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Renal and genito-urinary systems > Human herpes virus > Flashcards

Human herpes virus Flashcards

Structure and classification of Herpesviruses What disease are caused by Herpes viruses How Herpes viruses infect human cells Pathobiology of Herpes simplex virus and Pathobiology of Herpes simplex virus and other Herpes viruses

1
Q

Herpes virus structure

A

Herpes – herpeton, Greek for “creep”
Icosahedral capsid surrounding dsDNA
Virus size ~ 120-200 nm
Have around 80 genes coding for approx 100 proteins

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2
Q

HHV classification

A

α-herpesviruses
β-herpesviruses
γ-herpesviruses

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3
Q

α-herpesviruses

A
  • epidermal/ neuronal viruses with a wide host range

- HHV-1, HHV-2, HHV-3 (VZV)

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4
Q

β-herpesviruses

A

Slow growth, primarily in T-cells and leukocytes

  • HHV-5 (cytomegalovirus)
  • HHV-6
  • HHV-7
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5
Q

γ-herpesviruses

A

Primarily B-lymphocytes

  • HHV-4 (Epstein-Barr virus)
  • HHV-8
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6
Q

Diseases caused by HHV1 & 2

A

Oropharyngeal and genital herpes

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7
Q

Diseases caused by HHV-3 (VZV)

A

Chicken-pox (Varicella)/ singles (Zoster)

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8
Q

Diseases caused by Epstein-Barr Virus (HHV-4)

A

Infectious mononucleosis (glandular fever), burkitt’s lymphoma, nasopharyngeal carcinoma

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9
Q

Diseases caused by cytomegalovirus (HHV-5)

A

Cytomegalic inclusion disease in utero (newborns and immunocompromised)

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10
Q

Diseases caused by HHV-6

A 
Exanthem Subitum (6th disease)
Fatigue syndrome
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11
Q

Diseases caused by HHV-7

A

Pityriasis rosea?

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12
Q

Diseases caused by HHV-8

A

Kaposi’s sarcoma (in AIDS pts)

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13
Q

Infection and replication of herpes virus

A

Virus with glycoproteins sticking out –> stick to receptor on cell surface –> when they bind virus decouples and injects DNA into cell –> dsDNA uncoated, makes its way into nucleus –> co-opts host cell polymerase and DNA starts to transcribe viral genes –> translation –> makes viral proteins including viral factor which goes back to host cell polymerase –> this drives more viral DNA replication –> all bits get put together in nucleus –> viral DNA back into virus –> mature virus –> break out of nucleus –> cells get packed full, cell pops, spread to other cells around or further
Can make proteins out of very little DNA

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14
Q

Herpes Simplex Virus (HSV)

A

HSV 1
-mainly Oral Infections
HSV 2
-mainly Genital Infections

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15
Q

Herpes Simplex Virus (HSV) infection and reactivation

A
  1. Infection: herpetic gingivostomatitis

2. Reactivation: herpes labialis (cold sores)

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16
Q

HSV-1 - oral infections

A
  1. Herpes Simplex Infection
    - herpetic gingivostomatitis
    - virus enterstrigeminal sensory neurones
    - migrates to trigeminal ganglion
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17
Q

Herpes Simplex: becomes latent in trigeminal ganglion

A

In 50% of cases it becomes reactivated
Migrates to peripheral nerve endings
Where active viral particles are shed

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18
Q

Herpes Simplex Reactivation infection caused by

A

UV light
Stress
Illness
Immunosuppression

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19
Q

Herpes labialis

A

Coldsores
Lesion resolves
Virus lays dormant again in trigeminal ganglion until reactivated

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20
Q

Natural history of HSV infections

A

Source of virus:

  • skin lesions, saliva (usually HSV-1)
  • genital lesions, genital secretions (usually HSV-2)
  • passive immunity from maternal antibody in infancy
  • -> primary infection (90-99% asymptomatic, 1-10% symptomatic)
  • ->establishment of latent infection
  • ->reactivation of latent virus and secondary/ recurrent infection
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21
Q

Herpetic gingivostomatitis incidence

A 
Primary HSV
Very common
Mainly affects young children
-usually mild, may go unnoticed
Sometimes young adults
-often more severe
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22
Q

Herpetic gingivostomatitis clinical features

A 
Incubation period 3-10 days
Duration 5-14 days
Multiple vesicles - rupture to form
extensive sloughing ulcers
Gingivitis with erythema and sloughing
Malaise, pyrexia, lymphadenopathy
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23
Q

Herpetic gingivostomatitis diagnosis

A

Typical clinical appearance

Main diagnostic difficulty with erythema multiforme

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24
Q

Herpetic gingivostomatitis investigation

A

Not normally done
Rising antibody titre/ presence of IgM antibodies
Viral culture or now mainly PCR

25
Q

Polymerase chain reaction: basic method (DIAGRAMS)

A
  1. Denature DNA to single strands
  2. Annealing of specific primers to DNA
  3. Extension by polymerase
  4. Repeat 30-35 times
26
Q

Polymerase chain reaction

A

At the end of each cycle, the amount of DNA has doubled
By end of 30 cycles, you will have ~1 billion molecules from original one you started with
Band if positive, nothing if negative

27
Q

Management of herpetic gingivostomatitis

A 
Acyclovir (200mg 5x daily for 5 days) if found early in immunocompromised
Fluids and soft diet
Analgesics/ antipyretics (paracetamol)
Local antiseptics e.g. chlorhexidine
Topical analgesics e.g. Difflam
X-infection control
28
Q

Action of acyclovir

A

HSV thymidine kinase (TK) phosphorylates guanosine (G) when HSV DNA replicates
Human cells cannot phosphorylate ACV very well
In HSV-infected cells, ACV is phosphorylated by viral T enzyme to ACV-P
ACV-P then inhibits virus replication
-get incorporated into replicating viral DNA but further bases cannot be added as ACV-P lack a terminal hydroxyl gp. It is a chain terminator
-ACV-P acts on virus DNA complex and inhibits the activity of 1 or more of these enzymes, so virus DNA manufacture is markedly slowed up

29
Q

Clinical features of herpes labialis

A

Prodromal irritation
Vesicles at or near mucocutaneous junction of lips
Crusting lesions lasting 7-10 days
Usually re-occurs at same sites
Rarely: may occur, intra-orally, in nose or elsewhere on skin

30
Q

Management of herpes labialis

A

Acyclovir cream 5% if used v early

OTC drying and antibacterial agents

31
Q

Prophylactic treatment of herpes labialis

A

Rarely justified
Prophylactic acyclovir will prevent lesions in immunocompormised or those susceptible or those susceptible to erythema multiforme

32
Q

Value of acyclovir in herpes labialis

A

Prophylactic - oral ACV (600-1000mg/day in 2 doses) is effective

  • < duration of pain by 1.4 days
  • < time to lesion crusting by 2.1 days
  • < occurrence of new lesions by at least 50%
  • > mean time to next recurrence from 46-118 days
  • < mean number of reccurrences over 4 - month observation period
33
Q

Herpetic Whitlow features

A

Herpetic infection of fingers from handling oral tissues of someone active HSV1 or HSV 2 simplex lesions (mainly dentists)
Very painful
Very difficult to treat
Prevention better than cure - wear gloves

34
Q

HSV encephalitis

A

Mainly affects frontal loves of brain
70-80% mortality if untreated
Of survivors, only 3% return to normal
Usually only people >50 years (HSv-1) and neonates (HSV-2) affected

35
Q

HSV encephalitis - adults (HSV-1)

A

Headache and behavioural changes over several days
Fever
Only 11% of cases have history of recurrent HSV infections

36
Q

HSV encephalitis - neonates (HSV-2)

A

Skin rash, lesions and CNS symptoms
Virus present in liver, lung and adrenal glands
Respiratory distress
Fits and convulsions
> intracranial p
Incidence approx 1 in 300,000 live births in UK

37
Q

HSV-2

A

Mainly genital infections
Multiple vesicles
-rupture to form extensive sloughing ulcers

38
Q

HHV-3 (VZV)

A 
Many similarities in structure and infection to HSV-1 and 2
Primary infection
-chicken pox (varicella)
Secondary infection 
-herpes zoster (shingles)
39
Q

HHV-3 pathway

A

Chicken pox/ varicella (1. HZV) –> dormant in dorsal root/ trigeminal ganglia

  • ->reactivation (age [70% >50yrs], stress, illness, immunosuppression) –>herpes zoster (2. HZV) seldom reoccurs
  • ->remains dormant
40
Q

Incubation period of chicken pox

A

14 days
Natural infection of the nasopharynx - day 0
Viral replication in lymph nodes - day 4
Primary viraemia - day 6
Viral replication in host tissues - day 9
-viral antigens displayed on tissue cells and antigen presenting cells

41
Q

HHV-3 (VZV) - 1. infection

A

Mild or severe versions

42
Q

Herpes zoster - 2. infection

A

Most commonly affects chest and back
Classical “shingles” rash like belt around chest
Blisters –> rash –> release and heal

43
Q

Herpes zoster - oral disease

A 
Most commonly affects of the divisions of the trigeminal N.
3 phases
-pre-herpetic neuralgia
-rash
-post-herpetic neuralgia
44
Q

Pre-herpetic neuralgia

A

Pain in distribution of affected division of trigeminal nerve
Prior to development of rash
May mimic dental pain

45
Q

Rash (herpes zoster)

A 
Unilateral in distribution of branch of trigeminal nerve
-ophthalmic
-maxillary
-mandibular
Vesicles break down to form 
-ulcers (mucosa) 
-crusting lesions (skin)
Last 2-3 weeks
46
Q

Herpes zoster - eye involvement

A

Problems caused by zoster include glaucoma, cataract, double vision and scarring of the cornea

47
Q

Management of herpes zoster

A

Acyclovir 800mg 5x daily for 7 days if seen soon after lesions develop
Analgesics
Ophthalmic referral if eye involved
Avoid contact with children

48
Q

New alternatives to acyclovir

A

Valaciclovir
-1g 3x daily for 7 days
Famciclovir
-250mg 3x daily for 7 days

49
Q

Post-herpetic neuralgia

A

10% of pts go on to get extremely unpleasant intractable burning pain in distribution of affected nerve
More common in elderly
Effective early treatment of zoster may decrease risk of neuralgia
Treat pain with tricyclic anti-depressants and neuropathic pain drugs

50
Q

HHV-4 - Epstein-Barr Virus (EBV) associated with

A 
Infectious Mononucleosis (glandular fever)
-acute primary infection with EBV
Burkitt's lymphoma 
-a B-cell malignancy
Nasopharyngeal carcinoma
-an epithelial cell malignancy
Oral hairy leukoplakia 
-seen in AIDS pts and some transplant recipients
51
Q

HHV-4 - Epstein-Barr Virus (EBV)

A

Primary infection EBV replicates in oro-pharyngeal epithelial cells but then establishes latency in B-lymphocytes
EBV latent infection of B-lymphocytes is necessary for virus persistance, subsequent replication in epithelial cells and release of infectious virus into saliva

52
Q

Infectious mononucleosis (EBV)

A 
About 95% of the world’s population are infected with EBV
Most infections are asymptomatic
Symptoms include sore throat,
swollen cervical lymph nodes and
mild fever
Infections in the western world are
usually seen in young adults
The disease can run
a prolonged,
episodic course, interfering with
physical and scholastic
performance (good excuse for poor exam results )
53
Q

Oral infectious mononucleosis

A

Petechiae on soft palate
Creamy exudates on fauces
Cervical lymphadenopathy

54
Q

Burkitt’s lymphoma

A

A malignant, B-cell lymphoma of high
prevalence in children in tropical Africa at
elevations below 1500m where malaria is
present
EBV infects most children sub-clinically in
these areas
Severe, clinical EBV infections early in
childhood predispose to Burkitt’s Lymphoma
– EBV immortalises B cells
Treatment – cyclophosphamide (chemo)
Uually affects jaw bone - tumour mass

55
Q

HHV-5 - cytomegalovirus (CMV)

A 
In healthy individuals In healthy individuals rarely causes:
„ Glandular fever-like illness
„ Salivary gland swelling 
In immunocompromised / AIDS can
cause:
„ Large ragged oral mucosal ulcers
„ Salivary gland swelling
„ Retinitis
56
Q

HSV-8

A

In AIDS pts can cause

-Kaposi’s sarcoma

57
Q

Chicken pox rash timeline

A

Secondary viraemia: day 0
-skin rash/ fever
-natural killer cell activity
Cessation of fever; skin lesions +ve for virus: day 2/3
Cessation of new lesion formation; virus absent from skin lesions: day 5 to 6 weeks
-neutralising Ab to virus proteins present; cell-mediated immunity (CMI) present

58
Q

Chicken pox recovery and latent phase timeline

A

Months –> years: exposure to VZV; asymptomatic reactivation of latent virus
-maintenance of CMI; persistance of IgG antibody; disappearance of IgM antibody

59
Q

Chicken pox reactivation timetline

A

Ole age: reactivation of latent VZV to give clinical zoster

-decline of CMI

Renal and genito-urinary systems (3 decks)

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