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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
Polymerase chain reaction: basic method (DIAGRAMS)
1. Denature DNA to single strands 2. Annealing of specific primers to DNA 3. Extension by polymerase 4. Repeat 30-35 times
26
Polymerase chain reaction
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
Management of herpetic gingivostomatitis
``` 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
Action of acyclovir
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
Clinical features of herpes labialis
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
Management of herpes labialis
Acyclovir cream 5% if used v early | OTC drying and antibacterial agents
31
Prophylactic treatment of herpes labialis
Rarely justified Prophylactic acyclovir will prevent lesions in immunocompormised or those susceptible or those susceptible to erythema multiforme
32
Value of acyclovir in herpes labialis
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
Herpetic Whitlow features
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
HSV encephalitis
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
HSV encephalitis - adults (HSV-1)
Headache and behavioural changes over several days Fever Only 11% of cases have history of recurrent HSV infections
36
HSV encephalitis - neonates (HSV-2)
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
HSV-2
Mainly genital infections Multiple vesicles -rupture to form extensive sloughing ulcers
38
HHV-3 (VZV)
``` Many similarities in structure and infection to HSV-1 and 2 Primary infection -chicken pox (varicella) Secondary infection -herpes zoster (shingles) ```
39
HHV-3 pathway
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
Incubation period of chicken pox
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
HHV-3 (VZV) - 1. infection
Mild or severe versions
42
Herpes zoster - 2. infection
Most commonly affects chest and back Classical "shingles" rash like belt around chest Blisters --> rash --> release and heal
43
Herpes zoster - oral disease
``` Most commonly affects of the divisions of the trigeminal N. 3 phases -pre-herpetic neuralgia -rash -post-herpetic neuralgia ```
44
Pre-herpetic neuralgia
Pain in distribution of affected division of trigeminal nerve Prior to development of rash May mimic dental pain
45
Rash (herpes zoster)
``` 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
Herpes zoster - eye involvement
Problems caused by zoster include glaucoma, cataract, double vision and scarring of the cornea
47
Management of herpes zoster
Acyclovir 800mg 5x daily for 7 days if seen soon after lesions develop Analgesics Ophthalmic referral if eye involved Avoid contact with children
48
New alternatives to acyclovir
Valaciclovir -1g 3x daily for 7 days Famciclovir -250mg 3x daily for 7 days
49
Post-herpetic neuralgia
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
HHV-4 - Epstein-Barr Virus (EBV) associated with
``` 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
HHV-4 - Epstein-Barr Virus (EBV)
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
Infectious mononucleosis (EBV)
``` 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
Oral infectious mononucleosis
Petechiae on soft palate Creamy exudates on fauces Cervical lymphadenopathy
54
Burkitt's lymphoma
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
HHV-5 - cytomegalovirus (CMV)
``` 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
HSV-8
In AIDS pts can cause | -Kaposi's sarcoma
57
Chicken pox rash timeline
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
Chicken pox recovery and latent phase timeline
Months --> years: exposure to VZV; asymptomatic reactivation of latent virus -maintenance of CMI; persistance of IgG antibody; disappearance of IgM antibody
59
Chicken pox reactivation timetline
Ole age: reactivation of latent VZV to give clinical zoster | -decline of CMI

Renal and Genito-Urinary (3 decks)

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