Herpesvirus and HIV Pathophysiology Flashcards
Traube’s space
lower left lung where you percuss the spleen to see splenomegaly
CBC presentation of EBV
*atypical lymphocytosis: reactive cytotoxic T lymphocytes
heterophile (monospot) test
-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
EBV pathophysiology
*EBV induces a proliferation of B lymphocytes in the lymphoid tissue, causing B cells that resemble malignant lymphocytes on histology
what cell does EBV infect
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)
epidemiology of EBV
*one of the most common viruses in humans
*transmitted by saliva
pathogenesis of EBV
- initially infects oropharyngeal epithelial cells
- spreads to underlying lymphoid tissue
- mature B cells are infected; some are lytic and some are latent
EBV transforming latency genes
- EBNA 1 and 2
- LMP1
- vIL-10
EBNA 1 and 2 (Epstein-Barr nuclear antigens)
*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
latent membrane protein 1 (LMP1)
*a transforming latency gene of EBV
*drives B cell ACTIVATION
*PREVENTS APOPTOSIS (immortalizes the B cells) by activating Bcl-2
vIL-10 (homologue of IL-10)
*a transforming latency gene of EBV
*SUPPRESSES CELL-MEDIATED RESPONSES (inhibits macrophages and dendritic cells and suppresses antiviral T cell responses)
EBV infection results in?
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
EBV serology
- IgM antibody to Viral Capsid Antigen (IgM-VCA) increases FIRST
- IgG-VCA produced later
- EBNA persists and indicates latency
viral latency definition
persistence of viral genomes in cells that do NOT produce infectious virus
CMV clinical features
*immunocompetent people: asymptomatic or mono-like infection
*neonates/immunocompromised: devastating systemic infections (CMV pneumonia, CMV colitis)
EBV reactivation
*Burkitt lymphoma
*Nasopharyngeal malignancy
HIV labs
*reduced CD4+ cell count
*p24 ELISA test positive = HIV confirmatory test
Pneumocystis jirovecii pneumonia
opportunistic fungal infection, presents in HIV patients (and other immunodeficient patients)
*treatment with TMP-sulfa
AIDS and neurologic impairment
several different things can cause altered mental status in AIDS patients:
1. opportunistic diseases
2. neoplastic diseases
3. primary HIV-associated syndromes
common diarrhea-producing pathogens in AIDS
*mycobacterium avium-intracellulare
*cryptosporidium or isosporidium
*CMV
Kaposi sarcoma
*associated with HHV-8
*purple-red vascular lesions on the skin
*commonly occurs in immuno-compromised patients
HIV overview
retrovirus characterized by destruction of CD4+ T cells, leading to profound immunosuppression that leads to:
-opportunistic infections
-secondary neoplasms
-neurologic manifestations
HIV transmission
- sexual contact
- parenteral inoculation (sharing needles)
- mother-to-infant
important envelope proteins in HIV
- gp120 (binds to CD4+ T cells)
- gp41 (allows envelope to fuse to CD4 T cell)
important core protein in HIV
p24 (major capsid protein)
**used to DIAGNOSE HIV
acute viral syndrome in HIV
viremia dissemination and development of host immune response
-infection of CD4+ T cells
*death of many infected cells
chronic phase (clinical latency) of HIV
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
clinical AIDS
breakdown of host defense
serious opportunistic infections, secondary neoplasms, or clinical neurologic disease
