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PBD II > Viruses 2 - Retroviruses, HSV, etc. - KMS > Flashcards

Viruses 2 - Retroviruses, HSV, etc. - KMS Flashcards

1
Q

What is the genetic makeup of a retrovirus? What enzymes must be packaged in the capsule?

A

•Enveloped +ssRNA with reverse transcriptase (RNA-dependent DNA polymerase) and integration into host cell DNA

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2
Q

What viruses are pertinent from the Oncornavirus family?

A

•Oncornaviruses: HTLV 1, HTLV 2 (Human T-cell Lymphotropic Virus)

(a type of retrovirus)

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3
Q

Generally speaking, Oncornaviruses are what?

A

•Oncogenic transforming viruses

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4
Q

What does an HTLV-1 infection cause?

A

•HTLV-I produces HTLV myelopathy/tropical spastic paraparesis and T-cell leukemia/lymphomas

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5
Q

What does an HTLV-2 infection cause?

A

•HTLV-II associated with several cases of myelopathy/tropical spastic paraparesis and T cell lymphoproliferative disease (hairy-cell leukemia-like)

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6
Q

Why are Lentiviruses are clinically important?

A

Lentiviruses include HIV-1 and HIV-2

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7
Q

How is HIV spread?

A

•Spread by fluids (sex, transfusions, contaminated needles) or during pregnancy

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8
Q

How is an HIV virus able to gain access to a cell? What cells do they need to gain access to initially? What is essential for this process?

A

•Attach to CD4 receptor & CCR5 (mφ) or CXCR4 (TH cell) coreceptors

Absolutely need co-receptor for this process to occur

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9
Q

What cells does HIV-1 have a predilection for?

A

•Tropism for CD4+ (T-helper) cells

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10
Q

What are the initial symptoms of an HIV-1 infection?

A

•Lymphadenopathy, fever, weight loss and malaise

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11
Q

What is a common-ish neurological manifestation of AIDS? Why?

A

•AIDS dementia: mimics Alzheimer disease, may involve HIV infection of the brain and microglia

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12
Q

AIDS is frequently associated with what change in body habitus due to what syndrome?

A

•Wasting syndrome (“slim disease“) common in Africa.

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13
Q

Where is HIV-2 commonly found?

A

•HIV-2 similar to HIV-1 infection but restricted to W. Africa

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14
Q

How is AIDS diagnosed? What is tested for to help this Dx?

A
  • Dx- Occurrence of AIDS defining disease (opportunistic infection, malignancy, etc.)
  • Serology for HIV antibodies using the ELISA (Enzyme-Linked Immuno-Sorbent Assay) and Western Blot (tests for antibodies against viral proteins), PCR
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15
Q

How is HIV and AIDS treated?

A

•Rx – Antiretrovirals:

nucleoside/nucleotide analogues

nonnucleoside reverse transcriptase inhibitors

protease inhibitors

fusion inhibitors

chemokine coreceptor antagonists

integrase inhibitors

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16
Q

Why are the gag genes important for HIV infection? What genes are included, and what do they make?

A

Gag (group specific antigens) polyprotein

gag

p24 - capsid, early marker of infection

p7p9 - core nucleocapsid

p17 - matrix

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17
Q

Why are the pol genes important for HIV infection?

A

Pol (polymerase) polyprotein

pol:

Reverse transcriptase - produces provirus

Integrase - DNA integration into host DNA

Protease - cleaves viral polyprotein

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18
Q

Why are env genes important for HIV infection?

A

Envelope proteins

env:

gp120 - Binds CD4 & CCR5(mφ)or CXCR4(TH-cell)

gp41 - Host cell fusion protein

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19
Q

Why are LTR genes important for HIV infection?

A
  • LTR*: Long terminal repeat sequences
  • LTR* - Integration and viral gene expression
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20
Q

What is the genetic makeup of Herpesviruses? enveloped?

A

•Large, dsDNA and enveloped

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21
Q

What histological findings are common with Herpesvirus infection?

A

•Produce intranuclear inclusions and multinucleated giant cells

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22
Q

What unusual feature about Herpesviruses allow them to create recurrent infections? What types stay where in the body?

A
  • Capable of latency and can lead to recurrent infections
  • HSV-1, HSV-2 and VZV are “neurotropic”
  • CMV and EBV are “lymphotropic“
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23
Q

What is the natural reservoir of HSV, CMV, VZV, and EBV?

A

humans

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24
Q

Name the 8 types of HHVs and the diseases they cause.

A
  • *1.HHV 1 [α] - Herpes Simplex 1 (HSV-1)
    2. HHV 2 [α] - Herpes Simplex 2 (HSV-2)
    3. HHV 3 [α] - Varicella-Zoster virus (VZV)
    4. HHV 4 [ȣ] - Epstein-Barr virus (EBV) (Oncogenic transforming virus)
    5. HHV 5 [β] - Cytomegalovirus (CMV) (Oncogenic transforming virus)**
    6. HHV 6 [β]– Causes roseola infantum/exanthema subitum (sixth disease)
    7. HHV 7 [β]– Causes roseola infantum/exanthema subitum (sixth disease)
  • *8.HHV 8 [ȣ]– Kaposi Sarcoma-associated Herpesvirus (Oncogenic transforming virus)**
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25
Q

Where does herpes simplex initially replicate? How does reinfection manifest?

A

•Replicate initially in skin or mucosae followed by latent neural infection with subsequent recurrences of skin and mucosal lesions

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26
Q

What histological findings should you associate with herpes simplex infections?

A

•Have intranuclear acidophilic Cowdry type A inclusions

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27
Q

How is HSV-1 typically transmitted, and what can it cause?

A
  • Usually transmitted by saliva
  • “Cold sores” (herpes labialis)
  • Gingivostomatitis – oropharyngeal blister in kids
  • Herpetic keratitis - if accompanied by conjunctivitis can lead to corneal scarring and blindness
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28
Q

What is a potentially disastrous outcome of HSV-1?

A

•Fatal sporadic encephalitis, #1 cause in U.S.

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29
Q

What is the typical presentation of an HSV-2 infection?

A

•Genital herpes – blistering skin/mucosal lesions

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30
Q

What are 2 lesser known presentations of HSV-2 infections?

A
  • Whitlows – erythematous lesions on toes or nail cuticle
  • Neonatal herpes - local or disseminated (50% mortality if untreated) Herpetic meningitis & encephalitis also occur
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31
Q

How is HSV-2 typically transmitted? What other infection can it increase chances contracting?

A
  • Generally transmitted by sexual contact or during delivery
  • Increases risk of subsequent HIV infection
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32
Q

How is a HSV infection Dx’ed?

A

•Dx – cytology, immunostaining, PCR

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33
Q

How is an HSV infection treated?

A

•Rx – acyclovir (other “ciclovir” anti-virals)

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34
Q

How is Varicella-Zoster Virus (VZV) typically transmitted?

A

•Respiratory transmission

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35
Q

What does the “Varicella” half of VZV cause? What does this disease look like?

A

Chickenpox:
•Mild infection in children (worse in adults)
•Usually transmitted by saliva
•After 2 weeks, skin rash first on the head and trunk, and later on the extremities (asynchronous and centripetal spread)
•Macules to papules to vesicles to pustules to crusts
•Intranuclear inclusions at base of vesicle

36
Q

How does the chickenpox rash typically spread?

A

•Usually transmitted by saliva

  • After 2 weeks, skin rash first on the head and trunk, and later on the extremities (asynchronous and centripetal spread)
  • Macules to papules to vesicles to pustules to crusts
37
Q

What does the “Zoster” half of VZV cause?

A

Shingles - zoster

  • Older individuals with reactivation of latent infection
  • Skin areas innervated by sensory nerves of the dorsal root ganglia
  • Trigeminal nerve is common distribution
  • Very painful radiculoneuritis
  • Occasional debilitating transverse myelitis
38
Q

What is the distribution of the rash and the symptoms associated with shingles?

A
  • Skin areas innervated by sensory nerves of the dorsal root ganglia
  • Trigeminal nerve is common distribution
  • Very painful radiculoneuritis
  • Occasional debilitating transverse myelitis
39
Q

How is a shingles infection Dx’ed?

A

•Dx – clinical, cytology, PCR

(Rash will be very distinctive - often unilateral dermatome distribution)

40
Q

How is shingles treated?

A

•Rx - acyclovir

41
Q

How is shingles prevented?

A
  • 2 doses of varicella (VAR); 12 through 15 months & 4-6 years
  • Zoster vaccine (Zostavax®) for people aged 60 years and older
42
Q

What is the genetic makeup of Epstein-Barr virus (EBV)?

A

•dsDNA & envelope

43
Q

How is EBV typically spread?

A

•Human to human via saliva

44
Q

How does EBV gain entrance to cells, and what cells and receptors does it seek out?

A

•Attach via CD21
•= Complement receptor 2 = EBV receptor
•Normally acts as receptor for C3d, C3dg, and iC3b

45
Q

What common disease does EBV cause? What are the symptoms and findings?

A

•Infectious mononucleosis
•Fever, fatigue, malaise and pharyngitis
•Atypical activated T-lymphocytes (Downey cells)
•Can develop hepatitis, splenomegaly and other complications

46
Q

EBV latently affects what cells? What can this cause?

A

•EBV latently infects B-cells, potential for recurrence

47
Q

EBV also has what worrying characteristic? What other diseases is it associated with due to this characteristic?

A
  • Oncogenic transforming virus
  • Hodgkin lymphoma, Burkitt lymphoma, central nervous system lymphomas, & nasopharyngeal carcinoma

•Hairy oral leukoplakia in HIV patients

48
Q

How is an EBV infection Dx’ed?

A

•Dx – heterophile antibodies (Monospot), antibodies to viral capsid antigens

49
Q

How is an EBV infection usually treated?

A

•Rx - supportive

50
Q

What histological findings are associated with Cytomegalovirus (CMV) infection?

A

•Owl-eye basophilic intranuclear inclusions

51
Q

What cells does CMV infect?

A

•Infects monocytes and monocyte precursors

52
Q

Name 8 ways CMV is transmitted. (Or at least 4 important ones.)

A

•Transplacental - primary infection pregnant mother
•Neonatal - cervical or vaginal secretions during birth
•Perinatal -breast milk from a mother who has active infection
•Saliva – common during preschool years
•Genital - dominant mode after about 15 years of age
•Respiratory secretions
•Fecal-oral
•Iatrogenic - organ transplants or blood transfusions

53
Q

CMV infections are often asymptomatic. However, what 2 diseases are associated with infection?

A

•CMV mononucleosis-syndrome with fever, fatigue and atypical lymphocytes

•Congenital cytomegalovirus infection (cytomegalic inclusion disease of the newborn)-in utero infections with jaundice, purpura, hepatosplenomegaly and central nervous system development disorders

•Associated with mucoepidermoid carcinoma

54
Q

How is a CMV infection Dx’ed?

A

•Dx- cytology, serology. culture or viral DNA by PCR or antigens

55
Q

How is a CMV infection treated?

A

•Rx- supportive +/- ganciclovir

56
Q

What is the genetic makeup of the Poxviridae family?

A

•dsDNA with envelope

57
Q

Where do the viruses that make up the Poxviridae family typically replicate?

A

•Replicate in the cytoplasm of host cell

58
Q

What 2 clinically important diseases are caused by the Poxviridae family?

A

Smallpox

Molluscum contagiosum

59
Q

What is molluscum contagiosum? How is it spread? What does it look like?

A

Molluscum contagiosum

  • Common self-limited viral disease caused by Poxvirus
  • Spread by direct contact, particularly seen among young children and adults
  • 0.2 -0.4 cm nodules on face, trunk and anogenital area
60
Q

What is the genetic makeup of Papovariedae/Papillomaviridae/Human Papilloma Virus (HPV)?

A

•Naked with circular dsDNA (>100 HPV serotypes)

61
Q

What cells does HPV typically infect?

A

•Trophic for epithelial cells of the skin and mucus membranes

62
Q

How common is HPV? How can infection present?

A
  • Possibly the most common sexually transmitted disease in the world
  • Infections may be latent (asymptomatic), subclinical, or clinical
63
Q

HPV is considered an oncogenic transforming virus(es). What lesions can they cause, and what cell cycle regulators do they mess up?

A

•Oncogenic transforming viruses
•Verrucae, papillomas, condyloma, and cervical, anal and pharyngeal cancers
•Viral E6 inhibits p53 protein and E7 inhibits pRB protein

64
Q

What are the low risk HPV strains associated with?

A

•Low risk - types 6 and 11 cause condylomas and oropharyngeal papillomas

65
Q

What are the high risk HPV strains associated with?

A
  • High-risk - types 16 and 18 responsible for most cancers and high grade dysplasias
  • Genome is incorporated into the host genome
66
Q

How are papillomaviruses generally transmitted?

A

•Generally transmitted by direct contact

67
Q

What is the Dx for an HPV infection?

A
  • Dx – Clinical for verrucae and condylomas
  • PCR for viral RNA of specific HPV types (e.g. types 16 & 18)
  • Cytology and or biopsy for cytopathic effects
68
Q

What is the Tx for an HPV infection?

A

•Rx – Depends on lesion type, anywhere from nothing to surgery to radiation and chemo

69
Q

What is the prevention for HPV infection?

A
  • Prevention – Vaccination (females 9-26 years) and physical barriers
  • Gardasil© (types 6, 11, 16 and 18)-three shots (0, 2 and 6 months)
  • Cervarix© (types 16 and 18)-three shots (0, 1 and 6 months)
70
Q

What is the genetic makeup of the Papovariedae/Polyomaviridae?

A

•Naked dsDNA

71
Q

What are the 2 clinically important viruses of the Polyomaviridae family?

A

BK and JC viruses

72
Q

What is the reservoir and transmission of the BK and JC viruses? What kinds of patients do these cause disease in?

A
  • Respiratory reservoir and transmission
  • Cause infections only in immunocompromised patients
73
Q

What disease does the BK virus cause? How is it Dx’ed?

A
  • BK - Renal disease (failure) in AIDS or post-transplant patients
  • Dx - BKV DNA by PCR or urine cytology with decoy cells (basophilic nuclear inclusions)
74
Q

What disease does the JC virus cause? How is it Dx’ed?

A
  • JC - Progressive multifocal leukoencephalopathy in AIDS or post-transplant
  • Dx - JCV DNA by PCR
75
Q

What is the genetic makeup of Adenoviridae?

A

•Naked dsDNA with numerous serotypes

76
Q

What is the transmission of Adenoviridae?

A

•Respiratory and oral-fecal transmission

77
Q

What diseases does the Adenoviridae family cause?

A
  • Acute respiratory disease – serotypes 4,7 &21) upper respiratory infections in kids/young adults that can progress to pneumonia
  • Gastroenteritis - adenoviruses that lead to diarrhea
  • Pharyngoconjunctivitis – pink eye and sore throat
  • Epidemic form also exists
  • Acute hemorrhagic cystitis – in older boys
78
Q

How is a Dx of Adenoviridae infection made? How is it treated?

A
  • Dx – Serology or PCR
  • Rx – supportive
79
Q

How is infection by Adenoviridae prevented?

A

•Prevention – live adenovirus vaccine (types 4 and 7); two concurrent oral tablets only approved for military personnel 17 -50 years of age

80
Q

What is the genetic makeup of Parvoviridae/Parvovirus 19?

A

•Naked ssDNA in segments (some positive, others negative)

81
Q

What is some additional interesting information about parvovirus 19?

A

•Proteins not well characterized but NS1 protein is thought to possess site-specific DNA-binding, DNA-nicking, ATPase, transcriptional, and helicase activities

(In gray, prolly not a high-yield topic)

82
Q

What is the reservoir for parvovirus 19? Incubation?

A
  • Reservoir is human respiratory tract with respiratory & vertical transmission
  • 7-10 day incubation
83
Q

What 2 clinically relevant diseases can result from parvovirus 19 infection?

A

•Erythema infectiosum (fifth disease)
•Fever, arthralgias and cheek rash children

•Aplastic anemia (infects erythroblasts)
•Can cause hydrops fetalis via in utero infection

84
Q

How is parvovirus 19 Dx’ed and treated?

A
  • Dx- serology or PCR
  • Rx- supportive
85
Q
A

PBD II (18 decks)

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