Hepatatis virus Flashcards
Hepatatis viruses - types
HAV, HBV, HCV, HDV, HEV
Hepatatis viruses - RNA OR DNA?
all rna except HBV
Hepatatis viruses - transmission
HAV –> fecal-oral (shellfish, travellers, day care)
HBV –> parenteral, sexual, perinatal
HCV –> primarily blood (IVDU, post-transfusion)
HDV –> Parental, sexual, perinatal
HEV –> fecal-oral (espcecially waterborne, undercooked seafood)
Hepatatis viruses - carrier?
all except HAV and HEV
Hepatatis viruses - risk for hepatocellular Carcinoma
all except HAV and HEV
Hepatatis viruses - incubation
HAV --> short (weeks) HBV --> long (months) HCV --> long HDV --> if superinfection (after HBV), short. If coinfection with HBV, long HEV --> short
Hepatatis viruses - characteristics and family
HAV –> RNA-icosahedral-nonenveloped-SS+nonsegmented-Picornavirus
HBV –> DNA-icosahedral-enveloped-DS circular-Hepadnaviridaeg
HCV –> RNA-icosahedral-enveloped-SS+nonsegmented-Flavivirus
HDV –> RNA-NOT EXACTLY icosahedral nucleocapsid-enveloped-SS(-)circular
HEV –> RNA-icosahedral-nonenveloped-SS+nonsegmented-calcivirus (hepevirus)
HDV functional special characteristics
HDV is a “defective” virus that requires the presence of HBV to replicate
HDV superinfection (after HBV) vs coinfection (with HBV) according to prognosis
superinfection is more severe
HAV - how many serotypes / MC season
only 1.. MC season –> autumn
Symptoms and labs for all hepatitis virus (not biopsy)
- fever
- jaundice
- INCREASED ALT and AST
beside HAVb, Councilman bodies can also be seen in
yellow fever
HEV - liver biopsy
patchy necrosis
HAV - liver biospy
- hepatocyte swelling
- monocyte infiltration
- Councilman bodies
Fecal-oral hepatitis virus - mechanism
HAV, HEV
Naked virus do not rely on an envelope, so they are not destroyed by the gut
nonenveloped hepatitis virus
HAV
HEV
HBV - cycle of live
the DNA polymerase has both DNA- and RNA-dependent activities. Upon entry into the nucleus, the polymerrase functions to complete the partial dsDNA. The host RNA polymerase transcribes mRNA from viral DNA to make viral proteins. The DNA polymerase then reverse transcribes viral RNA to DNA, which is genome of the progeny virus
HCV - liver biopsy
Lymphoid aggregates with focal areas of macrovesicular steatosis
HBV - liver biopsy
- granular eosiniphilic “ground glass appearance”
- cytotoxic T cells
HDV - liver biopsy
- granular eosiniphilic “ground glass appearance”
- cytotoxic T cells
(SIMILAR TO HBV)
breastfeeding - HBV vs HCV according to transmission?
neither
Hepatitis serologic markers (all)
- anti-HAV (IgM)
- anti-HAV (IgG)
- HBsAg
- anti-HBs
- HBcAg
- anti-HBc
- HBeAg
- anti-HBe
HCV diagnosis
anti-HCV
direct dirextion of HCV RNA (gold standard)
anti-HAV (IgM) - marker?
IgM antibody to HAV –> best test to detect acute Hepatitis A
anti-HAV (IgG) - marker?
IgG antibody indicates prior HAV infection and/or prior vaccination
protects against reinfection
HBsAg - marker / indicates
antigen found on surface of HBV
indicates hepatitis B infection (acute or chronic)
anti-HBs - marker / indicates
antibody to HBsAg
indicates immunity to hepatitis B
HBcAg
antigen associated with core of HBV
anti-HBc - marker
antibody to HBcAg (HBV)
IgM = acute/recent infection (+ in window)
IgG = prior exposure or chronic infection
anti-HBc - window
IgM anti-HBc may be the sole positive marker of infection during window period
HBeAg - marker
a differnet antigenic determinant in the HBV core
indicates active viral replication and therefore high transmissibility (acute HBV or chronic high infectivity)
anti-HBe - marker
antibody to HBeAg
indicates low transmissibility (positive in window, recovery, chronic HBV infection with low infectivity)
HBV structure
DNA-icosahedral-enveloped-DS circular (PARTIALLY) diameter 42mm DNA polymerase Core antigens: HBcAg, HBeAG Coat proteins: HBsAG
HBV: DNA polymerase abilities
has both DNA- and RNA-dependent activities
HBV serologic markers
HBsAG anti-HBs HBeAg Anti-HBe anti-HBc
HBV - states
Acute HBV window Chronic HBV (high infectivity) Chronic HBV (low inectivity) Revocery Immunized
HBV - markes during acute infection
HBsAG
HBeAg
anti-HBc - IgM
HBV - markes during window
anti-HBc - IgM
Anti-HBe
HBV - markes during Chronic infection with high infectivity
HBsAG
HBeAg
anti-HBc - IgG
HBV - markes during Chronic infection with low infectivity
HBsAG
Anti-HBe
anti-HBc - IgG
HBV - markes during recovery
anti-HBs
Anti-HBe
anti-HBc - IgG
HBV - markes during immunized
anti-HBs
HBV infection - serology during incubation period
HBsAg
HBV infection - anti-HBc is getting + at (time)
the beginning of the acute state (2 months)
HBV infection - HBsAg is getting + at (time)
the incubation period (1 month)
viral hepatitis vs alchoholic hepatitis according to labs
viral: ALT>AST
alcoholic: AST>ALT
Hepatatis viruses - vaccines and types
HAV --> yes (killed) HBV --> yes (subunit) HCV --> no HDV --> no HEV --> no
viral subunit vaccines - types
HBV (HBsAG)
HPV (types 6, 11, 16, 18)
HBV - window period - when
5,5-6 months
HBV - anti-HBs if recovery - when
after windorw period (6 months)
HBV - acute disease - when
2.25-5.25 mounths
HIV - characteristics
RNA virus - icosahedral nucleocapsid - enveloped - SS+ diploid - Retrovirus -
Retrovirus - viruses?
- HIV
- HTLV - 1
- HTLV - 2
HIV - structural genes - how many and which
- env (gp120 and gp41)
- gag (p24 and p17)
- pol
HIV - structural genes - env is formed from
cleavage of gp160 to form envelop glycoproteins (gp120 and gp41)
HIV - structural genes - function
- env (gp120 and gp41)
gp120 –> attachment to host CD4+ T cells (docking protein)
GP41 –> fusion and entry - gag (p24 and p17)
p24 –> capsid protein
p17 –> matrix protein - pol –> reverse transcriptase, aspartate protease, integrase
HIV - gp120 and gp41 - according to location
both on lipid membrane
gp120 outer (non-transmembrane)
gp41 transmembrane
HIV - gp120 and gp41 -aquired through
budding from host cell plasma membrane
HIV - proteins from outer to inner
out - gp120 - gp41 - Matrix protein (p17) - capsid protein p24 - reverse transcriptase - inne
HIV1 vs HIV2
HIV1 –> worldwide and more severe and more transmissible
HIV2 –> primarily in West Africa, less severe, less transmissible
HIV - reverse transciptase - function
synthesize dsDNA from genomic RNA
HIV - synthesis of dsDNA - next?
dsDNA integrats into host genome
virus to enter the host cells –> ….
binds CD4 as well as coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on T cells (late infection)
HIV - mutations on host coreceptors:??
homozygous CCR5 mutation = immunity
Heterozygous CCR5 mutation = slower course
HIV diagnosis - protocol
Presumptive diagnosis made with ELISA –> positive results are then confirmed with Western blot assay
HIV diagnosis - characteristics of ELISA
sensitive, high false positive, low threshold, RULE OUT test
HIV diagnosis - characteristics of Western Blot assay
specific, low false-positive, rate and high threshold, rule in test
HIV diagnosis - rule in and rule out test
rule in –> Western Blot assay
rule out –> ELISA
HIV - ELISA/Western blot test look for
antibodies to viral proteins
HIV - ELISA/Western blot test - disadvantages
- falsely negative in the fist 1-2 months of HIV infection
2. falsely positive in babies born to infected mothers (anti-gp120 crosses placenta)
how to diagnose HIV in infants younger than 18 months (no antibodies production) born to seropositive mothers
p24 antigen test
PCR
viral culture (not common)
AIDS diagnosis?
- less than two hundred CD4+ cells/mm3
- HIV+ with AIDS-defining conditions
- CD4 percentage less than 14%
normal CD4 COUNT
500-1500 cells/mm3
HIV transmission
- sexual contact
- infected blood,
- cross placenta
- birth
- breast milk
HIV infection - first signs (and when)
acute HIV syndrome (not always) - flu like
2 weeks-2.5 months
HIV infection - stages (and when)
four stages (4fs)
- flu like (acute) –> 2 weeks-2.5 months
- Feeling fine (latent) –> 2.5 months-8 years
- Falling count
- Final crisis
constitutional symptoms of HIV (AND WHEN)
fever, night sweats, diarrhoea, weight loss.
8-11 years
HIV infection - death - when (if untreated)
11 years
HIV infection - opportunistic infection - when (if untreated)
9-11 years
mechanism of virus during the acute phase of infection
wide dissemination of virus
seding of lymphoid organs
mechanism of virus during the latent phase of infection
virus replicates in lymph nodes
Common diseases of HIV positive adults - mechanism
As CD4+ decreases:
- risks of reactivation of past infections (e.g. TB, HSV, shingles)
- dissemination of bacterial infections and fungual infections (e.g. coccidioidomycoses)
- increased risk for non-Hodgkin lymphomas
HIV - disease (and pathogen) IF CD4 lower than 500
- oral thrush - Candida ablicans
- Oral hairy leukoplakia (EBV)
- Kaposi sarcoma (HHV-8)
- Chronic Watery diarrhea (Cryptosporidium spp)
- SCC, commonly of anus (men who have sex with men, or cervix (HPV)
- Bartonella henselae
Candida related oral thrush - findings
Scrapaple white plaque
pseuohyphae on microscopy
Oral hairy leukoplakia - findings
Unscrapable white plaque on lateral tongue
Chronic Watery diarrhea (Cryptosporidium spp) - findings
acid-fast oocyts in stool
HIV - disease (and pathogen) IF CD4 lower than 200
- dementia (HIV)
- Progressive multifocal leukoencephalopathy (JC)
- Pneumocystic pneumonia (Pneumocystis jirovecii)
Brain abscesses (Toxoplasma gondi) - findings
Multiple ring-enhancing lesions on MRI
Progressive multifocal leukoencephalopathy (JC) findings
Non-enhancing areas of demyelination on MRI
Pneumocystic pneumonia (Pneumocystis jirovecii) - findings
Ground-glass opacities on CXR
HIV - disease (and pathogen) IF CD4 lower than 100
- Hemoptysis, pleuritic pain (Aspergilus)
- Meningitis (Cryptococcus neoformans)
- esophagitis (Candida)
- Retinitis, esophagitis, colitis, pneumonitis, encephalitis (CMV)
- B-cell lymphoma (non-Hodgkin, CNS) (EBV)
- Fever, weight loss, fatique, cough, dyspnea, nausea, vomiting, diarrhea (Histoplasma)
- Nonspecific systemic infection (fever, nigh sweats, weight loss) or focal lymphadenitis (M. avium-intracellulare)
- Brain abscesses (Toxoplasma gondi)
HIV - Hemoptysis, pleuritic pain (Aspergilus) - findings
Caviation or infiltrates on chest imaging
HIV - esophagitis (Candida) - findings
white plaques on endoscopy
yeast and pseudohyphae on biopsy
HIV - Retinitis, esophagitis, colitis, pneumonitis, encephalitis (CMV) - findings
linear ulcer on endoscopy
cotton-wool spots on fundoscopy
Biopsy: cells with intranuclear (owl eye) inclusion bodies
HIV - EBV - CNS lymphoma - findings
ring enhancing, may be solid solitary
HIV - IMAGING - toxoplasma vs CNS lymphoma
both ring enhancing
Toxoplasma –> multiple
CNS lymphoma –> solitary
HIV - Fever, weight loss, fatique, cough, dyspnea, nausea, vomiting, diarrhea (Histoplasma) - findings
oval yeast cells with macrophages
HDV - antigen / protection against
HBsAg
HBV vaccine
HIV - viral load test determine
the amount of viral RNA in the plasma
HIV - viral load test determinations - clinical importance
High viral load associated with poor prognosis
monitor effect of drug therapy