Herpesvirus and HIV Pathophysiology Flashcards

1
Q

Traube’s space

A

lower left lung where you percuss the spleen to see splenomegaly

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2
Q

CBC presentation of EBV

A

*atypical lymphocytosis: reactive cytotoxic T lymphocytes

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3
Q

heterophile (monospot) test

A

-shows the ability of the patient’s serum to agglutinate horse red blood cells
-used as a test for infectious mononucleosis
*a positive test is sufficient to CONFIRM a diagnosis
*a negative test does NOT exclude mono

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4
Q

EBV pathophysiology

A

*EBV induces a proliferation of B lymphocytes in the lymphoid tissue, causing B cells that resemble malignant lymphocytes on histology

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5
Q

what cell does EBV infect

A

infects B lymphocytes (resides in a latent state for the remainder of the patient’s life)
*in TISSUES (tonsils and lymph nodes - CD20 positive B cells)

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6
Q

epidemiology of EBV

A

*one of the most common viruses in humans
*transmitted by saliva

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7
Q

pathogenesis of EBV

A
  1. initially infects oropharyngeal epithelial cells
  2. spreads to underlying lymphoid tissue
  3. mature B cells are infected; some are lytic and some are latent
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8
Q

EBV transforming latency genes

A
  1. EBNA 1 and 2
  2. LMP1
  3. vIL-10
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9
Q

EBNA 1 and 2 (Epstein-Barr nuclear antigens)

A

*a transforming latency gene of EBV
*binds EBV genome to host cell chromosomes
**promotes B cell REPLICATION (turns on protein transcription that drive cell cycling)
*we can detect antibodies against EBNA

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10
Q

latent membrane protein 1 (LMP1)

A

*a transforming latency gene of EBV
*drives B cell ACTIVATION
*PREVENTS APOPTOSIS (immortalizes the B cells) by activating Bcl-2

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11
Q

vIL-10 (homologue of IL-10)

A

*a transforming latency gene of EBV
*SUPPRESSES CELL-MEDIATED RESPONSES (inhibits macrophages and dendritic cells and suppresses antiviral T cell responses)

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12
Q

EBV infection results in?

A

BOTH HUMORAL AND CELLULAR RESPONSE
1. humoral response - secretes antibodies with many specificities
2. T cell-response - CD8+ cytotoxic T cells and NK cells in peripheral blood

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13
Q

EBV serology

A
  1. IgM antibody to Viral Capsid Antigen (IgM-VCA) increases FIRST
  2. IgG-VCA produced later
  3. EBNA persists and indicates latency
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14
Q

viral latency definition

A

persistence of viral genomes in cells that do NOT produce infectious virus

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15
Q

CMV clinical features

A

*immunocompetent people: asymptomatic or mono-like infection
*neonates/immunocompromised: devastating systemic infections (CMV pneumonia, CMV colitis)

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16
Q

EBV reactivation

A

*Burkitt lymphoma
*Nasopharyngeal malignancy

17
Q

HIV labs

A

*reduced CD4+ cell count
*p24 ELISA test positive = HIV confirmatory test

18
Q

Pneumocystis jirovecii pneumonia

A

opportunistic fungal infection, presents in HIV patients (and other immunodeficient patients)
*treatment with TMP-sulfa

19
Q

AIDS and neurologic impairment

A

several different things can cause altered mental status in AIDS patients:
1. opportunistic diseases
2. neoplastic diseases
3. primary HIV-associated syndromes

20
Q

common diarrhea-producing pathogens in AIDS

A

*mycobacterium avium-intracellulare
*cryptosporidium or isosporidium
*CMV

21
Q

Kaposi sarcoma

A

*associated with HHV-8
*purple-red vascular lesions on the skin
*commonly occurs in immuno-compromised patients

22
Q

HIV overview

A

retrovirus characterized by destruction of CD4+ T cells, leading to profound immunosuppression that leads to:
-opportunistic infections
-secondary neoplasms
-neurologic manifestations

23
Q

HIV transmission

A
  1. sexual contact
  2. parenteral inoculation (sharing needles)
  3. mother-to-infant
24
Q

important envelope proteins in HIV

A
  1. gp120 (binds to CD4+ T cells)
  2. gp41 (allows envelope to fuse to CD4 T cell)
25
Q

important core protein in HIV

A

p24 (major capsid protein)
**used to DIAGNOSE HIV

26
Q

acute viral syndrome in HIV

A

viremia dissemination and development of host immune response
-infection of CD4+ T cells
*death of many infected cells

27
Q

chronic phase (clinical latency) of HIV

A

over a period of years, continuous cycling of virus infection, T cell death, and new infection leads to STEADY DECLINE IN # of CD4+ T cells
*usually asymptomatic

28
Q

clinical AIDS

A

breakdown of host defense
serious opportunistic infections, secondary neoplasms, or clinical neurologic disease