?

A

Virus is inhaled and replicates in upper respiratory tract

Internal and dermal tissues are seeded with virus after two rounds of viremia

Hallmark “pox” forms (Lesions that are seen)

Two varients of small pox: Variola major (15-40% mortality) and Variola minor (1% mortality)

52
Q

What are the Level A CDC procedures for dealing with a suspected case of small pox?

A

If patient has suspect rash, isolate patient in negative air pressure room

Rule out chickenpox

Obtain specimen from lesion pustules

Contact state public health lab for further guidance

53
Q

What is the appearance of a patient with poxvirus?

A

Rashes have vesicles that appear in a centrifugal pattern

All lesions are at the same stage of debvelopment

Patients appear moribund

54
Q

What is the basis for the modern smallpox virus?

A

Vaccinia

55
Q

What is Molluscum contagiosum?

A

This is a pox virus

Transmitted by direct contact or fomites

Virus infects the basal cell layer and replicates

Molluscum contagiosum leaves benign epidermal tumors that can occur in people given vaccinia based vaccines (esp. in people with HIV)

Lesions are smooth, firm, shiny flesh colored to pearly white hemispheric papules with umbilicated centers confined to the skin and mucous membranes

Children, people that live in tropical climates and HIV+ are most at risk

56
Q

What are the characteristics of the adenoviridae?

A

Adenoviruses are medium sized (90-100 nm), ds DNA

49 immunologically/serologically distinct types organized into six subgenera called A through F. All of these can cause human infections. This is a frequent cause of the common cold.

They have naked icosahedral nucleocapsids

These are very stable to chemical and physical agents as well as adverse pH. This allows for prolonged survival outside of the body.

There is a fiber with a terminal knob that projects from each penton.

57
Q

What are the clinical features of adenovirus infection?

A

Most commonly cause respiratory illness

Depending on the infecting serotype, they may also cause various other illness such as gastroenteritis, conjunctivities, cystitis, and rash.

Respiratory symptoms range from common cold to pneumonia, croup, and bronchitis.

Patients with compromised immune systems are especially at risk.

Acute respiratory disease was first recognized among military recruits during WW II. Can be caused by adenovirus infections during conditions of crowding and stress.