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Virology > Herpes > Flashcards

Herpes Flashcards

1
Q

HSV-1

A

Herpes Simplex Virus 1 (cold sores)

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2
Q

HSV-2

A

Herpes Simplex Virus 2 (genital sores)

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3
Q

EBV

A

Epstein Barr Virus (mono)

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4
Q

CMV aka HCMV

A

Human Cytomegalovirus

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5
Q

VZV

A

Varicella Zoster Virus

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6
Q

HHV-6

A

Human Herpes Virus 6

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7
Q

HHV-7

A

Human Herpes Virus 7

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8
Q

HHV-8

A

Human Herpes Virus 8

aka Kaposi’s Sacroma virus

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9
Q

Who does herpes infect?

A

Everyone and everything! Including shellfish

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10
Q

General Characteristics of Herpes Viruses

A

Large viruses

Enveloped

Icosahedral “capsid” or “nucleocapsid” dsDNA - linear- 125-230 kb

Pleomorphic

Tegument is between the envelop and the capsid and contains viral proteins that assist viral replication;

delivered into the cell at the time of the infection and tweak the cell in various ways primarily deciding whether the virus is productively infected or latent.

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11
Q

Herpes Virus Replication

A

tend to replicate in non-replicating cells (cells that are not dividing)

Herpes viruses replicate in the cell’s nucleus

The viral genome is transcribed by the cellular DNA-dependent RNA polymerase and is regulated by viral-encoded and cellular nuclear factors. So that decision between latency or activity is made by an interplay between viral factors and cellular factors!

During symptomatic infection, herpes simplex viruses and VZV replicate in a lytic manner - the cells die and skin lesions are formed.

Latent infection is established in specific cell types and only a small number of viral genes are expressed.

Virus is later reactivated, virions are made and lytic replication results, with attendant symptoms.

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12
Q

Antiviral Drug Target

A

Thymidine kinase

NOTE
Herpes viruses encode their own DNA polymerase and thymidine kinase (as well as other proteins that increase nucleotide levels in cells)
to assist in the replication of viral genome in non-replicating cells such as neurons.

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13
Q

Immune Avoidance

A

Cell to cell spread - via contact between cells - evades antibodies

Latency - immune system cannot “see” the virus if no RNA or proteins are being made

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14
Q

Immune Response

A

T cell responses are primarily responsible for resolving initial infection. Antibodies can protect from acquiring infection - VZV vaccine.

The course of disease is often very different in the immune-compromised.

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15
Q

HSV-1 Replicates and sets up latency where?

A

Trigeminal Ganglia

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16
Q

HSV-2 Replicates and sets up latency where?

A

Sacral Ganglia

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17
Q

Process of Infection in HSV

A

1) Undergoes a productive (lytic) infection epithelial cells of genital or oral mucosal surface (blister forms)
2) Nucelocapsid travels up axon to the ganglion (trigeminal or sacral), enters cell nucleus, and either replicates or establishes latency. Latency is always set up though.
3) A stimulus reactivates the virus, the virus will begin assembly new proteins, genome, etc. within the cell and it travels down the axon to the produce a lytic infection once again.

18
Q

Disease Mechanisms for HSV

A

Infection is initiated by direct contact between mucosal surfaces.

HSV replication causes cytopathic effects on epithelial cells. Forms syncytia - fusion between infected and uninfected cells.

Cell-mediated immunopathological effects contribute to symptoms. (With Herpes virus it’s the combo of lysis of cells by virus and the T cell immune response at the localized site that causes the blistering)

HSV avoids antibody neutralization by direct cell-to-cell spread.

HSV establish latency in neurons (hides from immune response).

HSV are reactivated from latency by various factors
Cell-mediated immunity is required for resolution of symptoms with a limited role for antibody.

DO NOT NEED TO HAVE BLISTERS TO BE INFECTIOUS FOR BOTH HSV-1/2

19
Q

Triggers for reactivation of herpes simplex viruses

A

Stress, fatigue
Temperature changes
U.V. light / Sun exposure Menstruation Immunosuppression (If T cell response is compromised, the virus will come out of latency much more readily)

20
Q

Diseases Caused by HSV

A

Herpes Labialis (cold sores)

Herpes Whitlow (on fingers)

Eczema Herpeticum (herpetic vesicles in people with eczema)

Herpes Gladiatorum

Keratoconjunctivitis (eye herpes)

Encephalitis

Primary Herpetic Gingivostomatitis

21
Q

Prevention and Treatment

A

Prevention - no vaccine – no specific form of prevention. Avoid contact with lesions – oral and genital.

Treatment – acyclovir (aciclovir) (ACV, sold as Valtrex, Zelitrex) – not a cure.

ACV is also used for shingles (zoster)

22
Q

Acyclovir

A

Nucleoside (guanosine) analog.
Converted to acyclo-GMP by viral thymidine kinase. Then converted into acyclo-GTP by cellular kinase. Then incorporated into viral genome and DNA synthesis is stopped because new nucleotides cannot be added: chain termination.

23
Q

Lab Diagnosis of HSV infections

A

Mucosal Smear looking for Tzanck cells or syncytial cells (– giant cells that are multinucleated; swollen cytoplasm; intranuclear bodies)

Viral antigen assays test antibody reactivity

PCR for viral nucleic acid provides definitive diagnosis

24
Q

HSV-2 Transmission

A

Virus can be shed even during asymptomatic periods.

Practice safe sex.

Acyclovir can reduce transmission.

Pregnant women with active HSV-2 should deliver by caesarean section to prevent infection of child.

Disseminated HSV disease is life threatening in children: The cellular immune system is underdeveloped in children leading to mortality or cognitive impairment

25
Q

Varicella Zoster Virus (VZV)

A

Causes chickenpox and shingles

Only herpes virus that spreads person to person by coughing or sneezing.

It can cause sever lung infections and be fatal in rare adult cases

26
Q

When does the rash appear in Chicken Pox?

A

After primary replication in lymphatics, primary viremia, replication liver, spleen, and other organs, and secondary viremia. So, it has gone through two cycles already before getting to your skin.

Even though the disease is apparent on the skin, it’s an inhalation disease primarily or a contact-transmission.

27
Q

Shingles (Herpes Zoster)

A

After a primary VZV infection (chickenpox), the virus remains latent (dormant) in the dorsal root ganglia until something reactivates it

More localized then chicken pox, usually staying along the dermatone.

It is contagious

28
Q

VZV Vaccine

A

available to adults 50+ and is super powerful

29
Q

Cytomegalovirus (CMV)

A

Infection is usually through the mother to the fetus or newborn or via sex in adulthood.

CMV is the most common viral congenital infection. 4000/yr in US show symptoms of in utero infection leading to mental retardation, deafness, microcephaly

Most of us are infected by middle adulthood.

Establishes latent infection in many cell types, but for months up to 2 years after acute infection, virus can be shed in saliva due to chronic replication in salivary glands.
Establishes latency in immune cells including lymphocytes and macrophages. Primary infection can result in mononucleosis-like symptoms.

30
Q

Leading cause of death in HIV patients not taking antivirals?

A

CMV

31
Q

Epstein-Barr Virus (EBV)

A

Causes 79% of infectious mononucleosis cases (CMV causes the other 21%)

EBV infects antibody-producing B cells and makes them hyperproliferate. These infected cells produce IgM antibodies that can be detected in the blood - heterophile ab.

T cell responses against the B cells causes both spleen inflammation and fatigue.

32
Q

Cancers associated with EBV

A

Burkitt’s Lymphoma and Nasopharyngeal carcinoma

33
Q

What causes mononucleosis symptoms?

A

an aggressive T cell response to the infection and hyperproliferation of the infected B cells

34
Q

Symptoms of Infectious Mono?

A 
Sore throat
Fever
Swollen Lymph Glands
Malaise
Enlarged spleen (sometimes)
Enlarged liver (sometimes)
Heart problems (rare)
Central nervous system (CNS) problems (rare)

Resolve in 1-2 months

BUT REMAINS LATENT IN THROAT AND BLOOD FOR LIFE

35
Q

Diagnosis of EBV?

A

1) Symptoms
2) Elevated mononuclear white blood cell count
3) Heterophile Ab test: antibodies that bind non-EBV antigens but are induced by EBV infection.
4) Staining of cells for viral antigens

36
Q

Differential Diagnosis EBV vs. CMV

A

1) Heterophile Ab is only in the EBV

2) too MANY white cells EBV vs. too FEW white cells CMV.

37
Q

Latency of EBV

A

In throat and blood for life. However, some latent infected cells undergo lytic replication in the oropharynx, resulting in production of virus with shedding of virus into the saliva or infection of epithelial cells with release of virus.

38
Q

HHV-6

A

Ubiquitous - spread by saliva and present in nearly everyone by adulthood. Is associated with various neurological problems, including multiple sclerosis.
Possible molecular mimicry of myelin basic protein may stimulate T cell responses that destroy neuron function.

HHV 6 and 7 – Roseola is a reddening condition in babies. Red rash in babies caused by both of these. Roseola is also called sixth disease.

HHV-6A associated with infertility in women

39
Q

HHV-6 and Alzheimer’s

A

HHV6 is recently thought to cause Alzheimer’s.
There is an association that has been made between finding HHV6 in brains of people generally who have Alzheimer’s at a higher incidence than people who don’t have Alzheimer’s

Research shows people on Acyclovir getting less Alzheimer’s disease

40
Q

HHV-8

A

Causes Kaposi’s sarcoma (KS) in people with AIDS/most likely requires immunosuppression

There’s a synergistic interaction between HIV and HHV8. HHV8 is the oncogenic trigger but HIV immunosuppresses the person, which allows the cancer to arise.

HIV also provides factors which boosts the virulence of HHV8.

Spread through kissing

Virology (11 decks)

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