I & I Part II > HSV II > Flashcards

HSV II Flashcards

(50 cards)

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1
Q

Varicella-Zoster Virus (VZV)

A
  • VZV genus of the Herpesviridae family
  • ds DNA icosohedral enveloped
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2
Q

Varicella-Zoster Virus (VZV) Transmission

A

•Virus entry through inhalation

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3
Q

Varicella-Zoster Virus (VZV) Incubation

A

•Incubation period 14-18 days

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4
Q

Varicella-Zoster Virus (VZV) Replication

A
  • Replicates in respiratory tract and invades lymph nodes
  • Viremia: spreads virus to target organs
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5
Q

VZV - Chicken Pox

A
  • Rash appears first on head, neck, trunk
  • Vesicles contain clear fluid (itch)
  • New vesicles appear during first week
  • Mild fever, malaise, headache
  • Recovery in 2 weeks
  • Adult infections more severe (VZV pneumonia)
  • Maternal varicella during pregnancy causes many neonatal developmental problems
  • Neonatal infection (encephalitis)
  • Immunosuppressed (severe progressive infection)
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6
Q

VZV Shingles

A
  • Shingles is a reactivation of varicella-zoster
  • DNA remains latent in ganglia
  • May occur in any age group, occurrence increases with age (50% over 50 years)
  • Onset of pain occurs before appearance of vesicles
  • Usually unilateral
  • Immunosuppressed patients especially vulnerable
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7
Q

VZV Bacterial Superinfection

A
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8
Q

VZV Diagnosis

A
  • Clinical picture (almost always)
  • Immunofluorescent antibody staining biopsy
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9
Q

VZV Treatment

A
  • Supportive
  • Acyclovir for extreme cases
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10
Q

Chicken Pox Prevention

A
  • Immune globulin for patients at risk
  • Vaccine: live attenuated vaccine, VARIVAX, approved by FDA on March 17, 1995.
  • Recommended dose: First dose at age 12-15 months and second dose at 4-6 years given IM
  • Two doses, 28 days a part for people above 13 years never vaccinated before
  • Single vaccine or combination-MMRV
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11
Q

Shingles Prevention

A
  • Recommended vaccine to prevent shingles: Single dose of ZOSTAVAX (live attenuated) or 2-doses of SHINGRIX (recombinant gE antigen) 2 to 6 months apart recommended for adults above age 50 to prevent shingles
  • Not recommended for immunocompromised or pregnant females
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12
Q

Cytomegalovirus (CMV)

A
  • Cytomegalovirus genus of the Herpesviridae family
  • ds DNA icosohedral enveloped
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13
Q

CMV Structure

A
  • ds DNA virus
  • largest genome of the herpes virus group (~240 kb)
  • similar to HSV but highly regulated by cisacting elements and regulatory proteins
  • slow replication and slow disease effects
  • Nuclear and cytoplasmic inclusion bodies, induction of giant cells
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14
Q

CMV Intranuclear Inclusion

A
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15
Q

CMV Transmission

A

•close contact, sexually transmitted, virus can be recovered from all body fluids much as saliva, urine, semen, & cervical secretions

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16
Q

CMV Clinical Disease

A
  • high infection rates in early childhood and early adulthood l usually asymptomatic
  • Heterophile-negative mononucleosis
  • Systemic CMV infection: pneumonia and hepatitis in immunosuppressed patients (transplant patients)
  • In AIDS patient; diarrhea, retinitis
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17
Q

Congenital CMV

A
  • most infants appear normal at birth
  • may develop hearing loss or some mental retardation often later.
  • Infants with symptomatic illness at birth demonstrate hepatosplenomegaly, jaundice, anemia, low weight, microcephaly, rash, thrombocytopenia
  • Neonatal – asymptomatic
  • Virus excreted about a year l
  • immunosuppressed…CMV pneumonia, disseminated CMV
  • CMV retinitis
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18
Q

CMV Diagnosis

A

•isolation of virus, electron microscopy, serology, DNA amplification by PCR

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19
Q

CMV Treatment

A

•hyperimmune globulin, ganciclovir

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20
Q

Epstein-Barr Virus (EBV)

A
  • Lymphocryptovirus genus of the Herpesviridae family
  • ds DNA icosohedral enveloped
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21
Q

EBV Structure

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A
  • DNA virus, enveloped, ~172 kb
  • Etiologic agent of infectious mononucleosis and African Burkitt’s Lymphomas
  • Recent study has linked with Hodgkin’s lymphoma
  • Cultured in only lymphoblastoid cell lines derived from B lymphocytes of humans and higher primates
  • Viral genome can be cultivated continuously and are transformed or immortalized
22
Q

When do EBNAs appear in EBV?

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A

•EBV nuclear antigens (EBNAs) appear in the nucleus prior to virus directed protein synthesis.

23
Q

When does VCA appear in EBV?

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A

•Viral capsid antigen (VCA) is detected in virus producing cell lines.

24
Q

EBV Transmission

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A
  • EBV can be cultured from saliva and thus infection is acquired by contact.
  • contact with infected secretions, low contagiousness, virus can be cultured from throat washings
25
EBV Clinical Disease
* usually asymptomatic * symptoms (young adults), low fever, headache, sore throat, fatigue, night chills (sweats), enlarged lymph nodes and spleen, elevated lymphocytes and monocytes, atypical lymphocytes
26
EBV Complications
•laryngeal obstruction, meningitis, encephalitis, hemolytic anemia, thrombocytopenia or splenic rupture may occur in 1 to 5% of the patients
27
EBV Diagnosis
* Clinical picture * Complete Blood Cell Count - Atypical lymphocytes (10% atypical lymphocytes – Downey Cells) * **Heterophile-positive antibodies** -Heterophile Antibodies (sheep erythrocyte agglutinins; used as Monospot test) - Positive in 50% on presentation and 90% at some point: quite specific •Culture: -Usually positive in acute illness, but asymptomatic viral shedding is so common, that culture is seldom helpfu
28
EBV Diagnosis Serology
* Expensive, but can be useful * Demonstrate antibody to viral capsid antigen (VCA) which rises quickly (IgM)and persists for life (IgG) * Antibodies to EBNAs rise later and decrease in about 1 month * A high titer of VCA and no titer of EBNA suggest recent infection * Antibodies to early antigen (EA) may be useful in correlating with nasopharyngeal CA and African Burkitt’s lymphomas
29
EBV Epidemiology
* Burkitt’s lymphoma-Central & East Africa tumor in jaw area * Nasopharyngeal carcinoma - China & Southeast Asia
30
EBV Treatment
* Supportive * Acyclovir can suppress the replication process
31
EBV Prevention
•No vaccine available
32
HHV 6
* Roseolovirus genus of the Herpesviridae family * ds DNA icosohedral enveloped * HHV-6 detected in PBMC from patients with lymphoproliferative diseases * Genetically distinct but morphologically similar to other herpes virus
33
HHV 6 Replication
* Replicates in lymphoid tissue preferentially in T lymphocytes * Cytopathic for T lymphocytes in cell culture * Establishes a latent infection and may be activated by mitogenic stimulation
34
HHV 6 Clinical Disease
* Serologic studies indicate that almost all children are infected by age 5 * Most communicable of all herpes virus * Spread by close personal contact or by respiratory route * Disease: Roseola infantum (rash like disease) * Reactivated in transplant patients
35
HHV 6 Treatment
•Acyclovir is 15 to 30% absorbed by oral route
36
HHV 7
* Roseolovirus genus of the Herpesviridae family * ds DNA icosohedral enveloped * HHV-7 discovered in 1990 * HHV-7 is distinct from all other known human herpes viruses but closely related to HHV-6 * Infects most children by age 2 and 97% of adults are seropositive * Culture restricted to specialized virology lab. * Diagnosis of acute infection by seroconversion
37
HHV 8 KSHV
* Rhadinovirus genus from the Herpesviridae family * ds DNA icosohedral enveloped * B lymphocytes
38
HHV 8 KSHV and AIDS
* Kaposi’s sarcoma (KS) occurred during the AIDS epidemic in ~30% of gay and bisexual males and ~1% of hemophiliacs with AIDS * KSHV or HHV-8 in AIDS related Kaposi’s sarcoma (KS) patients was discovered * HHV-8 DNA sequences found in 95% of KS tissues, both AIDS and non-AIDS related cases * KSHV DNA has also been detected in cells from lymphoproliferative diseases
39
Where is HHV 8 found?
•Like EBV, HHV-8 is found in B-lymphocytes
40
What are co-factors for KS?
•In addition to HHV-8, immunosuppression, and genetic predisposition are cofactors for KS
41
HHV 8 Epidemiology
•5% of healthy donors are seropositive in the U. S., 50% seropositivity in Africa, ~25% seroprevalence in Southern Italy
42
HHV 8 Transmission
* HHV-8 was believed to be sexually transmitted but the virus is found rarely in genital secretions. * The virus is shed mainly in saliva. * Likely transmission is due to prolonged intimate contact.
43
HHV 8 Pathogenesis
* KSHV infects the oral epithelium and shed in saliva for transmission. * It’s also found in B-lymphocytes in latent stage, although lytic infection can occur in some cells. * KSHV is found in main tumor cells.
44
HHV 8 Classical KS
•described in 1800s, rare, mainly found in lower extremities, seen in elderly men of Mediterranean origin and Ashkenazi Jews
45
HHV 8 Endemic KS
•described in 20th century, KS became common in central Africa Ø More aggressive than classical KS and seen higher on extremities and oral cavity
46
HHV 8 Iatrogenic KS
•seen in post transplant patients but regresses after off immunosuppressive
47
HHV 8 Epidemic or AIDS-associated KS
•This is most aggressive form of KS, with tumors found in the mouth, on the torso and face as well as on internal organs, leads to death if untreated (HIV treatment)
48
HHV 8 Diagnosis
•Immunofluorescence with patient’s sera, PCR from patient’s peripheral blood mononuclear cells
49
HHV Treatment
•Anti-herpesviral drugs could be used for lytic KSHV such as foscarnet, ganciclovir
50
HHV Prevention
•No vaccine
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