Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/58

Click to flip

58 Cards in this Set

  • Front
  • Back
Human Herpes Viruses
(general)
Large
Enveloped
dsDNA (makes sense b/c latency!)
Human Herpes Viruses
(Classification Scheme)
Alpha, Beta and Gamma Subfamilies
Human Herpes Viruses
(Alpha Subfamily)
Include HHV 1/2/3 and Herpes simiae (Herpes B)
Characterized by rapid cell growth, variable host range and latency in sensory ganglio
Human Herpes Viruses
(Beta Subfamily)
CMV (5) and HHV6
SLOW GROWTH (culture)
Latency in CD4/Monocytes/Macs/Mesenchymal cells
Human Herpes Viruses
(Gamma Subfamily)
4 (EBV) and 8 (Kaposi's Sarcoma HIV)
POOR GROWTH
Herpes
(Virus-Host Interactions)
All encode enzymes involved in NA metabolism (important in antiviral therapy!)
Lysis/latency
Reactivation of latent phase may be symptomatic or asymptomatic
Herpes Simplex Viruses
HHV 1 & 2
HSV
(Structure)
As HHVs, they're enveloped w/dsDNA
They're envelope is coated with glycoproteins that facilitate their attachment to cells but also enable serotyping
How do you serologically distinguish HSV1 and HSV2?
Serology is based on antibodies to gG (envelope glycoprotein)
HSV1 vs. HSV2
(Seroepidemiology)
HSV1: indidence begins at childhood (most adults seropositive)
HSV2: incidence at puberty & less than 1/2 adults seropositive
HSV Infections
(Pathogenesis)
Inoculate skin/mucous membranes
Productive infection of surrounding area and sensory neurons
LATENCY (in sensory ganglia)
External/internal stressors result in reactivation of infection (majority are subclinical)
HSV Primary Infection
Generally subclinical
Most common manifestation = PAINFUL vesicular rash
HSV Rash Evolution
Erythema, Papule, Vesicle, Pustule, Ulcer, Scab
HSV 1
(Typical Primary Infections)
Gingivostomatitis
Keratoconjunctivitis
HSV 1
(Typical Recurrent Disease)
Herpes labialis
HSV 2
(Typical Primary Infection)
Genital/neonatal herpes
HSV 2
(Recurrent disease)
Genital Herpes
HSV and the Immunocompromized Host
MORE FREQUENT
DISSEMINATED INFECTIONS are cause of significant mortality
Shared Clinical Syndrome of HSV 1 and 2
ENCEPHALITIS
HSV
(Diagnosis)
Tzank Smear (multinucleated giant cells w/inclusions)
Culture
or serology
Tzank Smear
Multinucleated Giant cells w/inclusions (seen in HSV lesions)
HHV 3
Varicella-Zoster Virus
Chickenpox and Shingles
VZV
(Epidemiology)
Majority of US adults are seropositive
Primary infections at childhood
Incidence of recurrent infection increase with age
VSV
(Pathogenesis)
Aerosol or direct contact
Latency established in sensory ganglia (note: you have this interstitial viremia which causes virus to set up shop in multiple dermatomes)
VSV
(Primary Infection)
Symptomatic
"Chickenpox"
Morbidity greater in adults vs. children
Serious complications if immunocompromized
Primary infection during pregnancy may give rise to birth defects
Reye Syndrome and VSV
Associated w/aspirin treatment
Reye Syndrome
Unexplained GI problems (vomiting/diarrhea)
Generally afebrile
"Brain Fevor" symptoms . . . lethary . . . delerium later, etc
Herpes Zoster
Reactivated latent VSV infection
Dermatomal banding pattern
More severe in immunecompromized host
VSV
(Prevention and Control)
Live vaccine recommended for 1 yr olds
Must isolate VSV infection in hospital
Immune globulin possible for those at risk for severe infecotion
Cytomegalovirus
CMV (HHV 5)
As HHV, tells you its dsDNA and enveloped
CMV
(Risk Factors)
Day Care
Promiscuity (Homosexuality)
Blood/transplant recipients
CMV
(Routes of Transmission)
Perinatal
Intimate contact
Blood transfusion/transplants
CMV
(Clinical Presentation)
Majority of infecotions are ASYMPTOMATIC but 3 groups of symptomatic infections exist (depends on host state)
CMV
(Symptomatic Infections)
(1) Fetus/Neonate
(2) Older children/adults
(3) Immunocompromized
CMV
(Fetal/Neonatal Infection)
Severe, disseminated disease
Fever, jaundice, hepatospenlomegaly, anemia/thrombocytopenia, lymphocytosis
What is the most common congenital infection?
CMV
What is the most common cause of viral-induced deafness/MR?
CMV
CMV
(Older Children/Adults)
Systemic infection mimics Infectious Mononucleosis (due to EBV)
CMV
(Immunocompromized Host)
Hepatitis
Retinitis
Encephalitis
Colitis
CMV
(Diagnosis)
Detect viral antigen/DNA (via PCR), IgM or histopathology (see cytoplasmic/nuclear inclusions)
EBV
(general)
Epstein-Barr Virus
HHV4 (tells you enveloped, as dsDNA)
EBV
(Seroepidemiology)
Vast majority seropositive
In children, infections are generally subclinical
Most common presentation in young adults
EBV
(Pathogenesis)
Replication in oropharynx and B cell infection
EBV stimulates proliferation of B cells and CMI/humoral response
What causes symptoms of EBV infection (mono)?
The immune response to B cell proliferation
EBV
(Clinical Manifestations)
(1) Infectious Mononucleosis (fever, sore throat and lymphadenopathy)
(2) OHL
(3) Cancer
OHL
Oral Hairy Leukoplakia
Seen in HIV patients
Lytic EBV replication on tongue epithelium
NOTE: EBV is required but not sufficient for OHL
EBV and Cancer
Nasopharyngeal carcinom
African-type Burkitt's Lymphoma
Non-Hodkin's Lymphoma
Hodkin's Disease
NOTE: these cancers arise in *10%* of transplant patients (b/c their immune system is so shoddy - if you cut back on immunosuppressive drugs, these cancers may regress)
EBV
(Diagnosis)
1) CBC w/diff: Lymphocytosis w/atypical lymphocytes
2) Heterophile antibodies (during acute infection)
3) anti-VCA (viral capside antigen) IgM antibodies (for specific diagnosis)
What should you look for to specifically diagnose acute EBV infection?
IgM antibodies to VCA (viral capsid antigen)
EBV
(Managment of Symptoms)
Steroids (if airway obstruction, thromobocytopenia/anemia, etc)
Avoid contact sports (splenic rupture)
HHV 6
(general)
Beta HHV Subfamily (?)
Tells you it's enveloped, dsDNA
HHV 6
(Clinical Manifestations)
MAJORITY of cases are SYMPTOMATIC
Causes Roseola (a.k.a. SIXTH disease) - high fever and following rash
HHV 8
(general)
Gamma HHV virus (enveloped, dsDNA)
a.k.a. Kaposi's Sarcoma-Associated Herpesvirus (KSHV)
HHV 8
(Epidemoiology)
Low seroprevalence in US
Higher seroprevalence in Mediterranean/East African Population
HIGH seroprevalence (75%) in HIV patients
HHV 8
(Transmission - Endemic Areas)
Oral and suggested mother-child
HHV 8
(Transmission)
Patterns of sexual transmission (virus predominates in saliva and other secretions)
NOTE: different route of infection in endemic countries (likely oral) b/c acquired during childhood
HHV 8
(Diseases)
Tumors (Kaposi's Sarcoma), primary effusion/body cavity lymphomas, AIDS-related multicentric Castleman's Disease
Herpes Simiae
Herpes B
Primate herpes that is highly infectious among humans, with severe CNS complications
Generally follows animal bites
NOTE: antiviral therapy EXISTS. Therefore, need to catch and treat early!