Herpesvirus and Papilomavirus Flashcards by John Fixari

Alphaherpesvirus Genome

dsDNA

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Alphaherpesvirus Virion

Enveloped

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Alphaherpesvirus Incubation

Anywhere from 2-14 days, but usually 4-5 days

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Alphaherpesvirus Strains

HSV-1: oral-oral, oral-genial; nearly 2/3 of adults are seropositive
HSV-2: genital-genital, oral-genital; more prevalent with sexual activity, approximately 1/5 of adults

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Alphaherpesvirus Replication

Nucleus - primarily infect epithelial cells in the skin or mucosa

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Alphaherpesvirus Immune inhibition

Cell mediated response system is required.

Viral proteins binds antibodies and compliment them, countering the effects of interferons

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Alphaherpesvirus Characteristics

Variable host range
Short reproductive cycle
Rapid spread in culture
Efficient destruction of infected cells
Capacity to establish latency in sensory ganglia

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Alphaherpesvirus Symptoms

Flu-like
Localized lesions - virus spreads to neighboring cells
Only 1/3 show symptoms
Can still transmit when asymptomatic
Symptoms last 8-12 days

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Alphaherpes virus Transmission

HSV-1: oral-oral, oral-genital

HSV-2: genital-genital; oral-genital

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Alphaherpes virus Complication

Latency

Genome circularizes and stays as an episome in the nucleus
Peripheral ganglia are a common site of latent infections
Can be triggered by sunburn, systemic infections, immune impairment, and stress

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Alphaherpesvirus Prevalence

HSV-1: 2/3 of adults

HSV-2: 1/5 of adults

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Alphaherpesvirus treatment

Acyclovir limits virus replication

Will not eliminate latent infection

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Alphaherpesvirus Prevention

Avoid contact during active herpes recurrence

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Betaherpesvirus characteristics

Restricted host range
Long reproductive cycle
Slow progress in cell culture
Enlargement of infected cells
Carrier cultures
Latent infection in a variety of tissues
Prototypical member - Cytomegalovirus (CMV)

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Gammaherpesvirus charachteristics

Restricted hist range
Targets T and B lymphocytes
Lytic infections
Latency in lymphoid tissues
Prototypical member - Epstein-Barr Virus (EBV)

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Betaherpesvirus/Gammaherpesvirus Genome

dsDNA

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Betaherpesvirus/Gammaherpesvirus Virions

enveloped

Betaherpesvirus/Gammaherpesvirus Replication

Nucleus

Betaherpesvirus/Gammaherpesvirus Symptoms

EBV - Burkett’s lymphoma, Hodgkin’s lymphoma

Burkett’s lymphoma

Most common childhood cancer in equatorial Africa
Tumor in jaw, eye socket, ovaries
In all cases, tumor cells have monoclonial EBV episome

What are the 3 types of Hodkin’s lymphoma

NL - nodular sclerosing
MC - mixed cellularity
LD - lymphocyte depletion

EBV’s role in Hodkin’s Lymphoma

EBV is present in 60-90% of MC and LD tumors
EBV is present in 20-40% of NL tumors
The exact role is not known

CMV latency

Persists in hematopoietic progenitor cells and macrophages in vitro
Chronic persistent infection, not latency
Controlled by healthy, actime immune system

EBV latency

Persistence of genome in memory B cells

Virus proteins ensure B cell proliferation and EBV genome replication

Betaherpesvirus/Gammaherpesvirus Prevalence

Common in the US

Betaherpesvirus/Gammaherpesvirus Treatment

Infections are usually self-limiting in healthy individuals Antivirals for immune compromised individuals Prophylaxis for transplant patients

Antiviral therapy for immune compromised individuals for CMV and EBV

Glanciclovir, foscarnet, acyclovir - Inhibit viral genome replication - Resistance can develop - Less effective for EBV-induced lymphoproliferation

Betaherpesvirus/Gammaherpesvirus Prevention

No vaccines

HPV Genome

circular dsDNA

HPV Virion

non-enveloped

HPV Strains

There are many different types associated with different diseases

HPV replication

Gain access through abrasion of the skin Virus production in differentiating cells Cell polymerase required

HPV Symptoms

Warts at infection sites | Can take moths to manifest, and 50% regress on their own within 2 years

HPV Transmission

Direct skin-to-skin contact -Mucous membrane is most susceptible and viruses enter through abrasions They are hardy to environmental stress, which allows for transmission via fomites

HPV Complications

Oncogenesis - cervical cancer | Respiratory papollomatosis

Respiratory papollomatosis

Complication of HPV Rare Respired virus Can be lethal

HPV role in cervical cancer

HPV requires actively replicating cells to replicate progeny | Actual path to cancer is unknown, either viral transformation or cell proliferation leading to cancer

HPV protein E7

Blocks retinoblastoma protein (Rb), which leads to continued cell proliferation May lead to cervical cancer

HPV protein E6

Blocks the p53 tumor suppressor pathway | May lead to cervical cancer

HPV Treatment

Most treatments are ablative Liquid nitrogen, surgical excision, laster, caustic chemicals Treatments may have to be repeated

HPV PRevention

Gardasil vaccination - protects against HPV-6, 11, 16, and 18