3 eserc. - lucidi

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285VIRAI HEPATITIS

Acute viÉl hepatitis is a systemic irilection a.ffecting the liver predoo-inantly. Alnost all cases of acute viIal hepatitis are caused by otre offrve vilal ageDts: hepatitis A virus (HAy), hepatitis B virus (HB\,),hepatitis C vins (IICV), the lIBv-associated delra agent or hepatitis

D virus QID\), and hepatitis E vi s (HED. Other transtusion-trans-mitted agents, e.g., "hepatitis G" vi s imd'TI" virus, have beenidentified but do not cause hepatitis. All these humalt hepatitis yiruses

arc RNA vi.uses, except for hepatitis B, which is a DNA virus. Al-ihough these agents caa be distinglished by the molecular and an-tigenic properties, all types of yiral hepatitis Foduce cliùicaÌly similarillnesses. These range Irom asymptomatic and inapparent to fulminantand fatal acute idections comrnon to all types, on the one hand,and from subclinical persistent hfections to rapidty Fogrcssivechrcnic liver disease with cirhosis and even hepatocellular calcinoma,common to the bloodbome t ?es (IIBV, HCV, atrd HDV), on theother.

Vltl)L()GY AilD m0[0GY I H.patili5 A Hepatitis A virus is a ronenvel-oped 27-nm, heat-, acid-, and ether-resistait RNA virus in the hepa-tovirus genus of tle picomavins family (Fig. 285-1). Its yirioD con-

tains foul capsid polr?eptides, designated \?l to VP4, which arecleaved postfanslationally from the polyprotein product of a 7500-nucleotide genome. Inaclivation of viral activjry can be achjeved byboiling for 1 min, by contact with formaldehyde and chlorine, or byultaviolet idadiation. Despite trucleotide sequsnce variatio[ of up to2070 among isolates ol HAV, all stains of this virus are itrlmùnolog-icaly indistinguishable and belong to one serotype. Hepatitis A hasan incubation period of approximately 4 weeks. Its replication is lim-ited to the liver, but the virus is present iII the liver, bile, Etools, alldblood dudng the late inorbation period and acute Feicteric phase olillress. Despiie p€rsislence of virus in Lhe liver, viml shedding in feces,vi-remia, and infectivity diminish rapidly once jaundice becomes ap-pareol. HAV can be cultivared reproducibly in viEo.

Antibodies to }lAV (anti-HAV) can be detect€d dudog acùte illnesswhen serum aminotransfetase activity is elevated and fecal HAV shed-

ding is still occuIrilÌg. This early antibody rcsponse is predominantlyof the IgM class and pe$ists for seveml months, Érely for 6 to 12months. DùinE convalescence, howevet, anti-HAV of the IgG classtrecomes the predominant antibody (Fig. 285-2). Therefore, the diag-nosis of hepatitis A is made duriag acute illness by demomfatiBg anti-HAV of the IgM class. Afle! acute illdess, a i-HAV of the Igc class,emains detectable indefrnitely, and patienls with serum anti-HAV areiiùnuoe to rcinfection. Neutratizing antibody activity parallels lhe ap-pea.rance of anti-HAV, and the IgG anti-HAV Fesent in imoune glob-ulin accounls for the protection ir affords against IIAV infectioo.

JaundicÉ Elnr-r [------l

Anti-HAV

cinomq and rcly on a replicative strategy unique amongbur q?ical of retroviruse§. I stead of DNA replication d

-0 4 I 12 18

Weeks atter exposurc

IIGURI 285-2 Scheme of tgp,crl clinical and labontory featurcs of

fl€patitis B Hepatitis B vims is a DNA virus with apact gedomic sEucturo; despite its small, circulaa,HBV DNA codes for four sets of viral Foducts wilh atiparticle structuie. HBV achieves its genomic economy byan efficieat strategy of encoding Foteins ftom fourS, C, P, alld X (Fig. 285-3), as detailed below. ODceùniqùe among viruses, HBV is now recogDized as one ofanirnal viruses, hepadnaviruses (hepatoùopic

DNAclassifed as hepadnavirus type 1 . Similar yiruses iofectof woodchuck, ground and uee squhrels, and Pekiù ducks,the most carefirlly characierized. Like HBV, all have ùetinctive thrce morphologic forms, have coùnterparts toand nùcleocapsid virus àntigens of IiBV, replicate iDthei{ extGhepatic sites, contain their orÀn endogenoùs DNAhave Éartially double-shanded aDd pattiallyare associated with acute and chrcoic hepatitis and

tl6l]ll 285-1 letr. Ele.lrcn dicroqraph of 2r-nm hepatils A virus panicle! purjfied from stoot of a patient lYithacule hepatitjs A virus infection and aqqrcgated bq hepatitis A anùbodu. Rig,tt. Bectron microqraph of concentratedserufi from a patient tyith hepatìls B infeclioa, demonsirating lhe 4z-nm $rions, tubular foms, and spherjral 22-nmparlicles oi hepatith B surface antigen. 132,000x. (Hepatitir D rcsembìes 42-nm vìfions of hepatitis B but is smaller,35 t0 3i nm, hepatilis E resembìes hepatilis A virus but is slightlu laEer, 32 to:t4 nm; hepatitis C ùas not beenrsualted defìnitivelU.)

18ZZ

DNA template, hepadnaviflses rcly on leverse traDscriptioby the DNA polymerase) of mirus-srand DNA from aRNA intermediate. Then plus-strand DNA is hanscdb€dnus-sfand DNA template by the DNA-depeodeDr DNAand converted in the hepatoc).te nucleus to a covalently

DNA, which sefles as . template for messenger RNA andRNA. Vilal proteins are taNlated by the messengerproteins and ge[ome are packaged into virions andhepaloc,,te. AldEugh IIBV is difficult to cultivate in vitroventional sense from clinical material, several cell linestransfected witi HBV DNA. such transfected cellsrcplication of the intact virus and its compoDent prcteiDs.

ylML FRlTElllS AND PARITCIES Ofthe three particulate formsble 285-l), the most numerous are the 22-nm particles,

as §pherical or longthese are antigenicallyfrom the outer surface orofHBV and arc thought toviral e[velope prctein.

rum by a factor of 100 or 1000parcd with the spheres aad

large, 42-nm. double-shelledticles, which Epresent theB virion (Fig. 285-l) . Theteilr eipressed on the outervtion afld on the smallerbular shuctuaes is refeEed to a§

surface antigen (HBsAg). Thetion of IlBsAg aod virusbtood may rcach 500 pgtnl- adparticles per milliliter,envelope Fotein, HBsAg, is drc

the S gene of IIBV,



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'285-4Srheme of Ìgpical clìnical and laboratoru features of aclle viral hep-

100

le or detectable at low levels (see'Laboratory Fearures,' below)285-51. During early chronic i{BV infecùon, HBV DNA can be

both in seùm and in hepatocyte nuclei, wherc it is preslnt inÌ episomal form. This replicatire Jrage of HBV infection is the

maximal infectivity and liver injury; HBeAg is a qualitativeand HBV DNA a quantitative ma*eÌ of this replicative phase,

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with current or recenl acuE hepadtis B. including ùose in ùewindow, have IgM anti-HBc in their serum. In patients who

from hepatitis B in the temote past as well as thoseHBV iDfection, a !ÌIBc is predominantly of the IgG

IDfrequently, in no more thaa 1 to 57o of patients wirh acute

levels of HBsAg are too low to be detected; in such

ùe presence of IgM a[ti-HBc estabìishes the diaglosis of acuteB. When isolated anti-Imc occuts h the rare patient with

hepatitis B whose HBsAg level is below the sensitivity thrcsh-eontemporary immunoassays (a low-level carrier), the anti-ÌIBc

IgG class. Geoerally, in pe$ons who have recovercd ftomB, anti-HBs and anti-ÌIBc persist indefinitely.

temporal association bètween the appearance of anti-HBs andof HBV infection as well as ihe observation that persons

in serum are protected against rcinfection with IIBVùat anti-HBs is the protectù)e antibod), Therclorc, strategies

of HBV inJection are based on Foviding susceptible

with circulating anti-HBs (see belov). Occasionally, in 10 topatients with chonic hepatitis B, ìow-level, low-affinity anti-be detected. This antibody is directed against a subtype de-different from Ìàat represented by the pÀrient's IIBsAg; irsis thought to reflect the stimulation of a rcìated clone of

cells, but it has no clinical rclevance and does notclearance of hepatitis B.

other readily detectable serologic marker of HBV infection,appea$ concùrrendy with or shtrfily after HBsAg. 1ts ap-

e coincides temporally with high levels of virus replication andihe presenge- of circulatirg intact vidons and detectabte HBV

Pre-Sl and prc-S2 proteins aÌe also expressed dudng periodsbut assays for the§e gene products are not routinely

In selflimited HBV iafections, HBeAg-becomes undetect-after peak elevations iII afiinotansfeÉse activity, beforc

of HBsAg, and gnti-HBe then becomes detectable,with a period of relatively lower infectivity (Fig. 285-4).harkers of IIBV replica'tion appear Ealsiently during acutetesting for such markers is of little clinical utility in typical

acùte IIBV iDJection. In contast, marke$ of HBV replicationvaluable information in patients \eith prohacted infections.

ftom the pattem §?ical of acute HBV infections, inHBV infection, HBsAg rcmains detectable beyond 6 months,

is primadly of the IgG class, and anti-HBs is either unde-

during which all three forms of HBV circulate, including intact vftiotrs.Over time, the replicative phase of chrcnic IIBV infection gives wayto a relatively nonreplicatiye praJe. This occurs at a Éte of apprcxi-mxely l\Vo per year and is accompanied by setoconve$ion ftomI{BeAg:positive to antiHBe-positive. In most cases, this seioconver-sion coincides wiù a aansient, aéute hepatitis-like elevation in ami-no[ansferase activiry, believed to rcflect cell-mediated immune cleat-ance of virus-infected hepatorytes. In the nomeplicative phase ofcfuonic'inlection. \yhen HBV DNA is demonstrable in hepatocyle nu-clei, it teDds to be integated into the host genome. In this phase, onlyspherìcal and tubular lolms of PBy, not intact yiriorr, circulate, atrdliver injùry tends to subside. Most such patie s would be character-ized as inactil)e HBV calar'?ru. In teality, the design tions replicatfuexrd nonreplicative ue only relativei even in the so-called nomepli-cative phase, HBV replication can be detected with highly sensitiveamplncation probes such as the polltnemse chain rcactio! eCR).Still, the distinctions are pathophysiplogically and clinicaly meaning-ful. Occasionally, noEeplicative HBV infection convefis back to rcp-licative infection, Such sponta{eous rcactivarions arc accompanied byreexpression of lIBeAg and HBV DNA, and sometimes of IgM aoti-HBc. as well as by exacerbarions of liver injury.

MAECUUR y;RA 15 Variation occurs throughout the HBV genome, aIlal

clhical isolates of HBV diat do not exp.ess srpical vial poteins havebeen attributed to mutations in individual or even multiple gene 1o-

cations. For example, variants have Leet described that lack nucleo-capsid proteins, envelope prcteins, or boih. Two categdries of HBVhave attractèd the most attention. One of these was identified initiallyin Mediterranean coùntries among patients with an unusual serclogic-clinical profile. They have severc chrcnic HBV infection and detect-able llBV DNA but with arti-HBe iNtead of IIBeAg. These patientswere found to be infected widr an HBV mutaflt that contained analteration in the precore rcgion rcndering the virus incapable of en-coding HBeAg. Although several potertial mutation sites exist_ifl thepre-C region, the regioriof the C gine necessary for the express'ion ofIlBeAg (see '.vfuology and Etiology," above), ihe most commonlyencountered in such patients is a single base substitutioq ftom G to

A, which occurs in the second to last codon of the pre-C gene atnìrcleotide 1896. This substitution results in the rcplacement of theTGG tryptoph;n codon by a stop coalon (TÀG), which plevent5 thetmnslation ol HBeAg. Another mutation, in the core prcmoter region,prcvents transcriptiofl of the coding region for IIBeAg and yields ar

AntiHBe

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0123456 12 24 36 4A 60 120

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flGURf 285-5 Scheme of tupical labordtoru features of chroni. viral hepatitis B.

iBeÀg ard HBv DNA can be oeteded rn seun during lhe replEonve phase ol ehrcnitinfedìon, whkh is assorìated with i fectir/itu and liver injuru. SeroconveEìon from the

replicative phase la the nonrcplicdlve phose occu6 at a Éte ot approrjmatelu l0 1o

15% per Uear aid is henìded bg an acute hepallis-likÉ elevaton of ALT actjvit!;du nq the nonreplicaiive phase, intectivitq and Iìver iijury are Iìrnìled.



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