Viral Hepatitis Treatment & Management

Updated: Jun 12, 2017
  • Author: Naga Swetha Samji, MD; Chief Editor: BS Anand, MD  more...
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Approach Considerations

No specific emergency department (ED) treatment is indicated for viral hepatitis, other than supportive care that includes intravenous (IV) rehydration. A liver abscess calls for IV antibiotic therapy directed toward the most likely pathogens and consultation for possible surgical or percutaneous drainage.

Admit patients with hepatitis if they are showing any signs or symptoms suggestive of severe complications. Admit and evaluate for hepatic encephalopathy any patients with altered mental status, agitation, behavior or personality changes, or changes in their sleep-wake cycle. Other admission criteria that are suggestive of severe disease include a prothrombin time (PT) longer than 3 seconds, a bilirubin level greater than 30 mg/dL, and hypoglycemia.

Admit any patients with intractable vomiting, significant electrolyte or fluid disturbances, or significant comorbid illness; those who are immunocompromised; and those who are older than 50 years.

Certain patients may benefit from pharmacologic therapy. For chronic hepatitis B virus (HBV) and chronic hepatitis C virus (HCV) infections in particular, the goals of therapy are to reduce liver inflammation and fibrosis and to prevent progression to cirrhosis and its complications. Because the treatment regimens for hepatitis are being actively researched, medication recommendations, indications, and dosages are all subject to change. Consultations with a gastroenterologist, hepatologist, or general surgeon may be indicated.

Most patients with viral hepatitis can be monitored on an outpatient basis. Ensure that patients can maintain adequate hydration, and arrange close follow-up care with primary care physicians. Instruct patients to refrain from using any potential hepatotoxins (eg, ethanol or acetaminophen). Advise patients to avoid prolonged or vigorous physical exertion until their symptoms improve. Patients who are found subsequently to have HBV or HCV should be referred to a gastroenterologist or a hepatologist for further evaluation and treatment.


Acute Hepatitis A

Treatment for acute hepatitis caused by hepatitis A virus (HAV) is necessarily supportive in nature, because no antiviral therapy is available. Hospitalization is warranted for patients whose nausea and vomiting places them at risk for dehydration. Patients with acute liver failure require close monitoring to ensure they do not develop fulminant hepatic failure (FHF), which is defined as acute liver failure that is complicated by hepatic encephalopathy.


Acute Hepatitis B

As is the case for acute hepatitis A virus (HAV) infection, no well-established antiviral therapy is available for acute hepatitis B virus (HBV) infection. Supportive treatment recommendations are the same for acute hepatitis B as for acute hepatitis A. Lamivudine, adefovir dipivoxil, and other antiviral therapies appear to have a positive impact on the natural history of severe cases of acute HBV infection. A study by Schmilovitz-Weiss described a rapid clinical and biochemical response in 13 of 15 patients with severe acute hepatitis B who received lamivudine. [62]


Chronic Hepatitis B

Ideally, treatment of chronic hepatitis B would routinely achieve loss of hepatitis B surface antigen (HBsAg). Indeed, loss of HBsAg is associated with a decreased incidence of hepatocellular carcinoma (HCC) and a decreased incidence of liver-related death in patients with hepatitis B virus (HBV)-induced cirrhosis. [63] However, loss of HBsAg is only achieved in relatively small percentages of patients with chronic hepatitis B, that is, about 3-7% of those treated with pegylated interferon (PEG-IFN) [64, 65, 66] and 0-5% of those treated with oral nucleosides or nucleotides. [67]

At present, the key goal of antiviral treatment of HBV is the inhibition of viral replication. This is marked by the loss of hepatitis B e antigen (HBeAg) in patients with HBeAg-positive chronic hepatitis B and by the suppression of HBV DNA levels. Secondary aims are to reduce symptoms, if any, and to prevent or delay the progression of chronic hepatitis to cirrhosis or HCC.

Agents currently used to treat hepatitis B include PEG-IFN alfa-2a and the oral nucleoside or nucleotide analogues. Typically, PEG-IFN treatment is continued for 48 weeks for both HBeAg-positive and HBeAg-negative chronic hepatitis. Oral agents may be used for as short as 1-2 years; however, most HBeAg-positive chronic hepatitis patients and almost all HBeAg-negative chronic hepatitis patients require indefinite therapy with these agents. Withdrawal of oral nucleoside/nucleotide analogue therapy in these individuals usually results in virologic relapse.

More detailed information regarding management of chronic hepatitis B is beyond the scope of this emergency medicine topic. The reader is referred to the following references:

  • Pyrsopoulos NT, Reddy KR. Hepatitis B. Medscape Drugs & Diseases. Updated: May 26, 2017. Available at:
  • Terrault NA, Bzowej NH, Chang KM, Hwang JP, Jonas MM, Murad MH, et al. AASLD guidelines for treatment of chronic hepatitis B.  Hepatology. 2016 Jan. 63 (1):261-83. [4]
  • World Health Organization. Guidelines for the prevention, care and treatment of persons with chronic hepatitis B infection. 2015 Mar. [5]

Acute Hepatitis C

Acute hepatitis C virus (HCV) infection is detected infrequently. When it is identified, early interferon (IFN) therapy should be considered. In one study, 44 patients with acute hepatitis C were treated with IFN alfa-2b at 5 million U/day subcuteaneously (SC) for 4 weeks and then three times per week for another 20 weeks. [68] About 98% of patients developed a sustained virologic response (SVR), defined as an undetectable level of serum HCV RNA 6 months after completion of antiviral treatment. Most experts now equate achievement of an SVR with viral eradication or cure of HCV infection. [68, 69]


Chronic Hepatitis C


Antiviral therapy has several major goals, including the following, to:

  • Decrease viral replication or eradicate HCV
  • Prevent progression of disease
  • Reduce the prevalence of cirrhosis
  • Decrease the frequency of hepatocellular carcinoma (HCC) as a complication of cirrhosis
  • Ameliorate symptoms, such as fatigue and joint pain
  • Treat extrahepatic complications of HCV infection, such as cryoglobulinemia or glomerulonephritis

Interferon (IFN) has been the drug of choice for the treatment of hepatitis C for more than two decades. It is often used in combination with another drug, ribavirin. Successful IFN-based therapy, resulting in a sustained virologic response (SVR), can improve the natural history of chronic hepatitis C and may reduce the risk of HCC in patients with HCV-induced cirrhosis. [70, 71]

IFN-based therapy appears to reduce the rate of fibrosis progression in patients with HCV infection. [72] One report described regression of cirrhosis in some—but not all—patients who responded well to antiviral therapy. [73] In this study, 96 patients with biopsy-proven HCV-induced cirrhosis were treated with IFN-based therapy.

At a median interval of 17 months after the conclusion of antiviral therapy, patients underwent a second biopsy. [73]  Overall, 18 patients (19%) had a decrease in fibrosis score on follow-up biopsy, from stage 4 to less than stage 2, and SVR had been achieved in 17 of these 18 patients. With a median follow-up of 118 months, these patients were found to have decreased liver-related morbidity and mortality compared with patients who were not histologic responders.

In this study, not all patients who achieved SVR experienced histologic improvements. [73] Thus, it remains important to continue routine surveillance in patients with HCV cirrhosis—even if SVR is achieved through antiviral therapy—in order to rule out the development of HCC as a complication of cirrhosis.

Another report retrospectively assessed 920 patients with HCV-induced cirrhosis who underwent IFN therapy in the 1990s. The mean follow-up period was 96 months (range, 6-167 months). Achievement of SVR decreased patients’ risk for hepatic decompensation, HCC, and liver-related mortality. [71]

When considering treatment of HCV infection, both the clinician and the patient must be clear about the goals of therapy. As an example, in the patient with advanced fibrosis or cirrhosis, the goal of treatment is virologic cure in the hope of preventing progressive liver disease.

Unfortunately, SVR cannot be achieved in everyone. Achievement of SVR, although always desirable, is not always necessary to obtain a desired clinical result. Indeed, partial suppression of HCV through antiviral therapy may be all that is needed to stabilize renal function in a patient with HCV-related glomerulonephritis or to prevent the progression of malignancy in a patient with HCV-related non-Hodgkin lymphoma.

Pharmacologic agents

IFNs are a class of naturally occurring compounds that have both antiviral and immunomodulatory effects. They remain the backbone of antiviral strategies used against HCV infection. Agents currently approved by the FDA for the treatment of HCV infection include the following:

  • IFN alfa-2b
  • IFN alfa-2a
  • Ribavirin, which is used in combination with IFN

The addition of a large, inert polyethylene glycol (PEG) molecule to a therapeutic molecule (eg, IFN) can delay the clearance of the therapeutic molecule from the bloodstream. Long-acting PEG-IFN alfa-2b and PEG-IFN alfa-2a are currently the most commonly used medications for hepatitis C therapy in the United States.

Other interferons under study include IFN beta, IFN gamma, and natural interferon. Future medications may target the enzymes responsible for HCV replication. Drugs that have activity against viral helicases, proteases, and polymerases are currently under study, as are ribozymes and antisense oligonucleotides.

Factors predictive of an SVR to treatment with PEG-IFN in combination with ribavirin include the following:

  • Genotype 2 or 3 status
  • Baseline HCV RNA level below 800,000 IU/mL or less than 2 million copies/mL
  • Compliance with treatment
  • Absence of cirrhosis

However, patients with well-compensated cirrhosis have a reasonable likelihood of achieving viral eradication and should be offered IFN therapy, provided no significant contraindication (eg, severe thrombocytopenia) is present. Ideally, HCV eradication in the cirrhotic patient may prevent or forestall the development of progressive hepatic fibrosis and liver decompensation. Patients treated with IFN may also have a decreased risk of HCC.

If a patient ultimately requires liver transplantation for the treatment of complications of cirrhosis, previous eradication of HCV obviates any concerns about potentially severe recurrent hepatitis C after transplantation.


Not all patients with chronic hepatitis C are appropriate candidates for therapy with IFN and ribavirin. First, the drugs have well-known adverse effects, which lead to discontinuance in approximately 15% of patients. IFN can induce fatigue, joint pain, emotional irritability, depression, and alopecia. Patients with underlying psychiatric disorders must be carefully screened before they receive a drug that can worsen underlying depression or schizophrenia or that can even induce suicidal ideation.

IFN can also induce the development of thyroid disease or exacerbate an underlying immune-mediated disease (eg, psoriasis or sarcoidosis).

It has long been recognized that adherence to prescribed doses of PEG-IFN and ribavirin will maximize a patient’s ability to achieve an SVR. Missed doses due to lack of patient compliance or to physician-ordered dose reductions (eg, on account of the new onset of anemia or cytopenias) will increase the chance for treatment failure.

Patients invariably need close clinical and laboratory follow-up during treatment. Treatment with PEG-IFN can induce neutropenia. In some patients with IFN-induced neutropenia, granulocyte colony-stimulating factor (G-SCF) must be added to the regimen in order to support a falling white blood cell (WBC) count.

Treatment with PEG-IFN can also induce thrombocytopenia. It was once assumed that most patients (typically cirrhotic) with baseline platelet counts lower then 70,000/µL would be unable to tolerate treatment because of the induction of severe thrombocytopenia. Eltrombopag received FDA approval in November 2008 for the treatment of thrombocytopenia in cases of idiopathic thrombocytopenic purpura (ITP).

Eltrombopag was studied in patients with HCV-induced cirrhosis and platelet counts lower than 70,000/µL. [74] Treatment with eltrombopag 75 mg orally once daily successfully improved platelet counts in 95% of the patients studied, permitting a majority to undergo IFN treatment. However, eltrombopag use has been associated with both venous thromboembolism and drug-induced liver injury. In the United States, the medication is only available through an FDA-mandated restricted-distribution program.

Ribavirin commonly produces rash and hemolytic anemia. Some patients with ribavirin-induced anemia need combination therapy with erythropoietin in order to support a falling hematocrit. Some clinicians believe patients should undergo baseline cardiac stress testing, given the potential for patients to develop severe anemia.

Both IFN and ribavirin have been associated with a low risk of inducing retinopathy. Clinicians may wish to consider having patients undergo pretreatment and posttreatment ophthalmologic examinations.

The presence of insulin resistance may reduce the chance of achieving viral eradication with PEG-IFN and ribavirin. [69] Excellent control of diabetes is recommended before patients embark on IFN-based therapy.

In spite of all of the potential concerns related to combination therapy with PEG-IFN and ribavirin, the vast majority of patients are able to tolerate their recommended 24-week (for genotypes 2 and 3) or 48-week (for genotypes 1 and 4) treatment course.

Treatment of special populations

Chronic renal failure

HCV infection is documented in 10-20% of patients receiving chronic hemodialysis. Anti-HCV therapy is often appropriate for such patients. Attempts to eradicate HCV should be made before renal transplantation is carried out. Indeed, the hepatic histologic abnormalities attributed to HCV infection may worsen dramatically after posttransplant immunosuppressant therapy is started.

Reduced doses of PEG-IFN are typically used. Ribavirin should be avoided in all patients with renal insufficiency and in patients receiving hemodialysis because of the increased risk of severe hemolytic anemia.

HIV-HCV coinfection

Approximately 25% of Americans infected with human immunodeficiency virus (HIV) are also coinfected with HCV (10% of HIV-infected people are coinfected with HBV), and 75% of HIV-infected persons who inject drugs have HCV coinfection. [75] Therefore, HIV testing should be routine in patients with diagnosed with HCV infection.

HIV-infected individuals appear to have an impaired immune response to HCV infection. This translates into more rapid progression of hepatic fibrosis and higher rates of liver-related death in coinfected patients than in those with only HCV infection. [7, 75] Indeed, HCV-induced cirrhosis is a major cause of death in the HIV-infected population in the United States. [18, 76]

Accordingly, physicians are now more aggressive than they once were with respect to diagnosing and treating HCV infection in their HIV-infected patients. It also appears that suppression of HCV by means of IFN therapy may improve a patient’s ability to tolerate antiretroviral therapy (ART). Drug-induced hepatotoxicity is common in patients treated with ART.

Treatment with PEG-IFN and ribavirin is usually offered to patients with a CD4 cell count higher than 200/µL. CD-4 cell counts lower than 200/µL—and certainly those lower than 100/µL—are associated with a poor response to therapy.

In general, HIV-infected patients tolerate treatment well. However, significant neutropenia, thrombocytopenia, and anemia may develop. A few case reports describe mitochondrial toxicity and lactic acidosis when IFN and ribavirin are used in combination with dideoxyinosine, zidovudine, stavudine, and efavirenz. Pancreatitis has been described in patients receiving IFN and dideoxyinosine.

Since the introduction of IFN therapy, patients with HIV-HCV coinfection have generally had a diminished rate of hepatitis C SVR in comparison with patients without HIV infection. However, in an early study of coinfected patients who received PEG-IFN alfa-2a 180 µg subcuteaneously (SC) once weekly and ribavirin 800 mg/day orally, patients with genotype 1 had a 29% SVR rate, and those with genotype 2 or 3 had a 62% SVR rate. [77]

There are multiple reports of liver transplantation being successfully performed to treat decompensated HCV-induced cirrhosis in coinfected patients. Potential candidates for transplantation include patients who have achieved a negative HIV viral load through ART.

Overall, however, 2-year posttransplant survival rates are lower in patients coinfected with HIV/HCV than in patients infected with HCV alone. [78] At present, only a small percentage of the more than 100 transplantation programs in the United States perform liver transplantation in HIV-infected patients.

Newer therapeutic agents

The development of direct-acting antiviral drugs (DAAs) has significantly improved treatment options for patients infected with hepatitis C. These newer agents, which are taken orally for 8-12 weeks, are becoming standard of care for patients with chronic hepatitis C because they have been shown to attain sustained virologic response rates of 90% and greater. [9]

Newer, all-oral, direct-acting antiviral agents [9] :

  • Simeprevir and sofosbuvir – approved in 2013. Used in combination with PEG-INF and ribavirin, or as an all-oral combination regimen
  • Ledipasvir/sofosbuvir (Harvoni) – approved in 2014
  • Ombitasvir, paritaprevir, and ritonavir tabliets; dasabuvir tablets (Viekira Pak) – approved in 2014
  • Elbasvir and grazoprevir (Zepatier) – licensed in 2016

Further reading

Detailed information on management and treatment of chronic hepatitis C is beyond the scope of this emergency medicine topic. Further guidance is available from the following references:

  • AASLD/IDSA HCV Guidance Panel. Hepatitis C guidance: AASLD-IDSA recommendations for testing, managing, and treating adults infected with hepatitis C virus (updated April 12, 2017).  Hepatology. 2015 Sep. 62 (3):932-54. [7]
  • Dhawan VK. Hepatitis C.  Medscape Drugs & Diseases. Updated: March 28, 2016. Available at:

Treatment of Hepatitis D and E

Treatment of patients coinfected with hepatitis B virus (HBV) and hepatitis delta virus (HDV) has not been well studied. The onl effective treatment for HBV/HDV coinfection is pegylated interferon (PEG-IFN) [4, 5] ; antiviral nucleos(t)ide analogues have limited or no effect on HDV replication. [5]  However, multiple small studies have demonstrated that patients with HBV-HDV coinfection are less responsive to IFN therapy than patients with HBV infection alone. [5] Treatment with PEG-IFN alfa-2b produced HDV RNA negativity in only 17-19% of patients. [79, 80] Lamivudine appears to be ineffective against HBV-HDV coinfection. [81, 82]

Treatment of patients infected with hepatitis E virus (HEV) infection is supportive in nature.



Hepatitis A

Improved sanitation, strict personal hygiene, and hand washing all may help prevent transmission of hepatitis A virus (HAV). The virus is inactivated by household bleach or by heating to 85°C (185°F) for 1 minute. In addition, travelers to endemic areas should not drink untreated water or ingest raw seafood or shellfish. Fruits and vegetables should not be eaten unless they are cooked or can be peeled.


In 1995, the US Food and Drug Administration (FDA) approved the first vaccine for HAV. Beginning in 1996, the Centers for Disease Control and Prevention (CDC) recommended vaccination against HAV for the following individuals:

  • People traveling to regions where HAV is endemic
  • Men who have sex with men
  • Users of illicit drugs

Beginning in 1999, the CDC recommended vaccination for children living in 17 states with consistently elevated rates of HAV infection. Since 2006, the CDC has recommended vaccination for all children at age 1 year as well as encouraged “catchup” vaccination programs for unvaccinated children. [83]

Active immunization with HAV vaccine is also recommended for the following individuals:

  • Persons with an occupational risk of infection (eg, persons working with HAV-infected primates)
  • Patients who may receive clotting factor concentrates
  • “Susceptible persons with chronic liver disease” [83]
  • “Susceptible persons who are either awaiting or have received liver transplants” [83]

The third recommendation stemmed from the observation that patients with chronic liver disease, although not at increased risk for exposure to HAV, were at increased risk for fulminant hepatic failure (FHF) if they were infected with the virus. [84] Notably, there are data to suggest that workers exposed to raw sewage do not have a higher prevalence of antibodies to HAV than a comparator population. [83]

The inactivated HAV vaccines Havrix and Vaqta are administered as 1-mL (0.5-mL in children) intramuscular (IM) injections given more than 1 month before anticipated travel. This approach results in a better-than-90% likelihood of stimulating production of immunoglobulin G (IgG) antibody to HAV (anti-HAV), with resulting immunity against HAV infection.

A booster dose of the vaccine is recommended 6 months after the initial vaccination. Whether HAV vaccine administration should be mandated in children (as HBV vaccination is) remains unclear.

An alternative vaccine, containing inactivated HAV and recombinant hepatitis B virus (HBV) vaccines, is Twinrix. This product is immunogenic against both HAV and HBV. The FDA has approved its use in adults. Typical administration involves three injections of 1 mL given IM on a 0-, 1-, and 6-month schedule. Alternatively, a four-dose schedule can be used, with Twinrix administered on days 0, 7, and 21-30, followed by a booster dose at month 12. [85]

Immune globulin

Passive postexposure immunization with hepatitis A immune globulin (HAIG) is an alternative to active immunization with HAV vaccine. [86] Its effectiveness is highest when it is given within 48 hours of exposure, but it may be helpful when given as far as 2 weeks into the incubation period.

Postexposure prophylaxis with HAIG is appropriate for household and intimate contacts of patients with HAV. It is also recommended for contacts at daycare centers and institutions. The typical dosing of HAIG is 0.02 mL/kg IM as a single dose. Postexposure prophylaxis is not recommended for the casual contacts of patients, such as classmates or coworkers.

For travelers who anticipate spending less than 3 months in an HAV-endemic region, the dose is 0.02 mL/kg IM. Travelers who are planning to spend more than 3 months in a region where HAV is endemic should receive 0.06 mL/kg IM every 4-6 months.

Hepatitis B

The primary strategies for prevention of hepatitis B are to reduce transmission of the disease and to improve health outcomes for individuals who are already infected with hepatitis B. [9]


Plasma-derived and recombinant HBV vaccines use hepatitis B surface antigen (HBsAg) to stimulate the production of anti-HBs in noninfected individuals. The vaccines are highly effective, with a greater than 95% rate of seroconversion. Vaccine administration is recommended for all infants as part of the usual immunization schedule, as well as for adults at high risk of infection (eg, those receiving dialysis and healthcare workers). Recommendations for hepatitis B vaccination are available from the CDC [87]  and the World Health Organization (WHO). [5]

The recommended vaccination schedule for infants consists of an initial vaccination at the time of birth (ie, before hospital discharge), a repeat vaccination at 1-2 months, and another repeat vaccination at 6-18 months. The recommended vaccination schedule for adults consists of an initial vaccination, a repeat vaccination at 1 month, and another repeat vaccination at 6 months. If Twinrix (the combined HAV-HBV vaccine) is used, it is given according to the schedule previously described for hepatitis A.

Because of the nonresponse rate, many recommend that healthcare workers undergo postvaccination testing to confirm response within 1-2 months of receiving the vaccine. The duration of immunity conferred by the vaccine is not clearly known. Some clinicians recommend that a booster be given at 5-10 years.

Vaccination of children is an effective means of preventing HBV infection and its complications. For example, although HBV infection is endemic in Taiwan, the institution of universal vaccination for neonates in Taiwan in 1984 reduced the HBsAg carrier rate in children from 9.8% to 0.7% over a period of 15 years. [88] There was also a resulting drop in the incidence of HCC in children from 0.54 to 0.20 per 100,000. Follow-up studies are needed to determine whether the overall incidence of HCC in Taiwan decreases as these children enter adulthood.

Vaccination is also recommended for older children and adolescents who were not vaccinated as infants; adults with diabetes; and household contacts and intimate partners of individuals with chronic hepatitis B infection.

Prevention of perinatal transmission

Mother-to-child transmission of hepatitis B most commonly occurs at birth, when the neonate is exposed to maternal blood and bodily fluids, or during early childhood. [5]  Because acquiring hepatitis B infection early in life poses a high risk of developing chronic infection, strategies to reduce mother-to-child transmission are of vital importance. For such strategies to be effective, it is important that all pregnant women undergo screening for HBV infection so that they and their newborns may be treated appropriately. [9]  Administering hepatitis B vaccination within 12 hours of birth to neonates born to mothers with hepatitis B infection is 80-95% effective in preventing transmission of hepatitis B infection. [4, 5] In some cases, depending upon the mother’s viral load and human immunodeficiency virus (HIV) status, there may be indications to treat the mother with antiviral agents during pregnancy. [4, 5]

Immune globulin

Hepatitis B immune globulin (HBIG) is derived from plasma. It provides passive immunization for individuals who describe recent exposure to a patient infected with HBV. HBIG is also administered after liver transplantation to persons infected with HBV in order to prevent HBV-induced damage to the liver allograft.

Recommendations for postexposure prophylaxis for contacts of patients positive for HBsAg are as follows:

  • Perinatal exposure – HBIG plus HBV vaccine at the time of birth (90% effective)
  • Sexual contact with an acutely infected patient – HBIG plus HBV vaccine
  • Sexual contact with a chronic carrier – HBV vaccine
  • Household contact with an acutely infected patient – None
  • Household contact with an acutely infected person resulting in known exposure – HBIG, with or without HBV vaccine
  • Infant (age <12 months) primarily cared for by an acutely infected patient – HBIG, with or without HBV vaccine
  • Inadvertent percutaneous or permucosal exposure – HBIG, with or without HBV vaccine

Improving health outcomes for those with HBV infection

Improving health outcomes for persons with HBV requires early identification so that they can be made aware of their infection and can receive appropriate treatment and education on risk reduction. To that end, it is recommended that individuals who are at high risk for HBV infection be offered appropriate testing and connection with care. [9]

Hepatitis C

No vaccine against HCV is available, and immune globulin is not proven to prevent transmission. In fact, immune globulin administration has been associated with HCV. At present, the major means of preventing transmission of HCV is to prevent infected blood, organs, and semen from entering the donor pools. The CDC also recommends meticulous infection control practices within healthcare settings. [9]  Additionally, individuals who are at risk for HCV infection should be offered appropriate testing, treatment, and health education to reduce the risk of transmission. 

Improving health outcomes for those with HCV infection

With newer treatments that can provide sustained viral response (SVR), health outcomes for individuals with HCV can be improved by linking them to care and providing appropriate treatment. [9]  Because many individuals may not be aware that they are infected with HCV, providers should offer testing to individuals at risk to include those with a history of injection drug use, persons infected with HIV, and healthcare workers with bloodborne exposures to HCV. [46]  Additionally, the CDC recommends one-time screening for all individuals born between 1945 and 1965 because this population is at high risk of HCV infection, and they are at highest risk for morbidity and mortality as a result of HCV infection. [9]

Prevention of perinatal transmission

The finding of HCV among increasing numbers of women of childbearing age raises the concern that more infants will be at risk for HCV as a result of mother-to-child transmission. [46] Providers should screen pregnant women to assess their risks for HCV and offer testing if they are deemed to be at risk; additionally, infants born to infected mothers should be tested for HCV. Women of childbearing age, pregnant women, and infants who test positive for HCV should be referred for care, monitoring, and treatment. [46]

Hepatitis D and E

Because HDV can infect patients only when HBV is present, transmission of hepatitis D can be decreased by effectively immunizing patients against HBV. Unfortunately, at this time, no means of preventing HDV superinfection in patients with chronic HBV is known.

No vaccine exists for the prevention of HEV infection. Administration of immune globulin does not prevent the development of clinical disease.