Term
|
Definition
-picoRNAvirus
-small (+) ssRNA
-naked--not killed by stomach acid
-VPg protein on 5' end; polyadenosine tail at 3' end |
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Term
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Definition
-fecal-oral transmission-->replicate in hepatocytes and Kupffer cells-->exocytosis into bile (other picornaviruses are cytolytic)-->excreted in feces
-slow replication |
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Term
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Definition
-kids less severe disease than when infect adults
-shellfish, water, contaminated hands
-15-50 days post exposure symptoms develop abruptly:
-first have: fever, fatigue, nausea, loss of appetite, abd
pain
-4-6 days before icteric period symptoms worsen
-icteric period = dark urine, jaundice, pale stools, puritis
-contagious 10-14 days before symptoms |
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Term
| HepA immunity, diagnosis, treatment |
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Definition
-IFN limits replication
-T cells and NK cells-->eliminate infected cells
-Antibody protection for life
-active infection: anti-HAV-IgM
-recovered, vaccinated: anti-HAV-IgG
-prophylaxis with immune serum globulin before or early in incubation period
-vaccine at 2 y.o. with killed HAV |
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Term
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Definition
-hepaDNAvirus
-small, circular, partially dsDNA
-virion = Dane particle
-stable enveloped virus
-protein kinase, polymerase, P protein, HbcAg for capsid, HBsAg for envelope |
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Term
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Definition
-bind to hepatocyte via HbsAg glycoproteins-->partial DNA strand completed by forming into dsDNA circle--> transcription in nucleus starts from different point with same 3' end -->3500b mRNA is the template for genome replication (900b mRNA encodes X protein to promote viral replication) -->RNA-dpdnt DNAP with reverse transcriptase transcribes RNA using P protein as primer-->covalently attached to 5' end-->RNA degraded by ribonuclease H--> envelop nucleocapsid (RNA-dpdnt-DNAP w/ reverse transcriptase and ribonuclease H activity)-->nucleocapsid captures RNA-DNA circles w/ different lengths of RNA--> further RNA degradation-->partially dsDNA genome
-coinfection with HepD
-HBV provides envelope for HDV RNA
-HDV exacerbates symptoms caused by HBV |
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Term
|
Definition
-3 month incubation period w/ insidious onset of symptoms
-5-10% get chronic infection
-primary hepatocellular carcinoma associated with
chronic infxn
-1/3 infected worldwide, with 5000 deaths/year in US
-sexual, parenteral, perinatal routes of infection
-up to 45 day incubation period
-but have replication after just 3 days
-acute infection:
-prodromal period w/ fever, malaise, anorexia
-then get nausea, vomiting, abd discomfort, chills
-then icteric symptoms: dark urine, pale stool, jaundice
-chronic disease:
-liver scarring, cirrhosis, liver failure, chronic passive
hepatitis
-primary hepatocellular carcinoma (HPC): integration into
host chromosome, directly stimulates growth
-HBV X gene may turn on transcription and stimulate
growth
-9-35 year latency b/w HBV infection and PHC
-vasculitis, arthralgia, rash, renal damage from immune complexes between HBsAg and anti-HBs
-type III hypersensitivity reactions |
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Term
| HepB diagnosis and serology |
|
Definition
-Early acute HBV infxn:
-HBsAg present
-Acute infxn:
-HBsAg, HBeAg HBV DNA, Anti-HBc-IgM
-Window phase (between HBsAg disappearance and anti-HBs presence):
-Anti-HBc-IgM
-Recovered from HBV:
-Anti-HBc-IgG
-Immunized:
-Anti-HBs
-"Healthy carrier":
-HBsAg, Anti-HBc-IgG
-Infective carrier:
-HBsAg, HBeAg HBV DNA, Anti-HBc-IgG
-negative Ab tests b/c all HBsAb is bound to HBsAg in plasma |
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Term
| HebB immunology and treatment |
|
Definition
-cell-mediated immunity and inflammation lead to symptoms
-HBcAg induces T cell-->protect against initial infection BUT HBsAg in serum blocks neutralizing Ab later in infection
-immune complexes b/w HBsAg and anti-HBs --> hypersensitivity type III rxns-->vasculitis, arthralgia, rash, renal damage
-Dx: HBsAg and HBeAg in blood = active infection
-IgM anti-HBc in serologic gap
Treatment:
-HepB Ig w/in 1 week of exposure or to newborns w/
HBeAg+ mothers
-IFn-alpha for chronic HBV
-vaccines: insert plasmid w/ S gene for HBsAg in yeast) |
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Term
|
Definition
-flavivirus
-(+)ssRNA, enveloped
-hypervariable regions-->difficult for vaccine making |
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Term
|
Definition
-binds CD81 (tetraspanin) surface receptors on hepatocytes and B cells
-can coat itself with LDL or VLDL and use LDL-R
-buds into ER
-HCV proteins inhibit apoptosis and IFN-alpha action by binding to TNF-R and protein kinase R
-remains cell-associated, prevents host cell death
-Cell mediated immunity causes infection and tissue damage |
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Term
|
Definition
-no host cell death so persistent infection --> liver disease later in life-->predisposed to primary hepatocellular carcinoma
-get from infected blood and sexual transmission
-chronic asymptomatic infxns-->more viral spread
-acute infxn milder than HAV and HBV
-can lead to recovery and clearance (15%)
-can lead to cirrhosis w/ rapid onset (15%)
-can lead to persistent infxn (70%)
-chronic infxn:
-40% stay asyptomatic carriers
-the rest get chronic hepatitis
-leads to: liver failure, cirrhosis, hepatocellular
carcinoma
-chronic fatigue = main symptom |
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Term
| HepC immunity, diagnosis, and treatment |
|
Definition
-cell-mediated immunity-->damage
-anti-HCV Ab NOT protective
-immunity likely not life-long
-Diagnose:
-anti-HCV Ab or detect RNA genome
-seroconversion in 7-31 weeks
-confirm with western blot (like with HIV)
-Treatment:
-recombinant IFN-alpha or
-pegylated IFN
-can also use with ribavirin |
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Term
|
Definition
-also a flavivirus
-similar to HepC
-predilection for chronic hepatitis
-diagnose with genome detection |
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Term
|
Definition
-deltavirus
-small (-)ss circular RNA
-forms rod shape b/c of extensive base-pairing
-genome surrounded by deltaAg core, which is surrounded by HBsAg-containing envelope
-requires HBV for replication |
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Term
|
Definition
-HBsAg coat for getting into hepatocyte-->host RNA pol II makes RNA copy-->ribozyme forms-->cleaves RNA circle to make mRNA for small delta Ag-->delta Ag gene mutated by dsRNA-activated adenosine deaminase during infxn--> produce large delta Ag-->limits viral replication but promotes viral genome association with HBsAg-->virion formation and viral release
-cytotoxic so replication and release cause direct cytopathic effect of delta agent if have underlying HBV disease |
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Term
|
Definition
-requires actively replicating HBV as a "helper virus" so only in patients with active HBV infection
-coinfection with HBV:
-less severe progression b/c HBV must establish infxn
before HDV can replicate
-superinfection with HBV:
-more severe progression b/c HDV can begin replicating
quickly b/c already have chronic HBV
-can get acute hepatitis that will go to fulminant hepatitis
-fulminant hep results in: hepatic encephalopathy,
extensive jaundice, massive hepatic necrosis (80% fatal)
-can also get cirrhosis or chronic delta infection
-get from blood, semen, vaginal secretions, drug use |
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Term
| HepD immunity, diagnosis, treatment |
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Definition
-cytotoxic damage
-Diagnose by finding RNA genome, delta Ag, anti-HDV Ab
-Treat by preventing HBV infection with vaccine |
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Term
|
Definition
-enteric encapsulated viras with (+)ssRNA
-resembles caliciviruses |
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Term
|
Definition
-fecal-oral spread, esp contaminated water
-disease resembles HAV:
-only acute disease
-symptoms may occur later than with HAV
-higher mortality than with HAV
-serious with pregnant women |
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Term
|
Definition
-2nd most common cause of pediatric diarrhea
-see in immunocompromised as well
-upon biopsy see nonspecific villous atrophy and compensatory crypt hyperplasia
-resolves in about 10 days |
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Term
|
Definition
-considered enteroviruses and rhinoviruses, depending on clinical symptoms
-Enteroviruses: grow pH range (3-10).
-Initial replication in the oropharynx
-survive the acidic environment of the stomach for a few
hours b/c is naked
-major invasion in small intestine (rep at 37 degrees)
-icosahedral with Viral Proteins 1-4 arranged, nonenveloped
-(+)ssRNA with polyadenylated 3' end
-VPg = small viral-encoded protein at 5' end
-VP1-3: their peptide backbones loop back on themselves to form a beta-barrell
-AA chain b/w beta-barrel is series of loop with many
antigen-sites
-cleft or canyon surrounds each pentameric vertex
-on canyon floor have receptor binding site for host cell
attachment |
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Term
| Picornavirus pathogenesis |
|
Definition
-replicate in cell cytoplasm of enterocytes in small intestine
-bind host cell on canyon floor-->conformational change in virion-->release viral RNA into cytoplasm of host-->VPg removed-->RNA associates with host ribosomes--> translation is cap-independent (uses internal ribosome entry site)-->translated into viral polyprotein-->rapidly cleaved into fragments by proteases that were encoded by polyprotein--> virus-coded RNA-dpndt RNAP produced--> copy RNA into (-) sense then back into (+) for replication--> coat precursor protein from poly protein (P1) cleaved to form VP1, VP3, VP1-->protomers assemble into pentamers--> VPg and RNA associated and are packaged as provirions--> VP0 cleaved to Vp4 and VP2-->mature virions released, host cell disintegrates
-takes 5-10 hours to replicate |
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Term
|
Definition
-Group A: diarrhea and hepatitis
-Group B: hepatitis
-many clinical diseases:
-aseptic meningitis, herpangina, hand-food-mouth dz,
common cold
-GI tract = primary site of replication
-disease not typically a problem in GI tract (some group A
associated with diarrhea in kids)
-Use reverse transcriptase PCR to identify b/c hard to culture
-vertical transmission occurs
-see world-wide in summer and early fall
-no vaccine or meds |
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Term
|
Definition
-aseptic meningitis, rashes in kids, infantile diarrhea, heptatitis (types 4, 9)
-Enterovirus 70 => acute hemorrhagic conjunctivitis
-neutralizing and hemagglutination-inhibiting antibodies may persist for years
-see in younger patients in summer and autumn; low income families
-avoid contact w/ infected patients
-no vaccine or antivirals (exception = poliovaccine)
-isn't polio from picornavirus? I'm confused on how viruses are arranged so any help would be great. |
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Term
|
Definition
-linear, segmented dsRNA
-double-capsid shell = encapsulated
-no envelope except for transient pseudoenvelope when buds into rER
-heat resistant at 50 degrees, okay in pH from 3-9, resistant to lipid solvents |
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Term
|
Definition
-attach to cell surface receptors via viral hemagglutinin alpha-1 proteins-->penetration and virion uncoating within lysosomes and cytoplasm (remove outer shell)-->core- associated RNA transcriptase is activated-->mRNA transcription from (-) strand w/in intact core--> viral replicase synthesizes (-)sense strands to form ds genome segments-->bud of single-shelled particles into rER--> pseudoenvelope removed-->outer capsids added (the major one is glycosylated = UNIQUE)-->cell lysis to release virions
-inclusion bodies w/in cytoplasm are associated with tubular structures
-inclusion bodies w/in cytoplasm associated w/ tubular structures
-outer capsid proteins VP4 and VP7 carry epitopes for neutralizing; VP7 = predominant antigen
-multiple in enterocytes, damage transport mechanisms
-NSP4 = viral enterotoxin
-impaired glucose and Na+ absorption
- |
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Term
| Reovirus Clinical disease |
|
Definition
-infect small intestine vili and multiply in enterocytes
-diarrhea from impaired sodium and glucose absorption
-watery diarrhea, fever, abdominal pain
-dehydration life threatening in infants/kids if untreated
-adults are usually asymptomatic
-recovery in 3-8 weeks if get the diarrhea |
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Term
| Reovirus immunity, diagnosis, treatment |
|
Definition
-sIgA, IFN important for protection
-supportive treatment to replace water and electrolytes
-oral bovine-based rotavirus vaccine |
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Term
|
Definition
-Include 4 genera
-Norovirus (includes Norwalk)--human but can't culture
-Sapovirus--human but can't culture
-Lagovirus--not human
-Vesivirus--not human
-small, linear, non-segmented (+)RNA
-nonenveloped |
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Term
| Norwalk virus clinical disease |
|
Definition
-type of norovirus (which is a calcivirus)
-most important cause of epidemic viral gastroenteritis in adults (half of all outbreaks world-wide)
-rapid onset and recovery of gastroenteritis with mild systemic signs
-rapidly spreads with no predilection for age or geography
-person-to-person and food-contaminated transmission
-water, food, shellfish associated; see in winter
-can live on steamed oysters
-see on cruiseships
-nausea, vomit, water diarrhea, abd pain
-self-limited |
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Term
| Norwalk virus immunity, diagnosis, treatment |
|
Definition
-biopsy is nonspecific: loss of brush border, crypt hypertrophy, lamina propria infiltration, epithelial vacuolization, villous shortening)
-Antibodies develop early on but only protective in the short term
-no vaccine
-supportive care b/c is self-limited |
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Term
|
Definition
-(+)ssRNA with star-like morphology
-shed a lot of viruses in feces
-diarrhea
-transmit by fecal-oral, food/water contamination, person-to-person, contaminated surfaces
-see most in infants/kids, elderly, institutionalized people, and immunocompromised pts (where see long-term shedding) |
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Term
| Hepatocellular Carcinoma (HCC) |
|
Definition
-associated with HBV or HCV infection (75-85%)
-HBV endemic to far east and to africa (52% HCC in china)
-HBV and HCV do NOT encode viral oncoproteins
-HCV = RNA virus so not integrated into host genome
-HBV put into human genome b/c is DNA virus
-HBx gene: directly or indirectly activate transcription
factors
-nodules have clonal HBV integration patterns,
suggesting viral integration precedes/accompanies
transforming event
-proliferation of hepatocytes, ROS, maladaptive immune response and blocking apoptosis
-NF-kappaB mutation = KEY STEP for hepatocytes blocking apoptosis
-in high prevalence areas, HBV is passed on vertically
-vaccinate against HBV and decrease HCC development |
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Term
|
Definition
-paramyxovirus = (-)ssRNA, enveloped
-causes acute, benign viral parotitis
-with fever, sudden onset, red and swollen ostium
-increases in parotid pain when drinking cirtrus juice
-lytic infxn in cells
-in upper resp tract epi
-in parotid gland (via Stensen duct or viremia)
-viremia spreads to testes, ovary, pancreas, thyroid
-CNS infxn in 50%
-Lifelong immunity
-person-to-person, respiratory droplets
-winter and spring
-virus found in saliva, urine, pharynx, Stensen duct secretions
-mumps specific IgM Ab = active infection
-live attenuated virus as part of MMR
-resolves spontaneously w/in 1 week |
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Term
|
Definition
-ssRNA
-no DNAP
-picornavirus (naked)
-fecal-oral transmission; diarrhea
-IgM HAV test for diagnosis
-vaccine present
-Asymptomatic (usually), Acute, Alone (no carriers) |
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Term
|
Definition
-dsDNA (interrupted circular)
-DNAP in virion
-HBsAg in envelope
-hepadnavirus
-blood, sex, birth transmission
-chronic carrier state
-Diagnose: HBsAg
-HBsAb, IgM HBcAb
-vaccine present
-associated with HCC (HbX gene) |
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Term
|
Definition
-ssRNA
-no DNAP
-flavivirus
-blood, sexual transmission
-Diagnosis: HCV Ab
-no vaccine
-associated with HCC
-Chronic, Cirrhosis, Carcinoma, Carriers |
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Term
|
Definition
-(-)circular ssRNA
-need HBV infection also to replicate
-no DNAP
-HBsAg in envelope
-deltavirus
-blood, sexual transmission
-Diagnose: Ab to delta Ag
-no vaccine |
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Term
|
Definition
-ssRNA
-no DNAP
-Calcivirus (naked)
-fecal-oral transmission; diarrhea
-no lab diagnosis available
-no vaccine
-Enteric Expectant mothers, Epidemics
-can get fulminant hepatitis, esp if pregnant |
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