HAV structural basics
- Picronaviridae family, genus enterovirus
- Non-enveloped icosahedral capsid
- < 7 kb ss RNA (+)
- Single serotype
- Human reservoir
- Family Caliciviridae, genus Hepevirus
- Non-enveloped icosahedral capsid
- 7.5 kb ss RNA (+)
- Single serotype
- Possible swine or other animal reservoir
- Mostly prevalent in developing countries
- 1 in 5 fatality rate in pregnant F (3rd trimester: don’t see this with any of the other hep viruses)
What is the pathogenesis of HAV?
- Fecal-oral route, and replication in GI tract
- Early childhood disease is most common and often asymptomatic (kids) -> common source of community outbreaks
- 33% of annual US acute hepatitis cases, and 1/3rd of US population has had this
- Weeks of symptoms in adults with viral shedding before symptoms
1. Anorexia, malaise, fever, headache, perhaps jaundice
- Vaccination has reduced this by >90% (no longer 33% of annual acute cases): still see community outbreaks
What groups are at-risk for HAV?
- Household or sexual contacts
- Travelers to endemic areas
- Inhabitants of American Indian reservations
- During outbreaks:
2. Day care center workers: kids are a prominent target, but usually asymptomatic
3. Gay men
4. IV drug users: not typically contracted parenterally, but possible during an outbreak
How is HAV diagnosed and controlled?
- DIAGNOSIS: presumptive based on appearance and history
1. Detection of anti-HAV IgM
- PREVENTION: hand-washing for 10-20 seconds
1. Passive immunization w/gamma globulin (IgG)
2. Inactivated vaccine (Havrix): >2-y/o
3. Combo vaccine for HAV and HBV (Twinrix): 18 years or older
4. Vaccine or IgG recommended for travelers to endemic areas (vaccine for kids too)
- CASE: 28, lives in Cooper Young. 2-yo child. Confirmed presence of anti-HAV IgM. Risk factors: child in daycare, bars and restaurants, denies IVDU (making C and B less likely)
How did the HAV vaccine affect the Memphis outbreak?
- Predicted decline rate shown here: actual decline rate MUCH faster
- Vaccine had a tremendous affect on the clearance of the infection in the Memphis outbreak
- Good candidate for eradication: 1 serotype, HUMANS ARE ONLY RESERVOIR
1. Why not eradicate: self-resolves, incidence dropping dramatically after intro of vaccine, bigger worries in underdeveloped countries
Hep B structural basics
- Hepadnavirus: enveloped (aka, Dane particle)
- Partially dsDNA genome, 3200 bp: one strand shorter than the other
- 5 major proteins:
1. DNA polymerase (reverse transcriptase)
2. HBsAg: surface antigen, attachment protein mostly found in 20 nm particles and filaments
3. HBcAg: core antigen, capsid protein
4. HBeAg: derivative of HBcAg, important serologic marker
5. X antigen: influences gene expression
How does HBV create a "smoke screen?"
- Phospholipid blebs from infected cell floating around in blood that act as “smoke screen,” and distract immune system from surface antigen
- So many that first vaccine was blood-derived, and made up of these things purified from blood (people get weird about these blood-derived vaccines, so not used anymore)
- NOTE: serology is very important -> can’t detect core antigen in lab, but can detect e antigen
Describe HBV replication. What is unique about it?
- Genome length RNA used as template for reverse transcription
- DNA can integrate into genome (probably not linked to cancer risk), but mostly maintained extra-chromosomally in chronic infections
- Completion of dsDNA during uncoating: now looks like a “plasmid” -> mRNA and (+) strand copy from host RNA polymerase that is pre-genomic RNA (virus has its own reverse transcriptase to now make strands of DNA: one is unfinished)
1. Opposite of HIV in this way: DNA virus with RNA intermediate rather than RNA virus with DNA intermediate -> both require reverse transcriptase
2. This is why some HIV drugs can be used to tx HBV too, opening up a lot of antivirals for use
- NOTE: don’t necessarily need to know all of this, but know that the REVERSE TRANSCRIPTASE is important due to this RNA intermediate
What is the epi of HBV?
- Endemic to China and sub-Saharan Africa
1. Early infection: 10-20% population rate
- Late infection in US and Europe: <1% population rate
How is HBV transmitted?
- Virus is present in blood, semen, and vaginal secretions
- Transmission by parenteral route:
1. Injection drug use
2. Sexual intercourse
3. Perinatal at delivery
What are the phases of Hep B infection? How do these correlate to serum markers?
- If not resolved in 6 months, considered chronic
- Chronic patients often remain asymptomatic until cirrhosis or HCC appears
- Scale for symptoms larger than for HAV: more insidious infection
1. Viral shedding before symptoms (like HAV)
- Graph shows acute resolved
What are the diagnostic HBV markers?
- HBsAg: ID of carriers or acutely infected persons
1. Anti-HBs: ID of persons who have had HBV infection or received vaccine
- HBeAg: ID of those at INC risk of transmission (active marker) -> means capsid protein being made
1. Anti-HBe: ID of HBsAg carriers with low risk of transmission -> immune response starting to contain the infection
- Anti-HBc: ID of persons with past infection
1. IgM Anti-HBc: ID of acute or recent infection
2. Can detect anti-HBc, but not HBcAg
- High-risk carrier: HBeAg + anti-HBc
- Encodes delta antigen, its core (capsid) protein
- Enveloped, circular ssRNA genome of 1.7 kb, and must incorporate HBsAg to infect hepatocytes (source of attachment to proteins)
- Uses host RNA polymerase
- Good anti-HBs = resolution of infection
- CO-INFECTION: primary acute infection can be more severe, but no increased risk of chronicity
- SUPER-INFECTION: HDV will trigger spike in ALT, and levels will never drop down to baseline -> makes chronic infection worse
Structural basics of HCV
- First described in 1989: Flaviviridae Hepacivirus
- Enveloped icosahedral capsid with 9.4 kb ss RNA (+) genome
- 6 major genotypes, divided into subtypes: 1a, 1b, 2a, 2b are worldwide -> 1a and 1b most comm in US
1. Pts also contain quasi-species (antigenic variants from E2 region)
- Translates one big polyprotein first:
1. 2 envelope proteins: E1 and E2 -> E2 is a prime source for antigenic variation (30 AA’s that can change, allowing virus to escape immune response)
2. PROTEASE: major target for antivirals
- CASE: contaminated blood transfusion -> Hep C (pre-1992 = tip-off that Hep C because prior to screening for it)
What is the epi of HCV? Risk factors?
- Highest incidence world-wide in Asia, Middle East, and North Africa
- New case incidence in US has dropped A LOT since the 80s -> general population rate is 2%, but estimates of 16-41% in prison population
- RISK FACTORS: born b/t 1945-65 (80% of chronic cases)
1. Illicit (injection) drug use
2. Perinatal infection at birth
What is the pathogenesis of HCV?
- Acute infections milder than HBV: resolved, acute infection lasts 2-3 wks
- CHRONIC pts have multiple bouts: immune response, but not sufficient to keep everything in check -> this may be where the antigenic variants come into play (some could also be reinfection with other serotypes): spikes in ALT every 2 years or so
- Emergence of quasi-species
What is the role of the immune response in HCV?
- Hepatitis viruses are not cytolytic
- Immune destruction (cytotoxic T cells) of infected hepatocytes leads to liver disease
What are the viral causes of chronic hepatitis?
- 40% of cases are due to HCV and 20% HBV (5% contain HDV)
1. Immunize HBV and HCV chronic pts against HAV and discourage alcohol use
2. HBV/HCV liver disease is leading reason for liver transplants
3. Despite HBV vaccine, HBV-related cancers and deaths have doubled in the past decade
- Remainder of unknown origin
- Devo depends on age of infection:
1. < 1 yo: 90% chronicity rate -> endemic in certain areas of the world due to EARLY infection
2. 1-5 yo: 30% rate
3. > 5 yo: 2% rate
- 1 in 4 chronic patients will die of liver disease, mostly in 6th decade
- 3 stages:
1. Immune tolerance phase
2. Immune clearance phase: eAg (+) to eAb (+)
3. Residual phase
- NOTE THE ATTACHED FIGURE
- 85% of untreated infections will lead to chronic infection
- 1 in 25 people will devo cancer from this infection: this is a very significant thing
- NOTE THE ATTACHED FIGURE
How can you diagnose viral hepatitis?
- Acute forms of ET- and PT-hepatitis can be similar
- Source of infection and ELISA:
1. HBV: HBsAg, anti-HBc IgM; HBeAg, HBe antibody, HBV DNA
2. HCV: anti-HCV antibodies, HCV RNA
- Determine HCV genotype
How is HBV controlled?
- Screen blood supplies for HBsAg, HBc antibodies, HBV DNA
- Vaccines: yeast expressed HBsAg
1. Twinrix: HAV + HBV -> NOT labeled for anyone under age 18
2. Childhood immunization recommended
3. NOTE: plasma-derived HBsAg not used anymore
- HBIg for exposed individuals: newborns, and can be used prophylactically for travelers
What is the goal of HBV antivirals? General criteria?
- GOAL: to reduce risk of progressive chronic disease, transmission, and complications (cirrhosis, HCC)
- General criteria:
1. >2000 units/mL HBV DNA
2. >2x upper normal limit of serum ALT
How is HCV controlled? Antivirals?
- Screen blood supplies for antibodies to core antigen, HCV RNA
- No vaccine in US yet, no passive immunization
- “HCV is relatively easily treated and can be eliminated in almost all patients," so the goal of therapy is to eliminate HCV RNA
1. Treatment varies by genotype
- ANTIVIRALS: Entecavir and Tenofovir target reverse transcriptase
1. Entecavir: directly INH polymerase molecule itself vs. Tenofovir, which is a chain terminator -> work 2 different ways to exploit reverse transcriptase
Why does it take so long to devo HCC and cirrhosis in chronic HBV and HCV pts?
Because liver can regenerate itself at first; virus is not what is destroying the liver, but the immune response
What are the 3 clinical presentations of viral hepatitis?
- Fulminant hepatic failure: really bad acute hep
- Chronic -> 20-30 yrs before cirrhosis with the following long-term complications:
2. Liver failure: ascites, jaundice, confusion, encephalopathy, bleeding
3. Hepatocellular carcinoma
- NOTE: while Hep C can cause acute hep, it most often presents as chronic
What is the "clinical picture" of acute hepatitis?
- Usually caused by HAV and HBV in the US
1. Acute HEV (zoonosis; India) and HCV (IVDU) are rare in clinical practice in US
- LABS: high AST/ALT: 1000- 5000 IU/L
1. High bilirubin, prothrombin time (INR)
a. Liver makes all clotting factors except Factor VIII (made in endothelium)
2. Very high INR may indicate progression to fulminant failure (serious disease)
a. Acute Hep and INR >4, worried about fulminant liver failure
- NOTE: jaundice with high AST/ALT, think Hep
What is the Ddx for acute hepatitis?
- Autoimmune disease
- Ischemic hepatitis (in ICU setting): shock -> no blood flow -> necrosis -> high ALT/AST + jaundice
- Alcohol/drug induced, Tylenol OD (esp. + alcohol)
- Wilson Disease
-NOTE: AST of 1,000 and jaundice = acute viral hepatitis, ischemic liver, or drug toxicity
1. High IgM + high ALT = acute viral hepatitis
HAV: dx and viral shedding
- DX: IgM anti-HAV in acute/early convalescent; generally present 5-10d before onset of symptoms, and no longer detectable in most pts 6 mos later
1. IgG anti-HAV appears early, and remains detectable for lifetime, conferring lifelong protection
2. Commercial tests available for IgM, and total (IgM + IgG)
- SHEDDING: HAV replicates in liver, is excreted in bile, and is shed in stool
1. Peak infectivity (concentration in stool highest) in 2-wk period before onset of jaundice or elevation of liver enzymes, and declines after jaundice appears
2. Children and infants can shed HAV in stool longer than adults, up to several mos after onset
- HAV RNA can be detected in blood/stool of most pts in acute phase with PCR -> not generally used for diagnostic purposes
What are the 3 possible clinical outcomes of acute hepatitis?
- Spontaneous RESOLUTION: most comm outcome
1. Hep A/E can rarely have relapsing course with cholestasis (95% of Hep B resolves)
- Progression to CHRONIC INFECTION: HCV 80%, HBV 5%
1. Chronicity NOT seen in Hep A or Hep E
- FULMINANT liver failure (<1%): rare, but most life-threatening complication
1. HBV, less commonly in HAV
2. HEV: 20% of pregnant F in 3rd trimester
- NOTE: tell people to rest if they come in with A and E -> most of them get better
How can you diagnose acute Hep A, E, B?
- Key test is IgM antibody:
1. Hep A: IgM anti-HAV antibody
2. Hep E: IgM anti-HEV antibody
3. Acute HBV: IgM anti-HB core antibody
4. No acute Ab (IgM) for Hep C.: have to rely on good history
- IgG antibody indicates previous infection, either resolved or active chronic infection
- Viral RNA or DNA: indicates active infection, but does not differentiate b/w acute v. chronic infection
What is fulminant hepatic failure?
- Most serious complication of acute viral hepatitis
- Usually caused by HBV, HEV (preggo), rarely HAV
- PRESENTATION: acute hep with altered mental status -> hepatic encephalopathy (cerebral edema)
- High mortality: brain herniation, infection
- TX: urgent liver transplantation is the only cure
1. Altered mental status: call transplant center b/c pt. will have brain damage in 2-3 days
- This is the most important cx of hepatitis
What are the clinical presentations of chronic viral hepatitis?
- CHRONIC HEP: persistent Infection > 6 months
1. Almost all cases HCV (MCC) and HBV
1. Asymptomatic: found incidentally
2. Mild elevations in AST, ALT (< 5x normal); some patients can have normal LFT
3. Liver failure or cancer in late stages: this is when many pts. present b/c they may be asymptomatic for a long time
4. Extra-hepatic manifestations
- Normal ALT: 3-5 (lab says 45 is normal, but it is really not -> above 40 out of normal range according to WebMD)
What factors can accelerate fibrosis in chronic HBV/HCV?
- Accelerated = progression to cirrhosis in 15-20y:
1. Obesity: fatty liver
3. Post-liver transplant
4. Alcohol consumption: def want <2 cups/d
- Tx algorithm recommend consideration of liver biopsy for monitoring -> useful in making tx decisions and assessing degree of damage
- IMAGE: progression of hepatic histology from normal through fibrosis to cirrhosis; also present on the far right, one can see cords of neoplastic hepatocytes in a patient with HCC
What US ethnic pop is disproportionately affected by HBV?
- Foreign-born Asian Americans and their kids
- Growing population in the US (8% of pop): 68.9% foreign-born -> many of the countries of origin are regions of high/intermediate HBV endemicity
- 2.7x more likely to devo hepatocellular carcinoma (HCC) and 2.4x more likely to die from HCC than their white counterparts
What are the CDC recommendations for routine HBV testing?
- Chronic Hep B: no symptoms, so SCREEN for it in high-risk pts
- While health care workers are not specifically mentioned by the CDC as a pop at risk, those with reasonably-anticipated occupational exposures to infectious body fluids should also be vaccinated
- NOTE: stars next to HIV+ ppl, and those who are immunosuppressed (b/c reactivation possible)
1. Other high-risk pops are those at high-risk for all parenterally transmitted infections
Describe the HBV serological markers.
- (+) HBsAg: active infection (acute or chronic)
- Anti-HBs Ab: resolved infection or prior exposure, vaccination
- Anti-HB core Ab: definite exposure (not seen in vaccination -> IgM: acute HBV, Ig G resolved or chronic infection)
- HBe Ag and high DNA: active replication & high risk of transmission
What is the course of chronic HBV infection (4 phases)?
- 4 PHASES:
1. Immune tolerant: little hepatic inflam despite high serum level of HBV DNA, & (+) HBeAg
2. Immune clearance: hepatic inflam, DEC in serum HBV DNA, and ultimate loss of HBeAg; known as the HBeAg+ phase
3. Inactive carrier: low level HBV DNA, (-) HBeAg, and normal LFT's
4. Reactivation: high levels of HBV DNA in serum + hepatic inflam; many pts HBeAg (-), but some may revert to HBeAg (+); HBeAg- CHB (some never enter this phase)
- 50+ pt w/chronic HBV probably in inactive carrier state, whereas teen who comes in w/chronic HBV more likely to be in immune tolerant stage
- Not all pts go through all 4 phases:
1. Immune clearance phase most common in young Asian pts with perinatally acquired HBV infection
2. Immune clearance phase and reactivation phases may be prolonged with recurrent exacerbations of hepatitis and fluctuations in serum HBV DNA levels
When do you treat chronic HBV?
- When there is evidence of liver injury (high ALT )
- Liver biopsy showing advanced fibrosis
- STARS: associated with liver injury
What are the goals of HBV treatment?
- Chronic HBV cannot be cured in most: only 5-10% of pts can be cured = loss of HBsAg
- TX GOAL: DEC HBV replication; lower DNA
1. Minimize liver injury, prevent progression
- SECONDARY GOAL: DEC risk of HCC
What drugs are used to treat HBV?
- ENTECAVIR, TENOFOVIR: oral, and require long duration (indefinite), well-tolerated
1. Once/day pills, but $900/mo. lifelong tx
2. Directly target HBV replication (reverse transcriptase), so viral resistance could be an issue
- PEG INTERFERON alfa-2: SQ injection, finite duration, several side effects, best for genotype A
1. CONTRAindicated in cirrhosis
2. Modulates immune system
- NOT a complete virus, unlike A, B, or E: needs HBsAg to infect -> seen only in pts with HBV
- Super-infection: infection in pt w/chronic HBV
- Co-infection: infection along with HBV
- NOTE: pt with Hep B is doing fine, goes to Europe, comes back with acute Hep, think of Delta
What are the implications of HDV in HBV? Dx?
- INC the severity of HBV, and risk of cirrhosis
- DX: delta Ab or RNA
1. All pts should have HBsAg
What is the most common chronic viral hep in the US?
- >50% of HCV not diagnosed
What is the liver-related burden of chronic HCV in the US?
- Rise in HCV-related cirrhosis and HCC due to manifestation of disease in aging baby boomers
1. Prevalence of HCV infection in HCC pts from 20-90%, and risk of HCC in HCV-related cirrhosis from 1-7%
- HCC rates projected to peak in 2019
What are the HCV screening guidelines for at-risk pts?
- All screening guidelines recommend screening BABY BOOMER population (1945-65 birth cohort)
- Guidelines also incl. screening recommendations based on risk factors and other medical conditions
How does HCV affect mortality?
- INC risk of:
1. Non-liver related cancers
2. Strokes, circulatory diseases
3. Heart attacks
5. Kidney failure: nephritis, nephrotic syndromes, nephrosis
- INC risk of dying from extra-hepatic disease
How does HCV progress (flow chart)?
- Image shows the natural history of hepatitis C virus (HCV) infection from acute infection to devo of disease complications
What are the recommended lab tests for chronic HCV?
- Screening test = Hep C Ab via EIA
- Positive results are to confirmed using PCR for HCV RNA
How do you interpret HCV assay test results?
- Hep C can be cured, but Ab persists
- HCV Ab's with no HCV RNA could indicate either resolution of prior infection or acute HCV infection in setting of intermittent or low-level viremia.
- HCV RNA w/no HCV antibody could indicate either early acute HCV infection or chronic HCV infection in those with immunosuppression or false-positive HCV RNA tests
- HCV Ab's and HCV RNA implies either acute OR chronic infection, depending on the clinical setting
- No HCV antibodies and no HCV RNA indicated the absence of HCV infection
What are the HCV genotypes? Where are they prevalent?
- Prevalence depends on geographic location
- Most common type in US is T1, then T2 and T3
1. 75% of HCV in US T1, but as high as 90-95% in African-Americans in the US
What is the HCV life cycle (image)?
What is the tx for HCV?
- HCV is curable w/tx (unlike HBV or HIV), but ACCESS TO CARE is the biggest issue
- Multiple direct-acting agents target HCV replication and prevent resistance: 90-95% cured
1. Shorter duration 3- 6 months
2. Less side effects
3. Less Drug Interaction
- SOFOBSUVIR: no major side effects, and no food interaction
1. Limited drug interaction
- NOTE: choose drug based on cost, and what insurance will accept
What is Harvoni?
- Indicated for tx of chronic HCV, genotype 1 infection in adults
- First and only once-daily, single-tablet regmin with Ledipasvir (NS5A INH), and Sofosbuvir (NS5B INH)
- Interferon (IFN)-free, ribavirin (RBV)-free regimen
How does HCV tx vary by genotype?
- G1: Sofosbuvir or Ledispavir 12-24 wks; cure 95%
- G2: Sofosbuvir + Ribavirin 12 wks; cure 90-95%
- G3: Sofosbuvir + Ribavirin 24 wk; cure 80%
- NOTE: two-stage HCV vaccine targeting cell entry and key HCV proteins undergoing phase 2 trials and likely to available in 2016
1. Vaccine could be used for prophylaxis, or as treatment along with other agents
How is HCV different than HBV and HIV, making it curable?
- Hep C does not have archived resistance
- High replication and mut rate of HCV (due to error-prone RNA poly that lacks proofreading func)
- Unlike HBV and HIV, which have been shown to archive resistance (as stable, covalently closed circular DNA persisting in nucleus or as integration in host genome, respectively), there is no known mechanism for HCV to be archived in the host
Why is curing HCV important?
- Achieving sustained virologic response assoc with DEC:
1. HCC incidence
2. Liver-related or transplantation mortality
3. All-cause mortality
What are the potential barriers to curing HCV?
- POOR ADHERENCE is the result of factors spanning several dimensions and issues related to:
1. Socioeconomic conditions
2. Therapy admin
3. Healthcare system
- Patient adherence is critical to good pt outcomes
For which hep viruses are there vaccines?
- HAV: 2-dose high-efficacy vaccine widely available
- HBV: 3-dose, high-efficacy vaccine widely available
- HEV: vaccine is not available in US, but 2 vaxes available outside US
1. Recombinant capsid antigen rHEV
2. HEV 239: China
- HCV: vaccines contain envelope protein E1, E2, and are designed to induce CD4/CD8 response against non-structural protein of HCV -> clinical trials results expected in 2016
1. This vax could be used for prophylaxis and tx, unlike HAV, HBV vaxes
- NOTE: every liver disease pt. (regardless of the etiology) should be vaccinated against A and B
1. Can check Ab response, and give vaccine again: 5% of pts don't respond to HBV vax
How is HIV related to viral hepatitis?
- All HIV pts should be tested for HBV and HCV
- Natural history of HBV and HCV worse in HIV+ pts, and chance of spontaneous clearance is low
1. HCV now leading cause of death in HIV pts
- Treatment of co-infected pts: many anti-HIV drugs have anti-HBV activity
1. In a co infected (HIV+HBV) pt, DOC to tx HIV is TENOFOVIR (Truvada*, Atripla*)
- No HCV drugs have anti-HIV activity
How are HBV and HCV related to HCC?
- 1 of most common cancers worldwide, and INC incidence in the US
- HCV causes HCC only with cirrhosis (0.8% of the time w/o cirrhosis), but HBV can cause HCC even without cirrhosis
- Cancer screening by imaging recommended in some HBV and HCV patients (US, CT)
- Transplant list: easiest to get is AB, hardest is O
What are the indications for liver transplantation in viral hepatitis?
1. Cirrhosis with liver failure (HCV and HBV, HDV): most patients (2/3rds)
2. Hepatocellular carcinoma (HCV and HBV, HDV): 1/3rd of pts
3. Fulminant hep failure (more in HBV>HEV>HAV): about 2%
What are the extra-hepatic manifestations in viral hepatitis?
- Membranoproliferative glomerulonephritis
- Porphyria cutanea tarda
- Mixed cryoglobulinemia (vasculitis,neuropathy)
- Lymphoproliferative conditions
- Extra hepatic manifestations may correlate with Viral RNA/DNA levels
- Treatment is indicated and can be successful if viral replication can be reduced
What other viral infections can cause acute hepatitis?
- Cytomegalovirus (CMV)
- Epstein barr (EBV): mononucleosis
- CLINICAL COURSE: ALT, AST range 300-600 IU/L
1. Self-limited in most patients
2. Serious infection in immunocompromised patients
What is this?
- CMV hepatitis: fever diarrhea (involvement of GI tract)
- DX: CMV DNA or tissue biopsy –> liver or GI tract
- TX: Ganciclovir
1. Prophylaxis is recommended w/Valcyclovir for organ transplant recipients
2. Long-term tx needed for some people
34-y/o admitted w/jaundice. Received 3 cycles of chemo for NHL. LFT's prior to chemo were normal. Now, ALT 600, AST 500, bilirubin 12, INR 1.9.
What is the clinical syndrome?
What are the possibilities?
- Possibilities: CMV or reactivation of latent HBV
- Differential: 1) drug-induced liver injury, 2) incidental acute infection w/A/B/E
- TREATMENT: specific antiviral RX is indicated for CMV and HBV
1. Always test for Hep B before chemo: treat before chemo if they have it
- NOTE: if this was a healthy 18-yo with same LFT’s and sore throat, what would you think? EBV (Mono)
What should all immunocompromised pts be tested for?
- HBV: natural history likely to be worse + chance of spontaneous clearance is low
- Acute presentation likely due to reactivation of “inactive infection”
- Prophylaxis for 6-12 months (Lamivudine or Entecavir) indicated in all pts on chemo if HBsAg+
Who needs to be tested for HCV, HBV?
- Baby boomers for Hep C
- Asians for Hep B
- Know the tables for HBV and HVB diagnosis