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ID Week 1 > ILC 1.13: Herpesviruses > Flashcards

ILC 1.13: Herpesviruses Flashcards

1
Q

how are herpesviruses categorized?

A

α, β and γ

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2
Q

where do α herpesviruses establish latency?

A

neurons

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3
Q

which herpes strains are in the α group?

A
  1. HHV-1 = herpes simplex virus type 1 (HSV-1)
  2. HHV-2 = herpes simplex virus type 2 (HSV-2)
  3. HHV-3 = varicella zoster virus (VZV)
  4. Herpesvirus B
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4
Q

where do β herpesviruses establish latency?

A

T cells

sometimes macrophages too

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5
Q

which herpes strains are in the β group?

A
  1. HHV-5 = cytomegalovirus (CMV)
  2. HHV-6 = human herpesvirus 6
  3. HHV-7 = human herpesvirus 7
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6
Q

which herpes strains are in the γ group?

A

HHV-4 = EBV

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7
Q

what is the structure of the herpesvirus virion?

A
  1. icasahedron capsid
  2. linear dsDNA
  3. matrix proteins present
  4. enveloped
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8
Q

what is tegument?

A

aka matrix proteins, they just have a specific name when it comes to herpes viruses

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9
Q

describe the genome of the herpesvirus

A

linear, dsDNA with repeat sequences at the ends

this means that the virus will circularize at some point during the replication process!

the repeats will be maintained during replication process, they’re intentional

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10
Q

how does the herpesvirus enter a cell?

A

pH independent OR pH dependent manner

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11
Q

what mechanism does the herpesvirus use to replicate?

A

rolling circle mechanism

like toilet paper

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12
Q

what is a persistent infection?

A

viral infection does not result in cell death

instead there is continuous production of low titers

mechanisms leading to this situation are unknown

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13
Q

what is a latent infection?

A

involves maintenance of the viral genome without replication

so there’s a primary lytic cycle but then it just stops replicating and goes to sleep

you might not have an antibody response during this phase because no virus is being produced

latently-infected cells can be reactivated, often by stress, or during periods of impaired immunity

reactivation is characterized by new virus production

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14
Q

how do you know when HSV-1 is in a latent phase?

A

latency is characterized by the generation of untranslated mRNAs called latency-associated transcripts (LAT)

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15
Q

how do you know when CMV is in a latent phase?

A

there is no detectable RNA or protein synthesis

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16
Q

when herpesvirus resurfaces after a latent phase, where does it appear?

A

in the same spot!!

HSV-1 and HSV-2 are α-herpesviruses that go latent in neurons so usually its the innervating neuron associated with the primary infection

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17
Q

what are the most common clinical features of HSV?

A
  • vesicular rashes
  • oral herpes = HSV-1
  • genital herpes = HSV-2
  • fetal infection in utero is often fatal

most infections are symptomatic so you can physically see that someone has herpes unlike other viruses that go under-diagnosed because they don’t have as many presenting symptoms

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18
Q

how can you differentiate between HSV-1 and HSV-2?

A

they’re both α-herpesviruses

but HSV-1 is usually oral herpes = above the waistline

HSV-2 is usually genital herpes = below the waistline

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19
Q

what are some other clinical presentations of HSV?

A
  1. herpes pharyngitis
  2. eye infection
  3. finger infection
  4. skin infection
  5. herpes encephalitis = most common cause of fatal sporadic encephalitis cases
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20
Q

how do you diagnose HSV?

A
  1. distinct vesicular blisters
  2. Tzanck smears = scrape the bottom of a lesion and look at it under a microscope –> you’ll see balooned cells and Cowdry inclusion bodies

Cowdry inclusion bodies = intranuclear inclusions where virus is replicating

  1. other diagnostic methods include virus isolation/culture in cell lines, electron microscopy, immunofluorescence, and PCR
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21
Q

what is the pathogenesis of HSV?

A

initial acute infection with the virus replicating at the site; you’ll have a normal replication cycle where lots of virus is being procued

then the cell dies; lots of times with HSV there is disease associated with this

after the initial infection, the virus will infect innervating neurons and hide in the neuron = not an acute infection anymore

the virus changes its replication program so that it’s no longer replicating like it does in the epithelium and fibroblasts

then when the conditions are right, the virus will come out of the neuron and travel back up the axon and infect those same epithelial cells

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22
Q

how do you prevent HSV?

A

there is no vaccine against HSV-1 or HSV-2….

health-care workers should use latex gloves to prevent infection

condoms help, but may not always be fully protective

patients with a history of HSV infection must abstain from sexual contact while they have prodromal symptoms or lesions; the latter must be fully reepithialized

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23
Q

how do you treat HSV?

A

acyclovir

acyclovir is phosphorylated by HSV-encoded thymidine kinase and acts as a terminator of viral DNA synthesis

other options include valacyclovir, penciclovir and famciclovir

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24
Q

what type of herpesvirus is VZV?

A

alpha herpesvirus

VZV = varicella zoster virus

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25
Q

what are the 2 disease outcomes of the VZV virus?

A
  1. chickenpox (varicella)

2. shingles (herpes zoster)

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26
Q

what are the clinical features of varicella?

A

varicella = chickenpox

may be asymptomatic but usually you get an exanthem (rash)

fever, followed by a maculopapular rash more severe in the trunk than in the limbs

each lesion develops to become a vesicle - the hallmark of varicella – and later becomes pustular and crusts

finally, scabbed lesions appear

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27
Q

how do you distinguish smallpox from varicella?

A

with varicella you get a rash that shows up in various stages; there are initial lesions and by the time it scabs up new ones have shown up

on the other hand, smallpox lesions are all the same age and all scab over/fall off at the same time

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28
Q

why does someone get shingles?

A

shingles = zoster

if there is VZV reaction and migration to the skin during adulthood

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29
Q

where does the shingles rash appear on the body?

A

so the varicella rash is all over the body so it’s traveling everywhere and infecting T cells; the infected T cells in your skin are what cause the rash

eventually the infected T cells will infect a neuron and the virus will lie latent in the neurons; usually its neurons in the trunk

the area innervated by the infected neurons becomes painful and the skin breaks with vesicles that are similar to those observed during chickenpox

when the virus reactivates, it’s usually in one spot that’s localized and extremely painful

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30
Q

which population is prone to zoster?

A

elderly patients

immunocompromised patients

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31
Q

how do you diagnose VZV?

A
  • rash
  • Tzanck smears
  • ELISA
  • PCR
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32
Q

how do you prevent VZV?

A

there is a highly effective, live-attenuated vaccine against chickenpox and one against zoster

composition is the same, the difference is dosage

you just have to be careful not to give it to immunocompromised patients since it’s a live vaccine

immunosuppressed patients may be treated with varicella-zoster immunoglobulin prepared from sera of seropositive people

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33
Q

how do you treat VZV?

A
  1. acyclovir

2. pain may be managed with analgesics or topical anesthetics

34
Q

what are some of the complications of VZV?

A
  1. can be fatal in immunocompromised people
  2. postherpetic neuralgia = chronic nerve pain that can persist for years due to damage caused by VZV

it’s confined to the dermatomic area following shingles outbreak

35
Q

what are the characteristics of herpesvirus B?

A

only zoonotic alpha-herpesvirus

4 practices for virus research

normally just effects monkeys but it could be transmitted to humans potentially

infection may be unapparent, or result in vesicular lesions

transmission by bite can lead to fatal encephalomyelitis (80% CFR is untreated)

36
Q

what class of herpesvirus is CMV?

A

beta herpesvirus

37
Q

what is the largest herpesvirus?

A

CMV

so this means it expresses many proteins to evade host antiviral responses

38
Q

which virus is the most common viral cause of congenital birth defects?

A

CMV

39
Q

which virus is the most common viral cause of solid organ transplant rejection?

A

CMV

especially renal allografts

40
Q

which population is at risk for CMV?

A

it’s increasingly prevalent in immunocompromised patient, in which it establishes opportunistic infections

41
Q

what does TORCH stand for?

A

Toxoplasma gondii

Other (HIV, syphilis, Zika, VZV, etc.)

Rubella

CMV

HSV/HIV

42
Q

what are TORCH viruses?

A

they’re transmitted from mother to child

each type of infection has a different prognosis

the stage of the pregnancy at the time of infection also can change the effect on the newborn

43
Q

what are common effects of TORCH viruses?

A

intrauterine growth restriction (IUGR)

microcephaly

intracranial calcifications

conjunctivitis

hearing loss

rash
hepatosplenomegaly

thrombocytopenia

44
Q

what can CMV develop into?

A

CMV is a sexually-transmitted disease and is usually asymptomatic

like 90% of us have CMV but there’s no symptoms because it’s just latent in T cells!

however, some patients may develop mononucleosis with symptoms similar to EBV

45
Q

how can you differentiate EBV and CMV that’s turned into mononucleosis?

A

in CMV there won’t be large/swollen lymph nodes!

pharyngitis and lymphadenopathy are less severe or absent

but both will have mononucleosis

46
Q

what is congenital CMV?

A

CMV is the most common viral cause of congenital defects

about 1% of babies born in US with congenital CMV and of those 10-20% with have symptoms but most are asymptomatic!

symptoms can be mild or severe: hearing/vision loss, microcephaly, muscle and brain development, mental disability, death – so its presenting in a lot of different places

we only treat symptomatic newborns

47
Q

which symptoms are immunocompromised CMV patients at risk for?

A

penumonia

retinitis

colitis

48
Q

how do you diagnose CMV?

A
  1. ELISA, testing for the presence of IgM (for in utero infections) or IgG antibodies
  2. virus can be isolated from blood, urine and saliva, and propagated in human fibroblasts
  3. histology of CMV-infected cells is very characteristic, and shows enlarged cells containing “owl’s eye” inclusions = viral nuclear inclusions
  4. immunofluorescence
  5. PCR
49
Q

what is the pathogenesis of CMV?

A

pathogenesis of CMV is similar to that of other herpesviruses and infections are often inapparent

virus is capable of establishing a persistent infection or, alternatively, latency in T cells and macrophages

spread occurs when the infected cells travel throughout the body (this is why CMV symptoms involve so many different parts of the body)

infected individuals shed virus in bodily fluids intermittently, but for life

reactivation, often with severe consequences, usually follows immunosuppression.

50
Q

how is CMV spread?

A

it’s transmitted by most bodily fluids and secretions

51
Q

how do we prevent CMV?

A

CMV vaccines are in all stages of clinical trials

maternal antibodies do no confer protection

52
Q

which drugs treat CMV?

A
  1. ganciclovir/valganciclovir
  2. cidofovir
  3. foscarnet
53
Q

what do ganciclovir/valganciclovir do?

A

used to treat CMV

same mechanism as acyclovir

the drug is activated when phosphorylated by a CMV-encoded kinase (UL97) and act as terminators of DNA synthesis

54
Q

what does cidofovir do?

A

used to treat CMV

it’s a cytidine analog that does not require phosphorylation to be active

it’s approved to treat CMV retinitis, especially in AIDS patients

55
Q

what does foscarnet do?

A

used to treat CMV

inhibits the DNA polymerase by mimicking the pyrophosphate in dNTPs

it’s selective because the viral polymerase is 100X more sensitive than human polymerase

it’s used with ganciclovir-resistant infections, especially AIDS and transplant recipients

56
Q

what are the characteristics of herpesvirus 6?

A

two variants: HHV61 and HHV6B

HHV6B causes the childhood exanthem: exanthem subitum or roseola (high fever and rash)

HHV6B reactivation associated with transplant recipients

HHV6A can be neurovirulent and associated with neuroinflammatory diseases like multiple sclerosis

57
Q

what are the characteristics of herpesvirus 7?

A

mononucleosis

lymphadenopathy

58
Q

which class of herpesvirus are HHV 6 and 7?

A

beta

59
Q

which class of herpesvirus is EBV?

A

gamma

60
Q

how is EBV transmitted?

A

saliva

it’s the kissing disease

61
Q

where is EBV latent?

A

Infection/latency in B cells (CD21 receptor)

62
Q

what is the main characteristic of EBV?

A

its ability to immortalize cells

if EBV can keep cells growing, since the infected cells are B cells this can lead to B cell cancers

63
Q

what are the clinical features of EBV?

A

causes infectious mononucleosis

symptoms include:

  • fatigue due to lymphocyte activation and proliferation
  • lymphadenopathy
  • splenomegaly
  • pharyngitis
  • high fever is frequent
  • rash is possible
64
Q

what happens when immunocompromised people get EBV?

A

in people with low immunity EBV infection can be life-threatening and induce several lymphoproliferative diseases

  1. African Burkitt’s lymphoma
  2. Hodgkin’s lymphoma
  3. nasopharyngeal carcinoma

also, a rare result of EBV infection is hairy oral leukoplakia, which results in mouth lesions seen in AIDS patients

65
Q

what’s the difference between EBV and CMV?

A

EBV can effect young healthy people….

also EBV will have a positive monospot test and CMV won’t

66
Q

how do you diagnose EBV?

A
  1. monospot positive
  2. presence of Downey cells (atypical T cells, 10-80% of WBC count)
  3. PCR
67
Q

how does the monospot test for for EBV?

A

EBV stimulates infected B cells to make non-specific heterophile antibodies that can be detected by agglutination of sheep RBCs

when the sheep RBCs clump, this is a positive monospot test

68
Q

which antigens can be used for diagnosis of EBV?

A
  1. EA = early antigen
  2. VCA = viral capsid antigen
  3. EBNA = nuclear antigens
  4. MA = glycoproteins of the membrane
69
Q

how do you prevent EBV?

A

you can’t, there’s no vaccine

70
Q

how do you treat EBV?

A

there’s no treatment….

EBV does not code for a thymidine kinase, so ACV is not useful

71
Q

what are some potential complications of EBV?

A

recurring replication can result in a disease similar to chronic fatigue syndrome

EBV can cause neurological complications and rupture of the spleen

the latter can be avoided by instructing the patient to rest

72
Q

EBV vingette

A

A 17-year-old high school student has had low-grade fever and malaise for several days, followed by sore throat, swollen cervical lymph nodes, and increasing fatigue. The patient also notes some discomfort in the left upper quadrant of the abdomen. The sore throat, lymphadenopathy, and fever gradually resolved over the next two weeks, but the patient’s full energy level does not return for another 6 weeks.

  1. low-grade fever
  2. swollen cervical lymph nodes
  3. fatigue
  4. LUQ discomfort
73
Q

CMV vingette

A

A 36-year-old man was brought to the hospital for complaints of persistent high fever, dry cough, and worsening shortness of breath for a week. He had been diagnosed with acute myelogenous leukemia 6 months before, and he received an allogeneic bone marrow transplant 6 weeks before. He was taking Bactrim for prophylaxis of pneumocystis pneumonia. Histopathology of lung biopsy specimens showed intranuclear inclusions in pneumocytes.

  1. high fever
  2. dry cough
  3. worsening shortness of breath for a week
  4. BM transplant 6 weeks before
74
Q

VZV vingette

A

A 32-year-old man presents to the emergency department with an itchy and painful rash on the back of his left leg. About 7 days ago, he began to feel an intense, burning pain behind his left knee. Over the subsequent days, small blisters began to pop up over the area but were the worst behind the knee itself. He treated the lesion with an over-the-counter antibiotic ointment and acetaminophen, but they did not relieve the pain. Any contact, however slight, with the apparent blisters immediately intensifies the pain. The patient reports having fevers, sneezing, and a runny nose over the last 2 weeks. He does not report any cough, shortness of breath, headaches, or fatigue. He also reports extreme stress at work with many deadlines and an ongoing threat of job loss because of continuing downsizing due to overseas corporate operations. Lesions are observed on the back of the left knee, and similar but smaller lesions appear in a band-like distribution along the posterior length of his left leg up to the buttock region. The affected leg is neurovascularly intact. Remaining findings on neurologic examination, cardiorespiratory examination, and the review of systems are unremarkable.

  1. intense, burning pain
  2. small blisters
  3. stress
  4. band-link distribution
75
Q

which class of herpesvirus is Kaposi’s sarcome herpesvirus?

A

gamma herpesvirus

76
Q

what are the characteristics of KSHV?

A

KSHV = Kaposi’s sarcome herpesvirus

linked to Kaposi sarcoma and other proliferative disorders…systemic disease that can present with cutaneous lesions/tumors

tumors originate due to immortalization of endothelial cells at multiple sites

most primary infections are asymptomatic, and the disease is the result of viral reactivation

in addition to the better-known skin lesions, KSHV can result in lung infection!!

associated with HIV-1 infections

77
Q

which populations is KSHV common in?

A

high prevalence among elderly men of Mediterranean (specially Jewish and Italian) and Eastern European ancestry

78
Q

how is KSHV transmitter?

A

mainly transmitted by sexual contact

but non-sexual transmission is possible

79
Q

how do you diagnose KSHV?

A

symptoms

PCR

serology

80
Q

KSHV vingette

A

A 31-year-old man presents with mucocutaneous lesions, breathlessness, cough, a fever, and wheezing. Chest X-rays are obtained and shown in the image. This patient is immunocompromised due to immunoaglobulinemia

  1. lung infection = cough and wheezing
  2. immunocompromised

KSHV is HIGHLY asscociated with immunocompromised patients; it’s not usually a healthy person that has KSHV

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