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IntroductionThose unfamiliar with the hmay wonder why this topic attention in an HIV/AIDS pubHIV/HCV co-infection. The mmate of the HCV infection raindividuals is 14 percent—126,000 individuals based on 650,000 to 900,000 (Cohen, 1rate is much higher among injHCV is the most prevalent bloUnited States, where the numexceeds 4 million. ApproxHCV-positive individuals dinfection, 70 percent develop and 10 to 20 percent develop to 10,000 persons die from United States alone (CDC, 199There is no vaccination or cuis expensive, and only succepatients. Like HIV, HCV now ately among the poor and unnew infections occur througSexual transmission of HCassociated with a high numand sexual activity without a Neither HCV nor HIV/HCV intstood. Many people are un

Inglesby TV, Rai R, Astemborski J, Gruskin L, Nelson K,Vlahov D and Thomas DL (1999). A prospective communitybased evaluation of liver enzymes in individuals withhepatitis C after drug use. y 29(2):590-596. [Online]Koop, CE (1998). Hepatitis C: An epidemic for anyone. [Online]Lesens O, Seschenes M, Steben M, Belanger G, Tsoukas C(1999). Hepatitis C virus is related to progressive liverdisease in human immunodeficiency positive hemophiliacsand should be treated as an opportunistic infection.

179:1254-1258.

National Digestive Diseases Information Clearinghouse(NIDDK) (1999). Chronic hepatitis C: Current diseasemanagement. NIH Publication No. 99-4230. [On-line]National Institutes of Health (1997). Management ofhepatitis C. NIH Consensus Statement March 24-26, 1997.15(3):1-41 [On-line] odp.od.nih.gov/consensus/cons/105/105_statement.htm.Piroth L, Duong M, Quantio C, Abrahamowicz M,Michardiere R, Aho L, Grappin M, Buisson M, Waldner A,Portier H, Chavanet P (1998). Does hepatitis C co-infectionaccelerate clinical and immunological evolution of HIVinfected patients? 12:381-388.Poynard T, Marcellin P, Lee SS, Niederau C, Minuk GS, Ideo G,Bain V, Heathcote J, Zeuzem S, Trepo C, Albracht J (1998).Randomized trial of interferon alpha2b plus ribavirin for48 weeks or for 24 weeks versus interferon alpha2b plus

placebo for 48 weeks for treatment of chronic hepatitis Cvirus. 352(9138):1426-1432.

Hepatolog

www.hepatitis-central.com.

www.epidemic.org .

The

Journal of Infectious Diseaseswww.niddk.nih.gov/ health/digest/pubs/chrnhepc/chrnhepc.htm .

AIDS

Lancet

Schiff E, deMedina M, Kahn RS (1999). New perspectives inthe diagnosis of hepatitis C.19(s1):3-15. [On-line]Sherman A (1999). HCV on the threshold.

16(2):92-94. [On-line] .

Soriano V, Rodriguez-Rosado R, Garcia-Samaniego J (1999).Management of chronic hepatitis C in HIV-infected patients.

13:539-546.

Sulkowski MS (1999). Hepatitis C & HIV coinfection: Asleeping giant awakes. January1999. [On-line] .Sulkowski M (1998). HIV and hepatitis C virus co-infection.

November 1998. [On-line] hopkinsaids.edu/ publications/report/nov98_5.html.

Thomas DL, Vlahov D, Solomon L, Cohn S, Taylor E, GarfeinR, Nelson K (1995). Correlates of hepatitis C virus infectionamong injection drug users in Baltimore.

74:212-220.

Yoshida H, Shiratori Y, Moriyama M, Arakawa Y, Ide T, SataM, Inoue O, Yano M, Tanaka M, Fujiyama S., Nishiguchi S,Kuroki T, Imazeki F, Yokosuka O, Kinoyama S, Yamada G,Omata M (1999). Interferon therapy reduces the risk forhepatocellular carcinoma: national surveillance programof cirrhotic and non-cirrhotic patients with chronichepatitis C in Japan.131(3):174-181.

Seminars in Liver Disease

www.medscape.com/thieme/SLD/

1999/1901s/ 1901.02.schi-01.html .

Infections in

Medicine www.medscape.comAIDS

The Hopkins HIV Report

www.hopkins-aids.edu/

The Hopkins HIV Report

Medicine

(Baltimore)

Annals of Internal Medicine

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Please forward comments, letters andquestions to:Office of CommunicationsHIV/AIDS Bureau, HRSA5600 Fishers Lane, Room 7-46Rockville, MD 20857Phone: 301-443-6652Fax: 301-443-0791or by E-mail to: www.hrsa.gov/habHRSA Care ACTION

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Continued from Page 1 . . . HEPATITIS C

Natural History

Epidemiology

Acute InfectionChronic Infection MortalityOnly 30 to 40 percent of individuals newly infectedwith HCV exhibit symptoms of acute infection; thesesymptoms occur anywhere from 3 to 20 weeks after

exposure (Hoofnagle, 1997;CDC, 1998). They often aremild and intermittent andinclude fatigue, nausea,muscle and joint pain, poorappetite and right upperquadrant tenderness ordiscomfort (NIDDK, 1999).Twenty to 30 percent of thoseinfected may have jaundice,a condition typicallyassociated with liver disease(CDC,1998). Illness associated with acute hepatitis C,when it appears at all, lastsfrom 2 to 12 weeks.Fulminate hepatitis (severeand rapid progression ofliver disease) resulting fromHCV is rare (Hoofnagle,1997).

Other markers for hepatitis C appear earlier than theonset of symptoms. HCV RNA can be detected in theblood as early as 1 to 3 weeks after exposure. Levelsof the liver enzyme alanine aminotransferase (ALT)may begin to rise after several weeks—although evenamong the chronically infected, ALT levels are notalways elevated. Antibodies to the virus appearsomewhat later than HCV RNA in the blood: in 80percent of patients within 15 weeks of exposure; 90percent within 5 months; and 97 percent by 6months (CDC, 1998).Virtually all infected persons develop liver celldamage within an average of 50 days of infectionand chronic infection develops in up to 85 percent ofthose who contract the virus; for reasons not wellunderstood, the remaining individuals eradicate thevirus without treatment (NIH Consensus, 1997; CDC,1998). Infection may not be apparent for decades,but the virus is not dormant. Cirrhosis of the liverdevelops in 10 to 20 percent of HCV-infected individuals, usually slowly—over a period of 20 to 30 years.Liver cancer may develop in up to 5 percent ofindividuals infected with HCV (CDC, 1998).

In 1 to 2 percent of HCV-infected individuals, extrahepatic (non liver-related) complications may appear.These include cryoglobulinemia, membranoproliferative glomerulonephritis and porphyria cutaneatarda (CDC, 1999).The long asymptomatic period of HCV, inadequateHCV screening, and lack of access to health care forpopulations among whom incidence is highest arejust three of the issues that make estimating HCVprevalence extremely difficult.The largest HCV prevalence study estimated 3.9million HCV-positive individuals in 1994, of whom2.7 million were chronically infected. HCV was mostprevalent in the 30 to 49 - year-old age group. AmongBlacks the rate was 6 to 7 percent, and it was higheramong Black men (9 to 10 percent)—compared to 1.8percent in the population as a whole. As indicated bythe study’s authors, this estimate was conservativebecause it excluded populations among whomprevalence is known to be high; e.g., incarceratedand homeless individuals (Alter et al., 1999).HCV prevalence in the United States is increasing—incidence is greater than mortality—however,incidence has declined dramatically from anestimated average of 242,000 from 1985 through1990 (CDC, 1999). Today, incidence is estimated atbetween 35,000 and 40,000. This decline is largelydue to the virtual elimination of transmissionthrough tainted blood products. Transmissionamong injection drug users has also decreased, butmuch less significantly. Most new infections occur inindividuals ages 20 to 39 years. Incidence is similaramong White and Black Americans, and is slightlyhigher among Hispanics .Between 8,000 and 10,000 Americans die annuallyfrom hepatitis C. Without substantial improvementin treatment options, that number will increase overthe next decade: large numbers were infected withHCV 20 to 25 years ago and are approaching the stageof infection at which severe complications typicallybecome apparent.





Injection drug use (IDU) has factor for HCV in the United Sthe epidemic. Hepatitis borne—much more so than candidate for transmission thnated syringes.The prevalence of hepatitiextremely high—more than samples. This means that thinto contact with contamisignificant, and that there is a those who ever injected drugs—One of the startling facts abrapidity with which IDUs constudy of 1,356 IDUs in which pants were HCV positive, prevaThe 405 HIV positive participmore likely to be HCV positparticipants—93.4 percent coEven among participants who needles, prevalence was 82.9 91.9 percent in those who sharing behaviors (Thomas, 1potential importance of indirand back loading” (dividing syringe into another) (CoutinhAlthough documentation is may be associated with a cocaine use (CDC, 1998). Tdelicate nasal membranes intranasal drug use and sharnated with infected blood. If tthrough this method, it appearTainted blood products wesource of HCV infection, but trin this manner is now very rathe likelihood of acquiring Honly .001 percent per unit tran

Injection Drug Use

Other Drug UseTransfusions and Transpla

HCV producesapproximately10 trillionhepatitis virionsdaily(Sulkowski).The HIVreplication rateis slower —approximately10 billion virionsdaily.

HCV Infection Among 

Duration of

injection drug use

< 1 year 

1 year 

> 5 years 

> 10 years

2

TransmissionHepatitis C virus is a blood-borne disease, andtransmission can occur in a number of ways.
4

Continued from Page3.. .HEPATITIS C

Vertical TransmissionNosocomial TransmissionOccupational ExposureHousehold ContactTattooing and body-piercing

Testing for HCV Antibodiesin HIV-positive Patients

The rate of HCV transmission from an HCV-infectedmother to her newborn is about 5 to 6 percent.However, if the mother is co-infected with HIV, thevertical transmission rate jumps to between 14 and17 percent (CDC, 1998).Nosocomial transmission (infection of patientsthrough contaminated medical equipment) isuncommon in the United States, but has beenreported in chronic hemodialysis settings.It is possible for health care workers to acquire HCVthrough needle sticks, but the prevalence in healthcare workers is about the same as that in the generalpopulation. The range of “needle stick conversionrates” is 0 to 7 percent, depending on the risk factorsof the individual in whom the needle was originallyused (Sherman, 1999).Infection from household contact is probablyextremely uncommon. It has not been documentedin the United States, although studies in Japan andItaly have shown that it does occur (Herrine, 1999).There is no documentation of transmission duringtattooing or body-piercing in the United States,although it has apparently occurred elsewhere in theworld (Herrine, 1999).HCV can be diagnosed by detecting HCV antibodies inthe blood. Two tests are FDA-approved for detectionof HCV antibodies: the enzyme immuno assay,commonly referred to as EIA or ELISA; and therecombinant immuno blot assay (RIBA). Both detectHCV antibodies in 97 percent of infected patients.The advantages of the EIA are ease of use and low cost.Disadvantages are: false positives occur more oftenthan with the RIBA, the interval between infection anddetection may be as long as 3 to 6 months, and peoplewho are immuno-suppressed or immunocompromised may not have detectable antibodies toHCV. The RIBA is more complex and considerablymore expensive to administer but has higher specificity.

Because false positive, false negative, and indeterminate results occur, a second “confirmatory” assay isrequired to confirm a positive result, or a negativeresult in an individual thoughtto be positive. In some cases, athird may be required. Neitherthe EIA nor the RIBA indicateswhether HCV infection is acute(new), chronic (long term) orresolved (past infection).Tests to directly detect hepatitisC RNA in the blood (viral load)are commonly available inclinical practice but are not yetstandardized. The reversetranscript polymerase chainreaction (PCR) and branchedDNA assay (bDNA) both detectthe nucleic acid of the virus inthe blood, and are indicators of active infection. ThePCR test has high sensitivity and may be able to detecta very low level of virus in the blood as early as 1-2weeks after infection. However, it is technicallydifficult to administer and false results are a commonproblem.Until very recently, HCV diagnostic testing wasavailable only in a physician’s office or clinic. InJune, the FDA approved an “at-home” test kit forhepatitis C. Individuals provide a small bloodsample, which is sent to a laboratory for testing.Results are available in about 10 days.The EIA is especially prone to false negatives in HIVpositive patients, because they may not developdetectable levels of antibodies to the virus (Schiff,1999). One study reported that HCV was undetectedin 30 percent of HIV/HCV-positive patients, whereasfalse negatives for the general HCV population were inthe range of 0.5 to 10 percent (Collier et al., 1998;Dieterich, 1999). The RIBA may be more likely to beindeterminate in co-infected individuals (Dieterich,1999). In one study of patients known to have HCVviremia in the blood, 14.7 percent of RIBA results werenegative or indeterminate in the HIV-positive group,while only 4 percent were indeterminate in the HIVnegative group and none were negative. (Cribier,1995).For a more complete discussion of HCV testing, seeMorbidity and Mortality Weekly Report, CDC, Volume

HCV Testing



Assessment of Liver DamagAlfa InterferonHCV tests cannot assess lienzyme, alanine aminotranmeasured to determine if Elevated ALT indicates active lA single ALT reading will be levels have a tendency to flucto 70 percent of chronically either persistently or intermlevels. In the remaining 30 to are normal (CDC, 1998). In positive individuals, researchmore ALT evaluations over a Forty-two percent showed values, 15 percent persistently 43 percent had intermitte(Inglesby et al.,1999).Liver damage also may be asbiopsy. It is used in conjumeasurement of ALT levels to and activity of the disease, fibrosis in the liver. It is treatment to both assess the stto exclude other types of livetions.Alfa interferon monotherapy Treatment

HCV appearsto be moreefficientlytransmittedfrom malesto femalesthan fromfemales tomales.

Anyone who has evagoAnyone who has bepositive for hepatitiAnyone who receiveAnyone who receiveAnyone who ever reAnyone who has evChildren born to HSource: CDC

Who 
Interferon and Ribavirin

Side Effects

Initiating TreatmentImpact of HCV on HIV

The FDA recently approved the combination of alfainterferon with ribavirin for the treatment of HCV.

Originally used only incases where patients hadrelapsed or not responded at all to interferonmonotherapy, it is nowused as an initialtreatment as well. In onerecent study, a sustainedresponse was achievedin 43 percent of patientswho received the interferon/ribavirin combination for 48 weeks(Poynard, 1998). Inanother study, 38percent of patients whoreceived the combination demonstrated asustained response after48 weeks of therapy,compared to 13 percent

of those who had received interferon alone (NIHConsensus, 1997). A number of other studies showsimilar results. Ribavirin alone has not proveneffect-ive in treating the hepatitis C virus.Interferon and ribavirin are not without sideeffects. The major side effect associated withribavirin is hemolytic anemia. The majority ofpatients treated with interferon suffer flu-likesymptoms, which can include fever, chills, malaise,headache, myalgia and tachycardia, but these tendto diminish with continued treatment. Later sideeffects include fatigue, alopecia, bone marrowsuppression, apathy, cognitive changes, irritability,and depression. Ten to 40 percent of patients undertreatment require a reduction in interferon dosagedue to side effects, and 5 to 10 percent must discontinue treatment. Severe side effects include autoimmune disease, depression with suicidal risk, seizuredisorder, acute cardiac and renal failure,retinopathy, interstatial pulmonary fibrosis,hearing impairment, and sepsis effects. They occurin less than 2 percent of patients. Infrequently, aparadoxical worsening of liver disease with therapy occurs (NIH Consensus, 1997). Therefore, ALTlevels must be monitored frequently.

It is not always clear who to treat for HCV and whento initiate treatment. The course of the disease isvariable and usually slow. CDC guidelines and theNIH Consensus Conference indicate that thosepatients most likely to progress to cirrhosis shouldbe treated—those with persistently elevated ALTlevels, detectable HCV RNA in the blood, and liverbiopsy indicating portal or bridging fibrosis, ormoderate degrees of inflammation and necrosis(CDC, 1998; NIH, 1997). New research confirms thattreatment with interferon before serious symptomsdevelop reduces the incidence of liver cancer(Yoshida et al., 1999).The magnitude of HIV/HCV co-infection in theUnited States is not yet clearly defined. The mostconservative estimates are that 14 percent of thoseliving with HIV disease are HCV positive (Cohen,1999). It is known that co-infection is much higheramong some sectors of the HIV-positive population,particularly IDUs. For example, in Baltimore—where IDU is the HIV transmission route in overone-half of all new AIDS cases—50 percent ofpatients in one HIV clinic are co-infected with HCV(Sulkowski, 1999). In drug treatment facilitiesacross the country, the HCV infection rate in HIVpositive patients often exceeds 50 percent.Even if HCV had been more prevalent and betterunderstood at the beginning of the AIDS epidemic,the immediacy and severity of HIV/AIDS would haveprecluded much concern over a disease in whichsevere symptoms may not develop for 20 years ormore. Today, however, because HCV prevalence hasincreased substantially and HIV-positive individuals are living longer, clinicians are increasinglyrequired to treat both diseases.Research on the effect of HCV/HIV co-infection onHIV has produced mixed results. Some studies havefound no significant impact on the progression ofHIV (Haydon, 1998; Wright, 1994; Botarelli, 1993;Quan, 1993 in Dieterich). Others have shown thatco-infected patients have increased risk for liverdisease, faster progression of HIV disease, greaterfrequency of hospital admissions, and greatermortality (Lesens, 1998; Piroth, 1998).

HIV/HCV Co-infection

70 to 80 percentof individualsliving with HCVin the UnitedStates areinfected withHCV genotype 1,which is lessresponsive tointerferon thanother strains.

There are indications that rferon in co-infected individuCD4 counts but, in any casepositive/HIV-negative patients While the combination of inhas shown improved sustaithose with hepatitis C infectirigorously tested among patients.Higher incidence of cirrhosis co-infected patients, and devperiod than in those patients HCV alone. One study of IDUcirrhosis was twice as high also living with HIV disease—to 15.3 in HCV-positive/H(Piroth, 1998). In a 1995 scirrhosis among HCV patienyears after infection, regarwere co-infected with HIV. incidence diverged, with 25 positive patients developing only 6.5 percent of HCVpatients (Sanchez-Qujano,19a more recent report, mean pin co-infected patients was 623.2 years in HCV-positive/(Soto, 1997 in Dieterich, 1999HCV replication appears to bimmune system has been (Beld, 1998; Thomas, 1995)inverse correlation between HCV RNA levels, where CD4 (Beld, 1998). Another study viremia in co-infected patienHCV-positive/HIV-negative pacorrelation between CD4 c(Cribier, 1995). All of these sprior to the introductioantiretroviral therapy (HAARSome research has shown thaeffect on the hepatitis C vinconclusive. One relativeImpact of HIV on HCV 

Continued from Page 5 . . . HEPATITIS C

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ReferencesAlter MJ, Kruszon-Moran D, Naina

F, Moyer LA, Kaslow RA, Margolis of hepatitis C virus infection in thThe New England Journal of MedicBall S (1997). Coverage from the 3on Antimocrobial Agents and ChOctober 1, 1997. [On-line] Beld M, Penning M, Lukashov Pakker N, van den Hoek A, Goudsboth HIV and HIV-induced immunreplication among HCV seroconv512.Centers for Disease Control Hepatitis C: Frequently Asked QueCenters for Disease Control and Hepatitis C Fact Sheet [On-li

.

Centers for Disease Control Recommendations for the PreHepatitis C Virus (HCV) Infection Disease. October 16, 1998: 1-39.Centers for Disease Control Hepatitis C Fact Sheet. October 5, 1

www.m

diseases/ hepatitis/c/fact.htm

Morbidity and Mortality 

httphttphttphttphttphttphttphttphttphttphttp

Genotypic and phenotypic tests for measuring resistance to antiretroviral therapy maybecome essential tools for making HIVtreatment decisions. These new tests areimportant since response to therapy iscompromised by drug-resistant strains of HIV.However, concerns abound regarding theiraccuracy, implications, and costs from$250 to over $1,000.Resistance to antiviral drugs is caused bymutations in the virus. HIV mutationsdevelop quickly because of its rapid rate ofreplication. Accumulation of drug-resistantmutations is accelerated by sub-optimaltreatment, non-adherence, and poor drugabsorption.A blood sample is analyzed to determine thepresence of mutant virions known to beassociated with resistance to certain drugs.Genotypic tests are appropriate only forpatients on antiretroviral therapy whoseviral load is above 1,000 copies. The test willnot detect resistant virus when it comprisesless than 20 percent of the total virus in theblood. Moreover, it is known that genotypingis not sensitive to at least one HIV mutation.Genotypic testing is less complex and lessexpensive (from $250 to $500 per test) thanphenotypic testing and results are usuallyavailable within a few weeks.An HIV sample from the patient is subjected todrug combinations in the laboratory todetermine the dosage levels required forinhibiting viral replication. When highdosage levels are required, resistance isthought to have developed. Like genotypetesting, phenotyping will not detect the

presence of mutant virions if they compriseless than 20 percent of the total HIV in theblood. Phenotyping is more complex andexpensive than genotype testing from $800to over $1,000. However, because it tests theresponsiveness of virus from the patient todrugs used in treatment, phenotypic testingoffers a unique advantage over other methods.Phenotype and genotype tests currently arenot FDA-licensed for clinical use and maytherefore not be covered by insurance. Littleresearch has been conducted on the value ofusing resistance testing in improving treatment outcomes. However, although manyquestions remain regarding genotype andphenotype testing, their use in HIV care islikely to expand.Additional information may be found in thefollowing resources:

New Mexico AIDS InfoNet, HIV ResistanceTesting Fact Sheet (#414) <http://www.aidsinfonet.org/414-resistance.html>Gay Men's Health Crisis' Treatment Issues,June 1998 <http://www.gmhc.org/aidslib/ti/ti.html>Project Inform: Descriptions of Genotypicand Phenotypic Resistance Tests<http://www. projinf.org/fs/GenoPheno.html>Johns Hopkins AIDS Service's Hopkins HIVReport, June 1999 <http://hopkinsaids.edu/publications/report/may99_1.html>

—

—

Genotypic testingPhenotypic testing

HIV Resistance Testing on Horizon
8 

What is it?IncubationperiodHow is itspread?

SymptomsTreatment ofchronicdiseaseVaccineWho is atrisk?Prevention

HAV is a virusthat causesinflammation ofthe liver. It doesnot lead tochronic disease.15 to 50 days.Average 30days.Transmitted byfecal/oral route,through closeperson to personcontact oringestion ofcontaminatedfood and water.

May have nosymptoms. Admay have lighstools, dark urfatigue, fever ajaundice.Not applicableTwo doses ofvaccine to any2 years of age older.Anyone withhousehold orsexual contactwith an infecteperson. Living an area with Houtbreak.Travelers todevelopingcountries. Menwho have sex men. Injectiondrug users.Immune globuor vaccination.Wash hands agoing to thebathroom. Clesurfacescontaminated feces, such aschanging table

HBV is a virusthat causesinflammation ofthe liver. The viruscan cause livercell damage,leading tocirrhosis andcancer.4 to 25 weeks.Average 8 to 12weeks.Contact withinfected blood,seminal fluid, andvaginalsecretions. Sexualcontact.Contaminatedinjection drugneedles, razors,unsafetattoo/bodypiercing and othersharpinstruments.Infected mother tonewborn. Humanbite.

HCV is a virus thatcauses inflammationof the liver. Thisinfection can lead tocirrhosis and cancer.6 weeks to 6 months.Average 6 to 7 weeks.Contaminated injectiondrug needles.Transfusion andtransplant recipientsbefore July 1992.Received treatmentwith blood productbefore 1987. Longterm kidney dialysis.Multiple sex partnersand/or sex with HCVinfected person.Infected mother tonewborn.Contaminatedtattoo/body piercingequipment, house-holdobjects (i.e. razors), orany other sharpinstruments.

HDV is a virusthat causesinflammationof the liver. Itonly infectsthose personswith HBV.4 to 26weeks.Infects peoplewho alreadyhave HBV.Contact withinfectedblood,contaminatedinjection drugneedles.Sexualcontact withHDV-infectedperson.

HEV is avirus thatcausesinflammationof the liver. Itis rare in theU.S. There isno chronicstate.2 to 9 weeks.Average 40days.Transmittedthrough thefeces of aninfectedperson. Veryuncommon inthe UnitedStates.

Hepatitis is defined as an inflammation of the liver.Non-viral forms of hepatitis can be caused by toxic agents (drugs or chemicals), alcohol, orautoimmune processes that cause a deterioration of the liver cells. Prolonged, repeated exposure tocertain medications may also create hepatitis-like reactions. Other viruses can also cause hepatitis as asecondary effect. Additional forms of non-viral hepatitis include certain disorders such as Wilson'sdisease, hemochromatosis, and galactosemia as well as nonviral infections including syphilis andbacterial sepsis.

Hepatitis A

(HAV)

Hepatitis 

(HAV)

Hepatitis B

(HBV)

Hepatitis C

(HCV)

Hepatitis D

(HDV)

Hepatitis E

(HEV)

HEPATITIS 101 

Source: Home Access Health Corpora