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HDID - Virology > Lecture 83_84: Herpesvirus' CMV, EBV, VZV, HHV 6, HHV 8 > Flashcards

Lecture 83_84: Herpesvirus' CMV, EBV, VZV, HHV 6, HHV 8 Flashcards

1
Q

Describe the basic structure of All herpes viruses

proteins for attachment?
Proteins for fusion?

A

Enveloped
Icosohedral capsin
Double Stranded DNA – Linear
Tegument

attachment – gB and gM
Fusion – gH

There is no cure for herpes viral infection
Common cause of illness in immuno compromised patients

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2
Q 
CMV -- 
Whats the HHV #? 
whats in the tegument? 
The genome -- IE, E, L genes? 
what other unique features?
A

HHV - 5

Tegument – contains pp65 and mRNAs

The Genome – 700 proteins – largest of the herpes viruses
IE genes – function in viral DNA synthesis (regulators)
Early genes – Function in DNA replication and Viral protein modification –
Late Genes – structural gene products

miRNAs – shut down the cell machinery

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3
Q

CMV – modes of transmission

A 
HEENT -- shedding in oropharynx, tears, saliva 
GU - urine, sexual transmission 
Blood transfusions
Breast milk 
Solid organ and BMT 
Congenital
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4
Q

CMV – describe a few disease manifestations?

What % are asymptomatic ?

A

80-90% Asymptomatic

Mononucleosis – Heterophile antibody Negative
Retinitis – Esp in AIDS patients – (white patches of infarct leading to “ketchup on scrambled egg” appearance)
Pneumonia –

Glomerulopathy
Hepatitis, Gastroenteritis

Periventriculitis – ventricles light up on CT
Transverse Myelitis – inflammation of the spinal cord – some paralysis or peripheral nerve involvement
Hearing Loss - 8th nerve involvement

Cytomegalic Inclusion Disease – vertical transmission at birth; Leading infectious cause of birth defects in the US; the early a mom infected during pregnancy, the worse
Mental Retardation

ITP

Immunosenecence

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5
Q

What are the different tissues types that can be infected during:
Permissive infection
latent Infection
Persistent infection

A

permissive – epithelial cells (mouth to anus)
Kidneys, lungs, colon

Latent – Hemopoeitic cells –
anemia, neutropenia, TTP

Persistent Infection – lymphocytes, endothelial cells, bone marrow

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6
Q

What is the Pathognomonic histological finding for CMV Infection?

A

“owl’s eye” inclusions

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7
Q

Immune Responses to CMV

A

Antiviral Antibodies:
1) Virolytic – attract complement for lysis of the virus

2) Non virolytic – complement independent

Cell mediated Immunity
- CD8, NK, — keep CMV from reactivating in the host

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8
Q

What are the criteria for diagnosis of CMV?

A

Evidence of viral replication + Systemic signs of disease

Evidence of viral replication = PCR, Histopath, IHC of antibodies or antigens; Shell vial method

Systemic Signs of Disease: Fever, Luekopenia, TTP, elevated transaminases

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9
Q

Prevention of CMV

A

Screening of solid organ and blood transfusion

Barrier protection for sexual intercourse

Antiviral Prophylaxis – Ganciclovir, Valganciclovir, Acyclovir

Bolster T cell mediated Immunity

Inactivated vaccine (Towne)

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10
Q

Treatment of CMV

A

Ganciclovir
Foscarnet – watch for renal toxicity
Hyperimmune Globulin – in combo with Gan or Fos
Valganciclovir – for retinitis

some resistance is developing

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11
Q

Epstein Bar Virus
- HHV #?
- Tropism
-

A

HHV - 4

Tropism – Complement Receptor 2 (CR2) – which is only on B lymphocytes and Oral/Nasopharyngeal epithelium (kissing disease)
Can also infect Cervical epithelium

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12
Q

EBV –
What % are symptomatic ?
Describe some clinical manifestations of disease

A

90% asymptomatic

Mononucleosis – Heterophile antibody positive
fever, pharyngitis, LAD
Rash when given Ampicillin

ITP, anemia, rash with ampicillin

Pneumonitis
Transverse melitis/peripheral neuropathies

immuno-senesence

Post Transplant Lymphoproliferative disease

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13
Q

What are some malignancies caused by EBV?

A

Burkitt’s Lymphoma
Hodgkins Lymphoma
Nasopharyngeal carcinoma

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14
Q

EBV manifestatins in the Immuno compromised

A

Hairy oral luekoplakia

Post Transplant Lymphoproliferative Disorder – may develop into lymphoma

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15
Q

Diagnosis of EBV

A

Evidence of Viral Infection + Replication

Evidence of Replication;
Quantitative PCR – evidence of EBV DNA
Positive Immunocytochemisitry — proteins/nucleic acid associated with EBV (LMP, EBER Stains)

+ systemic signs of disease: Fever, pharyngitis, LAD

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16
Q

Prevention of EBV

A

Don’t share food, drinking glasses, utensils
Barrier protection
Don’t donate blood 6 months afte rmono
Vaccines in trial

EBV PTLD – acyclovir, ganciclovir prophylaxis
bolster cell mediated Immunity

17
Q 
Treatment of: 
Mono 
Pneumonitis
Hairy leukoplakia
Burkitts Lymphoma/Naso-oro pharyngeal carcinoma 
PTLD
A

Mono – supportive care; corticosteroids for severe disease

Pneunmonitis/hairy luekoplakia – Aciclovir

Cancer – Chemotherapy

PTLD – Rituximab

18
Q

Differentiation of causative agents of mononucleosis

A

CMV and HHV6 – Heterophile antibody negative (Monospot negative)

EVC – Heterophile antibody positive (Monospot positive)

19
Q

Uses of Aciclovir

A

HSV 1 and 2: most sensitive

VZV: can use acyclovir, but need at higher doses bc there is some intrinsic decreased sensitivity 

EBV -- sensitive to acyclovir 

All over HHV -- inherently resistant to Acyclovir
20
Q

Varicella Zoster Virus (VZV)

aka HHV #?

primary infection ?
Reactivation of latent infection ?

A

HHV 3

Primary infection – Chicken pox
Latent infection reactivation - Shingles

21
Q

Clinical time course of the primary VZV infection?

A

transmission – respiratory secretions
Primary viremia – asymptomatic

9-13 days after infection – Secondary viremia; fever

10-20 days after infection – chicken pox (vesiculopustular rash); disseminated dew drop lesions

22
Q

Stages of VZV infection

A

primary infection – chicken pox

Latent Infection -
90% in DRG or Cranial Nerve ganglia – paresthesias
10% in anterior horn cells – paralysis

Reactivated infecitons – Shingles; can be lifethreatening inthe immuno compromised

23
Q

Complications of Primary VZV infection
who is the most susceptible to complications in general ?
describe some of the complications of primary infections

A

Susceptible: Immunocompetent Adults who get primary infections – 15-30x more likely
Immunocompromised persons – 1000x more likely

Complications: 
CNS- - meningitis, cerebellar ataxia 
Pnuemonitis 
Hepatitis 
Reye's Syndrome -- encephalopathy, hepatits, hyperglycemia associated with chickenpox + ASA

Disseminated disease - hemorrhagic chicken pox

24
Q

Shingles –

manifestations and symptoms

A

Manifestations: Vesiculopustular Rash involving 1-2 contiguous dermatomes; disappears in 10 days
Prodromal Paresthesia or Pain

Associated with Allodynia – uncomfortable sensation to light touch or temperature

Post herpetic Nueralgias –

25
Q

Shingles of the head and neck
Complications of Shingles

Complications in the immuno compromised

A

H&N shingles
- Herpes Zoster Ophthalmicus – reactivation of VZV within the first branch of CN V) – most concerning for encehalitis

-Poster Herpetic Angiitis – replication of virus in blood vessels of the brain; can lead to stroke like symptoms;

Complications of Shingles: 
Poster herpetic Neuralgias
Encephalalitis with CN V Involvement 
Ramsey Hunt Syndrome 
Transverse Myelitis 
Guillan Barre

Immunocompromised –
Disseminated Disease of the skin
Visceral disease – pneumonitis, Hepatitis, Meningoencephalitis

26
Q

Ramsey Hunt Syndrome

Poster Herpetic Angiitis

A

Reactvation of the geniculate ganglion

Symptoms:
Vesicles only present in the External Auditory canal
Ipsilateral Decreased of taste on ant 2/3 of tongue
Ipsilateral facial paralysis

Stroke like condition, complication of Shingles
- treat with both anti viral and anti-clotting

27
Q

Dx of VZV

A

For chicken pox and shingles – usually a clinical dx

but if in doubt: pap smear, DFA, PCR (for CNS manifestations)

28
Q

Prevention of VZV

A

patients are infectious before the rash state
avoid inhaling infectious drops

Avoid contact with skin lesions

Oka Vaccine

VZ Immunoglobulin – passive immune therapy use to prevent infection in newborns who had just contracted chichen pox;

29
Q

Treatment of VZV

A

Chicken pox:
immunocompetent : Aciclovir; can help shorten duration, but usually not given

Immunocompormised – Aciclovir IV

Shingles:
Immunocompetent: Aciclovir, famciclovir, valciclovir
Must treat Ophthalamic zoster

Immunocompromised: aciclovir IV

30
Q

HHV 6

general facts:

A

Beta Herpes Virus (like CMV – HHV 5)

Infection occurs earlier than EBV or CMV (usually by the age of 2)
95% infected by adulthood

For those infected; the disease becomes latent following primary infection; can insert but no evidence of malignancy

31
Q

HHV 6 Disease Manifestations

Children
Adults and Children

what is DRESS ?

A

Children :
Exanthem Subitum – roseola
Diffuse maculo-papuilar rash on trunk
Fever; malaise; resolves on own

Children and Adults:
Mononucleosis – Heterophile Antibody Negative

CNS complications in Immuno Compormised:

Bone marrow Suppression

DRESS – “Drug Reaction and Eosinophilia with Systemic Symptoms” —

No maligancies

32
Q

Diagnosis of HHV 6

A

Characteristic rash – self limiitng

SErology – igM and IgG

PCR – use for CNS dx

33
Q

Treatment of HHV 6

A

Resistant to Aciclovir

Use: Ganciclovir, Foscarnet, Cidofovir

34
Q

HHV 8 –
aka?
What herpes group is it in?
tropisms

what other features does this virus have?

what is LANA ?

A

aka – Kaposi’s Sarcoma Virus
gamma Herpesvirus –

Lymphotrophic and Angiotrophic
Urogenitial and GI Epithelial cells

Contains tumor promoters and oncogenes
11 proteins homooglous to cell proteins which may hlep it evade the immune system

Latent DNA is Episomal
but can insert and lead to malignancies
Expresses latency associated nuclear antigen

35
Q

Epidemiology of HHV 8

What groups are have the highest prevelence?
how is it transmitted?

A
  • Rare in the US but much higher is the HIV and MSM populations

93% prevelance in mediterranean countries and Africa

Sexually transmitted

36
Q

Clinical manifestations of HHV 8

Rare:

A

Kaposi’s Sarcoma – Cutaneous and Visceral

Primary effusion Lymphoma –

Metacentraic Castleman’s disease

Rare: Pneumonia

37
Q

Diagnosis of HHV 8

A

Serology - IgM, IgG

PCR of Tissue bx

LANA

38
Q

Treatment of HHV 8

A

Resistant to Aciclovir

Use ganciclovir, valaciclovir, foscarnet, cidofovir

Sarco

HDID - Virology (16 decks)

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