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Foundations Exam 3 > DNA Viruses > Flashcards

DNA Viruses Flashcards

1
Q

where do DNA and RNA viruses replicate, respectively?

A

DNA viruses replicate in nucleus (except Poxvirus)

RNA viruses replicate in cytoplasm

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2
Q

what virus does this describe?
- smallest pathogenic virus
- has linear (-)ssDNA
- replicates only in dividing cells, esp. erythrocyte precursors in the bone marrow

A

Parvovirus B-19!

common childhood infection with fever/rash (“slapped cheek”) or transient anemia (aplastic crisis!)

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3
Q

what kind of virus is Parvovirus B-19 and what kind of disease does it cause? (3)

A

Parvovirus B-19: linear (-)ssDNA

clinical:
1. Fifth disease: common childhood infection with fever and “slapped cheek” rash + trunk/extremities
2. aplastic crisis (patients with hematological abnormalities)
3. 1st trimester spontaneous abortions/birth defects

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4
Q

what kind of viruses are Papovaviruses and where did this name come from?

A

Papovaviruses: dsDNA viruses (require host cell replication machinery), named for its 3 original members:

  1. PApilloma - epithelial lesions
  2. POlyoma - tumor in animals, subclinical in humans
  3. Simian VAcuolating virus 40 - no human disease
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5
Q

where does Human Papilloma Virus (HPV) replicate, and on what terms?

A

HPV replicates in epithelial cells, but cells must differentiate for virus to go through full replication cycle -

therefore, virus early proteins keep infected cell in division cycle (ultimately kills cells)

*remember that HPV is Papovavirus, dsDNA genome

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6
Q

what disease does HPV most commonly cause? what is it a risk factor for?

A

most commonly causes condylomata (warts) - proliferative lesions

major risk factor for cervical cancer (sexual transmission)

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7
Q

what 2 viral proteins does HPV use to disrupt host cell cycle, and how do they work?

A

early viral proteins E6 and E7

E6: binds p53 (blocks apoptosis)
E7: binds Rb (Retinoblastoma) to disinhibit E2F (transcription factor)

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8
Q

how does HPV function as a major risk factor for cervical cancer? (how does malignancy occur?)

A

abortive HPV infection —> viral DNA fragment integrated into host DNA —> early genes expression

early gene expression drives cell into continuous division, but late proteins are not made so cells are not killed

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9
Q

what type of virus does this describe?
- transforms cell cultures but does not cause human cancers
- E1A and E1B drive infected cells into division
- 40+ types but only a few cause infection - respiratory, conjunctivitis, GI, febrile pharyngitis

A

Adenovirus

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10
Q

what family of virus does this describe?
- largest, most complex
- replicates in cytoplasm
- enveloped, brick-shaped
- lateral bodies contain proteins that modulate immune responses

A

Poxvirus: DNA virus but replicates in cytoplasm because it makes its own replication enzymes

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11
Q

which DNA virus replicates in the cytoplasm?

A

Poxvirus: largest and most complex, enveloped, brick-shaped

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12
Q

you identify a large brick-shaped, enveloped virus that contains lateral bodies - what virus is this, and what do the lateral bodies contain?

A

Poxvirus: largest, most complex, DNA virus but replicates in cytoplasm

lateral bodies contain proteins that modulate immune responses

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13
Q

what 3 Poxvirus are pathogenic to humans? (DNA virus)

A
  1. Smallpox
  2. Molluscum contagiosum virus: local infection (chest, face) of fleshy bumps (dome with little indentations/umbilications)
  3. Monkey pox
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14
Q

Pt is an 8yo M presenting with fleshy, dome-shaped bumps covering his chest, which began 3mo ago. Microscopy of one of the lesions reveals large, brick-shaped viruses within cytoplasm.

What is going on?

A

Molluscum contagiosum virus: type of Poxvirus (DNA virus), causes local (face, chest, back) infection of fleshy bumps with indentations (umbilications)

can last months, self-limiting

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15
Q

What are the 2 clinical forms of Smallpox (type of Poxvirus, DNA virus)?

A
  1. Variola major: severe, most common - extensive rash, high fever
  2. Variola minor: less common, less severe

*note epidemics were once widespread, but has since been “eradicated” - vaccination no longer performed, potential for bio-warfare

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16
Q

describe the transmission and pathology of Smallpox (DNA virus, Poxvirus)

A

Smallpox: transmission via respiratory droplets or fomites, infects macrophages

rash (oral cavity and body): macules —> papules —> vesicles —> pustules —> scab —> pox (scar)

recovery = lifelong immunity

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17
Q

how is Monkeypox (Poxvirus, DNA virus) transmitted, and what disease does it cause?

A

Monkeypox: transmitted via MSM and household contacts (via direct contact, respiratory secretions, fomites, vertical)

—> systemic febrile illness, rash (similar to smallpox but fewer), possible complications in immunocompromised

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18
Q

what type of vaccine is available for monkeypox (DNA poxvirus)?

A

live, attenuated vaccinia virus (also works for smallpox)

*remember that Vaccinia virus is the vaccine strain of smallpox, but smallpox vaccine is not given routinely anymore because it is “eradicated”

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19
Q

for the following forms of Human Herpesvirus, name what disease it causes:
a. HSV1
b. HSV2
c. Varicella-Zoster
d. Epstein-Barr

A

a. HSV1: cold sores
b. HSV2: genital herpes
c. Varicella-Zoster: Varicella = chickenpox, Zoster = shingles (but same virus)
d. Epstein-Barr: infectious mononucleosis

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20
Q

what kind of virus and shape is Human Herpesvirus?

A

enveloped linear dsDNA, icosahedral capsid

[recall that because it is enveloped, fusion occurs at host plasma membrane, leaving spike glycoproteins on surface, which can serve as red flags for immune system]

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21
Q

what is contained in the tegument of Human Herpesvirus (linear dsDNA virus)?

A

tegument: amorphous shape, contains viral proteins and mRNA

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22
Q

describe the protein synthesis cascade of Human Herpesvirus (linear dsDNA virus)

A

immediate early genes —> delayed early genes (trigger DNA replication) —> late genes (structural proteins)

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23
Q

how are Herpes viruses (linear dsDNA) classified? name the strains in each category

A

alpha: HSV1, HSV2, VZV
beta: CMV, HHV6, HHV7
gamma: EBV, HHV8

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24
Q

contrast the general features of alpha to beta to gamma herpes (linear dsDNA)

A

alpha: large host range, short reproductive cycle, spread rapidly, latent in sensory ganglia, kill infected cells (HSV1, HSV2, VZV)

beta: restricted host range, long reproductive cycle, slow infectivity, latent in monocytes, infected cells become large (CMV, HHV6, HHV7)

gamma: specific to T/B lymphocytes, latent in lymph tissue (EBV, HHV8)

25
Q

what category of herpes virus (linear dsDNA) does this describe?

large host range, short reproductive cycle, spread rapidly, latent in sensory ganglia, kill infected cells

A

alpha: HSV1, HSV2, VZV

26
Q

what category of herpes virus (linear dsDNA) does this describe?

restricted host range, long reproductive cycle, slow infectivity, latent in monocytes, infected cells become large

A

beta: CMV, HHV6, HHV7

27
Q

which category of herpes virus are restricted to infecting T and B lymphocytes?

A

gamma herpes: latent in lymph tissue (EBV, HHV8)

28
Q

how does herpes virus (linear dsDNA) evade the immune system, allowing for its latency? (4)

A
  1. cytokine homologs bind receptors
  2. remove MHC I chains from ER or induce endocytosis of MHC I from cell surface (hides from NK cells)
  3. inhibit interferon activity
  4. block apoptosis
29
Q

what 3 illnesses does HSV1 (alpha herpes) cause?

A
  1. herpetic gingivostomatitis
  2. herpetic keratoconjuntivitis
  3. HS encephalitis (usually immunocompromised)*

*usually herpes simplex virus is localized, rarely it invades CNS

30
Q

which herpes strain causes the following diseases:

  1. herpetic gingivostomatitis
  2. herpetic keratoconjuntivitis
  3. HS encephalitis (usually immunocompromised)
A

HSV1 (alpha herpes)

31
Q

what diseases (2) does HSV2 cause? (alpha herpes)

A
  1. genital herpes
  2. neonatal herpes
32
Q

which strain of herpes causes genital and neonatal herpes?

A

HSV2 (alpha herpes)

33
Q

how is herpes simplex virus (HSV1/2, alpha herpes) transmitted, and where does it establish latency?

A

HSV1/2: transmitted via contact of infected lesions

HSV1 - primarily oral/oral or oral/genital
HSV2 - primarily genital/genital

multiplies locally via mucous membranes, spreads along neurons (not systemic)

latent infection in 1 sensory nerve ganglion adjacent to site of infection

34
Q

what would you see under a microscope if you examined a cell infected by herpes simplex virus (HSV1/2, alpha herpes)?

A

focal necrosis, multinuclear giant cells with intra-nuclear inclusion bodies (HSV is dsDNA virus, replicates in nucleus)

35
Q

when can free virus be observed in HSV infection (alpha herpes)? what is the clinical relevance of this?

A

only see free HSV during initial infection - give human antisera as prophylaxis for high risk patients (small time window to catch free virus)

36
Q

what is the major immune player against HSV infection (alpha herpes)?

A

Cytotoxic T lymphocytes (CTLs) - recognize viral glycoproteins on surface of infected cells

remember that herpes is enveloped and invades cell via fusion, so it will leave some evidence behind on the plasma membrane!

37
Q

what is the function of latency-associated transcripts (LATs) of herpes virus (dsDNA)?

A

LATs: viral mRNA transcripts that keep herpes in latency - stops replication, avoids immune recognition

when stimulated by certain conditions (stress, UV light, etc), virus can travel back down latently-infected sensory neuron and infect epithelial/mucosal cells at same site as initial infection

38
Q

how does Varicella-Zoster differ from HSV (both alpha herpes)?

A

VZV:
- transmitted via respiratory secretions (HSV: via contact)
- systemic (HSV: local)
- rash itches (HSV: painful lesions)
- latent in multiple sensory ganglion because it is systemic (HSV: only 1 sensory ganglion)

39
Q

what kind of vaccine is available for Varicella-Zoster (alpha herpes)?

A

live attenuated vaccine

40
Q

primary vs secondary viremia of Varicella-Zoster (alpha herpes)

A

primary viremia: lymph nodes and organs

secondary viremia: skin via WBC, rash in crops (waves) —> macules-papules-vesicles-pustules-scab-pox (scar)*

*note that this is the same sequence as smallpox, but chickenpox (VZV) occurs in waves - may see rashes at every stage in different parts of the body, while smallpox will be the same stage of rash throughout

41
Q

how can you clinically differentiate between smallpox and chickenpox (VZV)?

A

both cause rashes that progress in this order: macules-papules-vesicles-pustules-scab-pox (scar)

however, chickenpox (VZV) occurs in crops (waves), so there will be rashes in different stages all over body, while smallpox rash will look uniform

42
Q

describe how recurrence of VZV (alpha herpes) occurs and what clinically manifests

A

VZV: chickenpox first (Varicella), then shingles (Zoster) - but same virus

recurrence induced by immunosuppression —> virus travels along sensory axons (from latency) to sensory dermatomes

produces painful/vesicular lesions - usually one per episode (not all over body)

43
Q

what kind of herpes does this describe?
- usually asymptomatic infection in children
- salivary gland disease of newborns (serious CNS disease) via breast-feeding of infected mother
- mononucleosis-like disease (lymphadenopathy, splenomegaly, etc)

A

Cytomegalovirus (beta herpes)

44
Q

what kind of diseases does cytomegalovirus (beta herpes) cause?

A
  • usually asymptomatic infection in children
  • salivary gland disease of newborns (serious CNS disease) via breast-feeding of infected mother
  • mononucleosis-like disease (lymphadenopathy, splenomegaly, etc)
45
Q

choose the correct choice for cytomegalovirus (beta herpes):
slow vs fast infectious cycle
and
destruction vs no destruction of infected cells

A

CMV: slow infectious cycle, does not kill infected cells (no necrosis) —> cytomegaly with owl eyes (2 nuclei with nuclear inclusions)

46
Q

what would you see under a microscope if you examined a cell infected by cytomegalovirus (beta herpes)?

A

it’s in the name - cytomegaly !

looks like owl eyes (2 nuclei with inclusions)

CMV does not kill infected cells and has slow infectious cycle

47
Q

how is cytomegalovirus (CMV, beta herpes) transmitted, which cells does it infect, and how does it spread?

A

CMV: transmitted via infected body fluids (sexual, blood)

infects epithelial cells and leukocytes, spreads to all organs, latent in neutrophils and monocytes

48
Q

how are HHV6 and HHV7 (beta herpes) transmitted, and what is their clinical significance?

A

HHV6/7: ubiquitous, transmitted via oral secretions, latent in peripheral blood lymphocytes, reactivated via pneumonitis/fever/hepatitis/encephalitis

HHV6 —> Roseola infantum (febrile, rash on trunk/neck), progression of HIV

HHV7 - asymptomatic

49
Q

which herpes causes Roseola infantum and is also associated with the progression of HIV to AIDs?

A

HHV6 (beta herpes): ubiquitous, transmitted via oral secretions

Roseola infantum: febrile illness with rash on neck/trunk

50
Q

which herpes virus is associated with several human tumors, including Burkitt’s, nasopharyngeal carcinoma, and Hodgkin’s? what illness does it definitely cause?

A

Epstein-Barr virus (gamma herpes) - causes infectious mononucleosis

[recall that EBV is associated with African Burkitt’s - lymphoma in jaw]

*recall that gamma herpes are latent in lymph tissues, which makes sense considering these associations

51
Q

how is Epstein-Barr (gamma herpes) transmitted and where does it establish latency?

A

EBV: transmitted via respiratory secretions (saliva) with repeated exposure

infects and establishes latency in B cells (transfusions can then spread infected leukocytes)

carriers shed virus for life!

52
Q

which herpes virus can cause infected cell proliferation, but has no cytopathic effects or inclusion bodies?

A

Epstein Barr (EBV): gamma herpes, infects B cells, associated with several cancers (African Burkitt’s, Hodgkin’s)

53
Q

describe the host immune response to Epstein Barr (EBV, gamma herpes)

A

infected B cells produce nonspecific/polyclonal heterophile antibodies to viral membrane antigens

Downy cells: activated CD8 cells, “atypical lymphocytosis”, which kill infected B cells

*note that in immunosuppressed patients with ineffective cell-mediated immunity, lymphomas occur

54
Q

with what herpes virus are Downy cells associated and what are they?

A

Epstein Barr (EBV, gamma herpes): infected B cells produce heterophile (polyclonal) antibodies against viral membrane antigens

Downy cells: reactive CD8 T cells kill infected B cells (“atypical lymphocytosis”)

55
Q

how does EBV maintain latency in B cells of lymph tissue? (gamma herpes)

A

latent B cells express viral proteins (not antigenic for CTLs) necessary for latency maintenance

56
Q

what test can be used to diagnose EBV (gamma herpes)?

A

EBV causes infectious mononucleosis

Paul-Bunnell Test (MonoSpot): detects heterophile antibodies, which agglutinate RBCs (polyclonal but specific to EBV)

[remember that heterophile Abs are polyclonal Abs produced by infected B cells]

57
Q

what 2 kinds of serology (based on time frame) can be used to diagnose EBV (gamma herpes)?

A

early: anti-viral capsid antigen

3-6 weeks post infection: anti-EBV nuclear antigen

58
Q

which herpes virus does this describe?
- rare, NOT ubiquitous
- associated with several lymphoproliferative disorders (Kaposi’s sacroma)
- AIDs-associated virus

A

Human Herpesvirus 8 (HHV, gamma herpes): aka Kaposi’s sarcoma virus

AIDs associated virus, rarely found in healthy individuals

associated with: Kaposi’s sarcoma, Body Cavity Lymphoma, Multicentric Castleman’s Disease

59
Q

HHV8 (gamma herpes) is also known as

A

HHV8 = Kaposi’s sarcoma virus

rarely found in healthy individuals, associated with several lymphoproliferative disorders (Kaposi’s sarcoma, Body Cavity Lymphoma, Multicentric Castleman’s Disease), AIDs-associated

Foundations Exam 3 (28 decks)

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