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Microbiology and immunology > Herpesviridae > Flashcards

Herpesviridae Flashcards

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Biology 101 flashcards
1
Q

What are the members of the virus family Herpesviridae?

A
  • HHV-1 (herpes simplex virus, type 1 [HSV-1])
  • HHV-2 (herpes simplex virus, type 2 [HSV-2])
  • HHV-3 (varicella-zoster virus [VZV])
  • HHV-4 (Epstein–Barr virus [EBV])
  • HHV-5 (cytomegalovirus [CMV])
  • HHV-6
  • HHV-7
  • HHV-8 (Kaposi sarcoma herpesvirus [KSHV])
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2
Q

What are the subfamilies of the family Herpesviridae?

A
  • Alphaherpesvirinae: HHV-1, HHV-2, HHV-3
  • Betaherpesvirinae: HHV-5, HHV-6, HHV-7
  • Gammaherpesvirinae: HHV-4, HHV-8
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3
Q

What is the general structure of human herpes viruses?

A

Enveloped viruses with double-stranded DNA genomes

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4
Q

What is the common feature shared by all herpes viruses?

A
  • They establish lifelong persistent latent infection, with periodic reactivation
  • The reactivation can be asymptomatic or symptomatic (especially if cellular immunity is suppressed)
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5
Q

Which human herpes viruses belong to the subfamily Alphaherpesvirinae?

A
  • HHV-1 (HSV-1)
  • HHV-2 (HSV-2)
  • HHV-3 (VZV)
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6
Q

Which herpes viruses are herpes simplex viruses?

A
  • HHV-1 (HSV-1)
  • HHV-2 (HSV-2)
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7
Q

To which subfamily do herpes simplex viruses belong?

A

Alphaherpesvirinae

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8
Q

How are herpes simplex viruses transmitted?

A
  • Direct contact
  • Saliva
  • Sexual transmission (especially for HSV-2)
  • Vertical transmission
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9
Q

What is the clinical manifestation and progression of primary infection with herpes simplex viruses?

A

The virus infects the skin and mucous membranes, causing lesions. The lesions progress as:

  • Macules (small, flat lesions)
  • Papules (small, raised lesions)
  • Vesicles (small, raised lesions filled with a clear fluid)
  • Ulcers (vesicles which have opened)
  • Crusting over of the ulcers

These lesions last 1–2 weeks and can be very painful

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10
Q

How do herpes simplex viruses become latent?

A
  • The nucleocapsid (i.e. the virion without the capsule) enters sensory nerve endings
  • The virus is transported by retrograde axonal transport to the dorsal root ganglion
  • The virus establishes latency in the nucleus
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11
Q

What are the common sites of latency for the herpes simplex viruses?

A
  • HSV-1: trigeminal nerve
  • HSV-2: sacral ganglia
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12
Q

How do latent herpes simplex viruses escape immune detection?

A

There is no active replication of the virus, so no virus proteins are produced for detection

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13
Q

What can trigger reactivation of herpes simplex viruses?

A
  • Stress
  • Fever
  • Suppressed cellular immunity
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14
Q

How are herpes simplex viruses reactivated?

A

The virus moves by anterograde axonal transport to the sensory nerve endings and establishes infection in the skin and mucous membranes

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15
Q

What is the clinical manifestation of reactivated herpes simplex virus?

A
  • Mostly asymptomatic (up to 90% for HSV-1)
  • The patients are still infectious
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16
Q

What are the diseases caused by herpes simplex virus?

A
  • Gingivostomatitis (inflammation of the gums and oral mucosa)
  • Pharyngitis and tonsilitis
  • Conjunctivitis
  • Keratitis
  • Cold sores (i.e. fever blisters, herpes labialis)
  • Cutaneous herpes
  • Herpetic whitlow (in the fingers)
  • Eczema herpeticum (more severe whitlow in those with allergic dermatitis)
  • Genital herpes
  • Herpes encephalitis
  • Herpes meningitis
  • Neonatal herpes
  • Disseminated severe disease (usually in immunosuppressed patients, e.g. AIDS patients)
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17
Q

Which disease caused by HSV-1/HSV-2 is most associated with occupational exposure, especially in dentists?

A

Herpetic whitlow

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18
Q

How severe is neonatal herpes?

A

Very severe, with a mortality rate of around 60%

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19
Q

How is herpes simplex virus diagnosed?

A
  • Clinical presentation (although the lesions don’t point definitively to HSV)
  • PCR
  • Serology: IgM for primary infection, IgG for past infection
  • Nuclear inclusions in cells (using a Tzanck smear)
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20
Q

How is herpes simplex virus treated?

A

Antiviral nucleoside analogs: acyclovir, valacyclovir, vidarabine. These do not affect the latent virus

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21
Q

Is there a vaccine for herpes simplex virus?

A

No

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22
Q

What is the epidemiology of herpes simplex viruses?

A
  • More than 90% of young adults have already been infected by HSV-1
  • HSV-2 is much less prevalent due to its sexual spread
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23
Q

How is varicella-zoster virus transmitted?

A
  • Direct contact
  • Aerosols (droplet nuclei)
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24
Q

What is the clinical manifestation and progression of primary infection with VZV?

A
  • The virus accesses the upper respiratory tract and replicates there
  • It spreads into the blood (primary viremia), followed by replication in the liver and spleen
  • It spreads in the blood again (secondary viremia) to the skin, giving rise to chickenpox (varicella)
  • The chickenpox rash is highly pruritic (itchy)
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25
Q

In VZV infections, what is the difference between primary and secondary viremia?

A
  • Primary viremia: the first spread of the virus into the blood, occurring after replication in the upper respiratory tract
  • Secondary: the second spread of the virus into the blood, following replication in the liver and spleen
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26
Q

What is the clinical manifestation and progression of secondary infection with VZV?

A
  • The virus causes lesions (called shingles or zoster) in one or a few skin segments innervated by the dorsal root ganglion it was latent in (along a dermatome)
  • The lesions are extremely painful
  • Pain may continue for months after the lesions disappear (post-herpetic neuralgia)
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27
Q

A man who has never been exposed to VZV is infected by a colleague with shingles (zoster). Which disease, varicella or zoster, will he develop?

A

Varicella (as it will be primary infection)

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28
Q

What are potential complications of chickenpox?

A
  • Pneumonia and meningitis
  • Mortality is very low (1 per hundred thousand; slightly higher in adults)
  • Neonatal infection is severe with a mortality rate of 30%
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29
Q

How is VZV diagnosed?

A
  • Clinical presentation
  • PCR
  • Serology: IgM for pirmary infection, IgG for past infection
  • Nuclear inclusions in cells (using a Tzanck smear)
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30
Q

Which virus is referred to as varicella-zoster virus (VZV)?

A

HHV-3

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31
Q

To which subfamily does varicella-zoster virus belong?

A

Alphaherpesvirinae

32
Q

How is varicella treated?

A

Symptomatic treatment

33
Q

How is zoster (and resultant post-herpetic neuralgia) treated?

A
  • Antivirals acyclovir, valacyclovir, and famciclovir can reduce the length and severity of infection
  • For neuralgia: tricyclic antidepressants, gabapentin (an anticonvulsant), pregabalin (an anticonvulsant), opioids, tramadol (an opioid and SNRI)
34
Q

Is there a vaccine for VZV?

A
  • Live attenuated virus to prevent chickenpox
  • Therapeutic vaccines to reduce occurrence of zoster (both recombinant subunit and live attenuated vaccines)
35
Q

What is the epidemiology of VZV?

A
  • Childhood infection is extremely common in countries where vaccination is not offered (due to the cost of the vaccine)
  • Incidence of zoster increases with age
36
Q

Which virus is referred to as Epstein–Barr virus?

A

HHV-4

37
Q

To which subfamily does Epstein–Barr virus belong?

A

Gammaherpesvirinae

38
Q

How is EBV transmitted?

A

Saliva (so, primary infection is called “kissing disease”)

39
Q

Primary infection with which virus is referred to as “kissing disease?”

A

EBV

40
Q

What is the tropism of EBV?

A
  • B cells
  • Epithelial cells
41
Q

What is the site of latency of EBV?

A

B cells

42
Q

Which receptor does EBV use to enter cells?

A

CD21 (complement receptor 2)

43
Q

What are the clinical manifestations of primary infection with EBV?

A
  • Most infections are asymptomatic, especially in children
  • In adults, infectious mononucleosis may occur
  • The classical triad of infectious mononucleosis is fever, pharyngitis, and cervical lymphadenopathy
  • Adults may also develop fatigue, headache, and splenomegaly
44
Q

Which cancers are linked with EBV?

A
  • Burkitt lymphoma
  • Nasopharyngeal carcinoma
  • Gastric carcinoma
  • Hodgkin and non-Hodgkin lymphomas
45
Q

Which disease linked to EBV infection is prominent in AIDS patients?

A

Oral hairy leukoplakia: a benign wart-like growth on the tongue

46
Q

How is EBV diagnosed?

A
  • Clinical presentation
  • Blood film showing atypical lymphocytes: these are large T cells reacting to the infected B cells
  • PCR
  • Serology: IgM to viral capsid antigen (VCA) in primary infection; IgG to EBV nuclear antigen (EBNA) for past infection
47
Q

How is EBV treated?

A

Supportive treatment

48
Q

Is there a vaccine for EBV?

A

No

49
Q

What is the epidemiology of EBV?

A
  • More than 90% of young adults have already been infected
  • In developing countries, infection occurs in early childhood
  • In developed countries, infection occurs in mid-/late-adolescence with the onset of sexual activity and kissing
50
Q

What virus is referred to as cytomegalovirus?

A

HHV-5

51
Q

To which subfamily does cytomegalovirus belong?

A

Betaherpesvirinae

52
Q

How is CMV transmitted?

A
  • Saliva
  • Direct contact
  • Vertical: CMV is the most common congenital infection
53
Q

Infection with which virus is the most common congenital infection?

A

CMV

54
Q

What is the clinical manifestation of primary infection with CMV?

A
  • Most infections are asymptomatic, espeically in children
  • In adults, mononucleosis-like syndrome may occur (with the same symptoms as mononucleosis)
55
Q

What is the result of congenital infection with CMV?

A
  • Deafness
  • Blindness
  • Mental retardation
56
Q

What diseases can be caused by CMV in immunosuprressed patients?

A
  • Pneumonia
  • Gastroenteritis
  • Retinitis
57
Q

How is CMV diagnosed?

A
  • Clinical presentation
  • Blood film showing atypical lymphocytes
  • PCR
  • Serology: IgM in primary infection, IgG for past infection
58
Q

How is CMV treated?

A
  • Normal primary infection: supportive therapy
  • In immunocompromised patients and congenital infection: ganciclovir
59
Q

Is there a vaccine for CMV?

A

No

60
Q

What is the epidemiology of CMV?

A

More than 90% of young adults have already been infected

61
Q

What viruses are referred to as roseola viruses?

A

HHV-6 and HHV-7

62
Q

To which subfamily do the roseola viruses belong?

A

Betaherpesvirinae

63
Q

How are HHV-6 and HHV-7 transmitted?

A

Saliva

64
Q

What are the clinical manifestations of roseola virus infections?

A
  • Infection is usually acquired in the first year of life
  • The disease (roseola infantum, aka exanthema subitum, sixth disease) is characterized by high fever and skin rash
65
Q

How are roseola viruses diagnosed?

A
  • Clinical presentation
  • PCR
66
Q

How are roseola viruses treated?

A

Supportive therapy, especially using antipyretics to lower the fever

67
Q

Are there vaccines for HHV-6 and HHV-7?

A

No

68
Q

What is the epidemiology of roseola viruses?

A

More than 90% of children have already been infected

69
Q

What virus is referred to as Kaposi sarcoma herpesvirus?

A

HHV-8

70
Q

To which subfamily does Kaposi sarcoma herpesvirus belong?

A

Gammaherpesvirinae

71
Q

How is KSHV transmitted?

A
  • Saliva
  • Sexual transmission (especially among homosexual males)
  • Vertical transmission (especially in Africa)
72
Q

What are the clinical manifestations of infection of KSHV?

A
  • Primary infection is asymptomatic in immunocompetent people
  • In AIDS patients or the elderly, Kaposi sarcoma (cancer of the blood and lymph vessels) can occur. This appears on the skin or mucous membranes
73
Q

How is KSHV diagnosed?

A
  • Histopathology
  • PCR
74
Q

Is there a vaccine for KSHV?

A

No

75
Q

What is the epidemiology of KSHV?

A
  • Low prevalence in the general population
  • Prevalence is higher among male homosexuals

Microbiology and immunology (33 decks)

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