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Block 6 - week 4 > Enveloped DNA viruses - Verma > Flashcards

Enveloped DNA viruses - Verma Flashcards

1
Q

Name the families of enveloped DNA viruses.

A
  1. Poxviruses
  2. Herpesviruses
  3. Hepadnaviruses
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2
Q

Name the three groups of Herpesviruses.

A
  1. Alpha-herpesvirus:
    * HSV1 - cold sores
    * HSV2 - genital ulcers
    * Varicella Zoster virus - chicken pox and shingles
  2. Beta-herpesvirus:
    * Cytomegalovirus
    * HSV6 - roseola virus
    * HSV7 - roseola virus
  3. Gamma-herpesvirus
    * Kaposi’s sarcoma associated virus - causes cancer
    * Epstein-Barr virus - causes cancer
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3
Q

Describe some general properties of Herpesvirus.

A
  1. enveloped dsDNA viruses
  2. sets up latent or persistent infection following primary infection
  3. reactivation are more likely to take place during immunosuppression
  4. both primary and reactivations are more likely to be more serious in immunocompromised patients
  5. Herpesviruses encode their own DNA polymerase: targets of anti-viral drugs
  6. primary and reactivation infections exhibit symptoms while latent infections do not
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4
Q

Describe the replication of Herpesviruses.

A
  1. enter host cell via receptor mediated mechanism.
  2. once inside, viral DNA is translocated to the nucleus.
  3. replication involves the use of viral polymerase.
  4. not all genes are transcribed at once.
  5. immediate early genes are transcribed first - these are regualtory genes i.e. - transcription factors.
  6. Early genes are transcribed next - these are enzymes needed for DNA replication - i.e. viral polymerase.
  7. Late genes are transcribed next, these are the structural genes.
  8. Transcription utilizes cellular RNA polymerase.
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5
Q

What are some diseases caused by HSV-1?

A
  1. skin - vesicular lesions above the waist
  2. mouth - gingivostomatitis
  3. eye - keratoconjunctivitis
  4. CNS - temporal lobe encephalitis
  5. neonate - rare but can acquire after birth from HSV-1 infected person
  6. dissemination to viscera in immunocompromised patients - Yes
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6
Q

What are some diseases caused by HSV-2?

A
  1. skin - vesicular lesions below the waist - especially the genitals
  2. mouth - rare
  3. eye - rare
  4. CNS - meningitis
  5. Neonate - skin lesions, encephalitis and disseminated infection. Acquired during passage thru birth canal
  6. Dissemination to viscera in immunocompromised patients - rare
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7
Q

Where does latency occur for HSV 1 and 2?

A

In neurons:
HSV 1 - Trigeminal ganglion
HSV 2 - DRG
Not many proteins are produced during latency.

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8
Q

Describe the clinical manifestations of HSV-1.

A
  1. Gingivostomatitis - occurs primarily in children. Symptoms include fever, irritability and vesicular lesions in the mouth. Primary disease more severe than recurrences.
  2. Herpes labialis - recurrent form, characterized by the crops of vesicles at the mucocutaneous junction of the lips or nose.
  3. Encephalitis - rare but virus can travel to brain and cause a necrotic lesion of the temporal lobe with symptoms of fever, headache and seizures.
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9
Q

Describe the clinical manifestations of HSV-2.

A
  1. Genital herpes - characterized by painful vesicular lesion on the genitals that are more severe in primary disease than recurrences. Primary infections present with fever. Many of these infections can be asymptomatic.
  2. Neonatal herpes - acquired by contact with vesicular lesions within the birth canal. Can cause mild disease with local lesions to the skin, eye and mouth or can cause more severe disease with encephalitis. Also can be asymptomatic.
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10
Q

How is HSV-1 spread?

A

Spread through saliva. Can get HSV-1 lesions on the genitals by oral-genital sexual contact. 50-60% of US infected, infection usually occurs in childhood.

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11
Q

How is HSV-2 spread?

A

Spread by sexual contact. Can get HSV-2 lesions in oral cavity by oral-genital contact. Antibodies if present appear at the age of sexual activity.

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12
Q

Describe the laboratory diagnosis of HSV 1 and 2 infection.

A
  1. The most definitive method of diagnosis is by virus isolation and growth in culture.
  2. Serology - only good for diagnosing primary infection.
  3. PCR-rapid diagnosis used for testing DNA in spinal fluid if encephalitis is present.
  4. Tzanck smear - multinucleated giant cells are seen with Giesma stain of base of vesicles.
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13
Q

Describe the treatment and prevention of HSV 1 and 2 infection.

A
  1. Treatment of choice for encephalitis is Acyclovir - also called acycloguanosine and Zovirax
  2. To treat acyclovir resistant HSV-1 use Foscarnet
  3. Valcyclovir and Famciclovir are used to treat genital herpes.
  4. prevention - avoid contact with vesicles
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14
Q

Describe some characteristics of HHV-3 or Varicella zoster virus.

A
  1. primary infection causes chicken pox
  2. incubation period of 14-21 days
  3. primary infection presents with fever, lymphadenopathy, and widespread vesicular rash
  4. latency occurs in DRG
  5. Reactivations cause shingles - blister like lesions along the dermatome associated with site of latency
  6. complications (especially in immunocompromised) - rare but can cause viral pneumonia, encephalitis and hemorrhagic chickenpox
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15
Q

What age group is more vulnerable to Shingles?

A

Patients 50 years and older.

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16
Q

Describe the diagnosis of HHV-3.

A
  1. cytology - direct IFA, PCR
  2. virus isolation - difficult to isolate because virus is very labile
  3. serology - antibody titers are normally low
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17
Q

Describe the treatment of HHV-3.

A
  1. no antiviral therapy in immune competent children.
  2. Acyclovir, famciclovir and valcyclovir can reduce duration in adults.
  3. vaccines (live-attenuated) - Varivax (children 1-12 years) to prevent varicella and Zostavax (60+ year age group) for Zoster (shingles)
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18
Q

What can be given to immunocompromised patients to prevent HHV-3 disease?

A

VZV - immunoglobulin.

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19
Q

Describe HHV-4 or Epstein-Barr virus.

A
  1. causes infectious mononucleosis (primary infection), B-cell lymphoma and nasopharyngeal carcinoma (reactivation infections)
  2. The most important antigens of the virus are - viral capsid antigen, early antigens and nuclear antigen.
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20
Q

Describe the clinical findings of HHV-4.

A
  1. symptoms of mono in children are usually subclinical.
  2. symptoms of mono - fatigue, fever, sore throat, headache, malaise, pharyngitis. Symptoms are usually self-limiting but can last for months.
  3. cancer causing diseases - Nasopharyngeal carcinoma and African Burkitt’s lymphoma.
  4. Can cause post-transplant lymphoproliferative disease.
  5. Can cause Oral hair leukoplakia (mostly seen in HIV patients) - whitish, non-malignant hair surface on the lateral side of tongue.
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21
Q

Describe the transmission of Epstein-Barr virus.

A
  1. EBV is transmitted via saliva and more than 90% of those infected shed virus for life.
  2. At least 70% of US population is infected by age 30.
  3. AIDS and immunodeficient people are at high risk for lymphoproliferative disorders.
  4. Burkitt’s lymphoma - mostly seen in Africa for unknown reasons.
22
Q

How does EBV spread?

A

Transmitted by saliva, infection occurs in oropharynx and spreads to blood where it infects B lymphocytes.

23
Q

What type of antibodies are formed against EBV and to what viral antigen?

A
  1. IgM are made against viral capsid antigen initially- indicate acute infection.
  2. IgG antibodies are made against viral capsid antigen and persist for life - indicate prior infection.
  3. IgM and IgG antibodies are also made to the early antigens and nuclear antigen.
24
Q

Describe who EBV may be diagnosed.

A
  1. Hematologic - 30% of B cells will be atypical with enlarged nucleus and vacuolated cytoplasm.
  2. Immunologic - presence of heterophile antibody and EBV specific antibody.
  3. PCR
25
Q

What treatment is available for EBV infection?

A

Acyclovir has limited activity and there is no vaccine available.

26
Q

Describe HHV-5 or Cytomegalovirus.

A
  1. is the most common viral cause of congenital birth defects.
  2. acts as an opportunistic pathogen in immunocompromised patients.
  3. can cause pneumonia, retinitis and colitis in immunocompromised patients such as recipients of bone marrow.
  4. latency occurs in stromal cells of the bone marrow.
27
Q

How is Cytomegalovirus spread?

A

It is transmitted by saliva in children and sexually in adults - is present in all bodily fluids. Also passed from mother to fetus through the placenta. 0.5 -2.5% of all newborns are congenitally infected.

28
Q

What diseases are caused by Cytomegalovirus infection in immune competent adults?

A
  1. heterophile negative mononucleosis fever - does not induce heterophile antibodies but does present with abnormal lymphocytes.
29
Q

What is the risk for infants if mom has a primary CMV infection during pregnancy?

A

The risk for serious birth defects is extremely high.

30
Q

How is CMV infection diagnosed?

A
  1. histology - look for cytomegalic cell
  2. Assay for antibodies, DNA probes
  3. PCR
  4. Easy to culture
31
Q

What is the treatment for CMV infection?

A
  1. Ganciclovir
  2. Foscarnet
  3. no vaccine available
  4. a high titer immune globulin called CytoGam is used to prevent disseminated CMV infections in organ transplant patients
32
Q

Describe HHV-6 and HHV-7.

A
  1. causes Roseola infantum - a spiking fever over 2 days followed by a maculopapular rash on the neck and trunk and spreading to the extremities in young children
  2. the main target cell is the T lymphocyte but B lymphocytes may also be infected.
  3. both strains share limited nucleotide homology with one another and antigenic cross-reactivity.
  4. both strains are related to eachother in a similar manner to HSV 1 and 2.
  5. both strains are ubiquitous and are found worldwide.
33
Q

How are HHV-6 and 7 spread and what is their pathogenisis?

A
  1. they are spread through contact with saliva and via breast feeding.
  2. infection is acquired in infants after the age of 4 months when maternal antibodies decrease.
  3. 90-99% of the population becomes infected with both viruses.
  4. Symptoms are very mild and occur with primary infection.
  5. primary HHV-6 infection is associated with Roseola infantum.
34
Q

How is HHV-6 and 7 infection diagnosed and treated?

A

Serology - detection of IgM and IgG.

No specific antiviral therapy or vaccine available.

35
Q

Describe HHV-8 or Kaposi’s Sarcoma herpes virus.

A
  1. originally isolated from cell so Kaposi’s sarcoma.
  2. associated with other malignancies such as Castleman’s disease and primary effusion lymphomas.
  3. most patients with KS have antibodies against HHV-8.
  4. the seroprevalence of HHV-8 is low among the general population but high in groups susceptible to KS such as homosexuals.
36
Q

How does Kaposi’s sarcoma and HHV-8 infection present?

A

Bluish-purple spots and lymphadenopathy with a history of fatigue, and intermittent diarrhea.

37
Q

Is there a treatment for HHV-8 infection?

A

No, there are no specific antivirals to treat.

38
Q

What is the most common AIDS-related malignancy?

A

Kaposi’s sarcoma.

39
Q

Describe pox virus/variola virus.

A
  1. has been completely eradicated via vaccine - easier because only has one serotype.
  2. is a category A select agent
  3. the virion particle is dsDNA and DNA-dependent RNA polymerase.
  4. virus replicates in the cytoplasm.
  5. causes smallpox.
40
Q

How is pox virus spread?

A

Transmitted by respiratory aerosol or by direct contact with the virus.

41
Q

Describe the pathogenesis of pox virus.

A
  1. infects upper respiratory tract, spreads to lymph nodes and then blood - primary viremia.
  2. travels to internal organs then re-enters blood - secondary viremia - before infecting the skin.
  3. rash is due to replication of virus in the skin. Also causes fever and malaise.
  4. Rash is worst on the face and extremities.
  5. incubation period is 7-14 days.
42
Q

How is smallpox diagnosed?

A
  1. culture of virus

2. detection of viral antigens

43
Q

How was smallpox eradicated?

A
  1. the virus has one serotype and no animal reservoir so a vaccine was easier to make.
  2. the vaccine is a live, attenuated vaccine that is given intra-dermally and forms a vesicle at the site of injection.
  3. first responders are still vaccinated and if someone were exposed they could be immunized up to 4 days post infection and still be protected.
  4. complications can be treated with high titer antibodies.
44
Q

Describe Molluscum Contagiosum virus.

A
  1. causes small flesh-colored papule of the skin or mucus membrane - often on face and trunk
  2. the lesions are non-itchy, painless and non-inflamed
  3. lesions occur in clusters
  4. incubation period is 2-8 weeks
  5. diagnosis is made clinically - no cultures can be grown
  6. is a pox virus that is transmitted via direct body contact, can be transmitted sexually
  7. no therapy available, lesions resolve over time
45
Q

Describe HBV - Hepatitis B virus.

A
  1. small, enveloped dsDNA virus
  2. viral particles are resistant to low pH, freezing and moderate heating hampers disinfection.
  3. the envelope contains proteins called surface antigen - HBcAg - can be used for diagnosis.
  4. other antigens are core antigens HBcAg, and HBeAg.
  5. humans are the only natural host.
46
Q

How is Hepatitis B virus transmitted?

A
  1. blood - prevalent in IV drug users
  2. sexual contact
  3. perinatal - mother to newborn contact
47
Q

Can Hepatitis B cause cancer?

A

Yes, it can cause hepatocellular carcinoma - high incidence in Asia. The HBV vaccine is the first to prevent human cancer.

48
Q

What are the symptoms of HBV infection?

A
  1. acute - fever, fatigue, nausea, loss of appetite, joint pain, pain associated with hepatomegaly. Many infections asymptomatic.
  2. chronic - cirrhosis, jaundice and liver failure, occurs in 5-10% of the those infected.
  3. 80% of cases of primary hepatocellular carcinoma are duet o chronic HBV infection.
49
Q

How is Hepatitis B virus infection diagnosed?

A
  1. many acute infections are asymptomatic and are detected via IgM antibody to HBsAg.
  2. HBsAg and anti HBc antibodies also associated with chronic infection.
  3. biochemical diagnosis - levels of liver enzymes
50
Q

How is HBV infection treated?

A
  1. acute - no treatment
  2. chronic - interferon-alpha, lamivudine, adefovir or entecavir.
  3. neonates of infected moms given HBV IgG therapy.
  4. immunization - recombinant HBsAg vaccine.
51
Q

Describe HDV - Hepatitis D virus.

A
  1. considered sub viral- only propagates in presence of HBV.
  2. has small, circular enveloped RNA genome and codes for a protein called delta agent that surrounds the genome
  3. transmitted by blood and sexual contact
  4. replication of delta agent leads to liver damage
  5. diagnosis - detection of RNA genome, delta antigen or anti-HDV antibodies
52
Q

Describe HEV - Hepatitis E virus.

A
  1. enveloped DNA virus
  2. presents with fatigue, anorexia, nausea, vomiting, low grade fever, dark urine, clay-colored stools, hepatomegaly.
  3. infections are acute only - no chronic infections
  4. transmitted by fecal-oral route, seen in developing countries with poor sanitation
  5. diagnosis - HEV specific IgM and IgG
  6. no specific treatment or vaccine, prevent by improving sanitary conditions

Block 6 - week 4 (9 decks)

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