Hepatitis in Pregnancy 

Updated: Aug 12, 2021
Author: Sarah Cassity, MD; Chief Editor: Christine Isaacs, MD 


Viral hepatitis remains the leading cause of liver inflammation and liver cancer requiring transplantation. Viral hepatitis can affect members of all populations worldwide, including pregnant people. There are six identified viral hepatitides—A, B, C, D, E, and the more recently described, G. Each varies in its epidemiology, clinical course, and long-term sequelae. Important considerations in pregnancy include the degree of liver inflammation, risk of fulminant hepatitis, vertical transmission risk, treatment, and prevention. The majority of acute infections are subclinical.

Hepatitis A virus (HAV) and hepatitis E virus (HEV) are important causes of maternal infections in endemic regions, and HEV can be associated with considerable maternal morbidity and mortality. Hepatitis D virus (HDV) is an incomplete virus that when co-infected with hepatitis B virus (HBV) can cause disease that is more severe and can lead to fulminant hepatic necrosis. Hepatitis G, an RNA flavivirus renamed as human pegivirus, or "HPgV," causes a parenterally transmitted infection of the reticuloendothelial system. It does not demonstrate hepatotropicity, and there is no evidence it causes clinical hepatitis; therefore, it will not be reviewed in this article.[1]  Hepatitis B and hepatitis C are antenatally screened for and are more likely to lead to chronic infections.

Recommendations for appropriate screening and risk stratification, as well as antepartum, intrapartum, and postpartum considerations to reduce vertical transmission risk and minimize maternal and neonatal morbidity of viral hepatitis, will be reviewed in this article. For more information regarding viral hepatitis, please see the following resources from the Centers for Disease Control and Prevention (CDC):


Hepatitis A


HAV is a highly contagious, single-stranded RNA virus, which is transmitted by the fecal-oral route.[2, 3, 4]  Transmission can occur from person-to-person contact or by exposure to contaminated food and water. HAV infections are more common in areas where sanitation is poor and living conditions are crowded.[5]

Acute infection

Once infected, patients may display symptoms such as fever, chills, gastrointestinal (GI) upset, and jaundice. This symptomatology is secondary to a T-cell mediated immune response leading to inflammation and necrosis of hepatocytes.[2, 3, 4]  In a large majority of patients, this is a reversible process without chronic sequelae.[3]

Screening and diagnosis

The diagnosis of acute hepatitis A is made through serologic evaluation. HAV infection can be differentiated from other viral hepatitides by identifying elevated anti-HAV immunoglobulin M (IgM) in the serum.[6, 7]  Because HAV infection induces lifelong protection against reinfection, an elevated IgG antibody would indicate a prior infection or prior vaccination.[8, 9]

Management and perinatal considerations

Following diagnosis, clinical management is usually supportive to maintain comfort and adequate nutritional balance. The administration of immunoglobulins may improve the clinical manifestations of the disease if given within 2 weeks of infection, but this treatment is of no help in the acute phase of HAV infection.[3]  Hospitalization is reserved for patients with evidence of severe disease, including coagulopathy, encephalopathy, or severe malaise and asthenia. Rare cases of fulminant hepatic necrosis may require liver transplantation.

There is practically no maternal-fetal transmission of HAV, as anti-HAV IgG antibodies present during the initial stages of HAV infection cross the placenta and provide protection to the infant after delivery, which poses a minimal risk to the fetus and newborn.[3]  Additionally, there is no evidence of congenital HAV infection.[10]  Thus, pregnancy should not impact a physician’s management of HAV infection or vice versa.


Prevention of HAV infection is possible through vaccination and improved sanitary precautions when traveling to endemic regions. Immunization is recommended for pregnant patients at high risk for exposure via the inactivated HAV vaccine.[2, 3, 4]  Additionally, HAV infection is not a contraindication to breastfeeding.[11]  If exposure has been encountered, postexposure prevention can be achieved through administration of HAV immunoglobulin within 2 weeks of exposure, which may decrease the risk of acquiring the disease and the severity.[12]


Hepatitis B


Hepatitis B is an important disease worldwide because of its ability to cause chronic infection leading to cirrhosis, liver failure, and hepatocellular carcinoma. The prevalence of hepatitis B is highest in sub-Saharan Africa and Asia.[13]  In endemic areas, the majority of HBV infections are attributed to the high rates of perinatal transmission. In the United States, the incidence of HBV infection in children and adolescents has remained low owing to effective childhood vaccination. According to the CDC 2019 surveillance report, there were 3192 cases reported, with an estimated 20,700 cases accounting for underreporting. The majority of these cases were in adults aged 30-49 years, and 35% of persons infected reported injection drug use.[14]


HBV is a small, enveloped double-stranded DNA virus that is unique from the other RNA-containing hepatitis viruses (A, C, D, E).[15]  It has three antigens of clinical importance: the hepatitis surface antigen, HBsAg, and two core antigens, HBcAg and HBeAg. It is a hepatotropic virus but is not directly cytopathic. The immune response to the virus leads to cell-mediated destruction of infected cells, causing liver inflammation and symptoms as well as resolution of illness. Because of an immature T-cell immune response in infants, perinatal transmission is much more likely to result in chronic infection.

Laboratory tests often reveal elevated serum aminotransferase levels. HBsAg becomes detectable about 4 weeks after infection. The presence of hepatitis B E antigen (HBeAg) indicates greater infectivity owing to high viral replication.[15, 16]  The antibody response occurs first with anti-HBcAb IgM. Anti-HBs appears only after resolution of infection or with immunity from vaccination.

Acute infection

Transmission of hepatitis B occurs via the parenteral route after exposure to the blood or bodily fluids of an infected person, typically through injection drug use, sexual intercourse, or childbirth. The prodromal period is about 3 months (60-150 days), and many HBV infections are asymptomatic. The most common presenting symptoms of acute HBV infection include fatigue, malaise, anorexia, nausea and vomiting, abdominal pain, and jaundice. Resolution of illness occurs by 3-4 months. Severe manifestations may include coagulopathy and hepatic encephalopathy, which indicate fulminant hepatitis—a life-threatening complication—and require hospitalization.

Chronic infection

Chronic HBV infection is defined by the persistence of detectable HBsAg for more than 6 months. Chronic infection occurs more frequently in younger as well as in immunocompromised persons, owing to the dependence on the cell-mediated immune response to clear the infection. Persistent infection is seen in 5-10% of infected adults, 25-50% of infected children, and 90% of infected neonates.[15]  Viral replication and damage from cell-mediated immune responses can eventually lead to cirrhosis and hepatocellular carcinoma. Death resulting from complications of chronic HBV infection ultimately occurs in about 20% of persons with persistent disease.[17]  Chronic infection can also lead to extrahepatic manifestations due to immune complexes, including arthritis, vasculitis, and glomerulonephritis.[18]

Screening and diagnosis

Universal screening for hepatitis B at the initial prenatal visit is recommended by the American College of Obstetricians and Gynecologists and the US Preventive Services Task Force. Identifying women with chronic HBV infection and providing appropriate postnatal immunoprophylaxis to the newborn have significantly reduced perinatal transmission of the virus to 10%. All pregnant people should be tested at the initial prenatal visit for the presence of serum HBsAg, which is present in both acute and chronic infection. If the initial screen is negative but the patient is at high risk for infection, repeated testing should be performed later in pregnancy and after delivery. A positive HBsAg test should be followed by a quantitative HBV DNA test to determine transmission risk and potential need for treatment.

The presence of anti-HBsAg antibody indicates resolution of a past infection or serologic response to prior vaccination. Anti-HBsAb is a neutralizing antibody and binds to the surface antigen, which is a decoy particle that does not contain viral DNA. Therefore, anti-HBsAb will not be detectable when there is ongoing viral replication. The antibody response occurs first with anti-HBcAb IgM followed by IgG, which persists following resolution or progression to chronic infection. Anti-HBcAb will not be present in serum from vaccinated individuals who have not been infected. The HBe antigen is a marker for high viral replication.[19]  The risk of perinatal transmission reaches 80-90% in the setting of positive anti-HBeAg and a high viral load near the time of delivery.[20]

Management and perinatal considerations

Acute HBV infection can mimic other pathologies affecting pregnancy, including gallbladder disease, severe preeclampsia, HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome, and acute fatty liver of pregnancy (AFLP). Diagnosis can be aided by the absence of gallbladder pathology on imaging; relatively lower aspartate aminotransferase (AST), alkaline phosphatase, and gamma-glutamyl transferase levels than those seen in gallbladder disease; absence of new or worsening hypertension or proteinuria; and the presence of positive serologic testing for HBV.  

Treatment of HBV infection is supportive, although hospitalization may be required for more severe complications, including coagulopathy, encephalopathy, dehydration, and severe metabolic derangements.[21]

Antiviral monotherapy should be considered at 28-32 weeks when HBV DNA levels exceed 6-8 log10 copies/mL, owing to significantly increased risk for transmission.[17]  Tenofovir disoproxil fumarate, or TDF, (Category B) is an HBV DNA polymerase inhibitor and is a preferred agent because of its well-established safety profile and low rates of resistance.[22]  Alternative options include lamivudine and telbivudine, but both have been associated with increased resistance.[23]

Invasive diagnostic procedures, including amniocentesis and chorionic villus sampling, may be offered to women if warranted, but women should be counseled on the increased risk of vertical transmission in conditions where viral load exceeds 7 log10 copies/mL. Fetal scalp electrode placement during labor is relatively contraindicated. HBV infection alone is not an indication for cesarean delivery.[17, 24]  Breastfeeding has not been shown to increase risk of transmission and should be encouraged following appropriate immunoprophylaxis of the newborn.[25]


The hepatitis B vaccine is recommended for all at-risk adults and for anyone desiring vaccination. HBV vaccination is not contraindicated in pregnancy and can be administered at any point during the pregnancy.[26]  Women at increased risk for acquiring hepatitis B include those who have had more than one sex partner in the past 6 months, are undergoing evaluation or treatment for a sexually transmitted infection (STI), have recent or current intravenous (IV) drug use, and have a HBsAg-positive sexual partner.

The available vaccines on the market are recombinant DNA vaccine and do not contain any live virus. There are three vaccines currently licensed in the United States, including Engerix-B, Recombivax-HB, and HEPLISAV-B. There are limited data on the safety of HEPLISAV-B in pregnancy; therefore, it is advised that pregnant people receive one of the other two available vaccines.

For adults and children, the three-injection vaccine series should be administered at 0, 1, and 6 months. Confirmatory testing for immune response to vaccination is recommended in higher-risk groups, including health care workers, immunocompromised individuals, infants of mothers with HBsAg, and sex partners of individuals with chronic HBV infection. This can be accomplished with anti-HBsAb drawn 1-2 months following the last dose of the series.[27]

Susceptible individuals who have been exposed to HBV should receive the hepatitis B vaccine as well as hepatitis B immunoglobulin to prevent infection as soon as possible after exposure and no more than 14 days after exposure.[27]  The administration of hepatitis B immunoglobulin and HBV vaccine is 85-95% effective in preventing HBV infection.[26]  Newborns born to mothers who are HBsAg-positive or HBsAg-unknown should receive hepatitis B immunoglobulin and HBV vaccine within 12 hours of birth.[17, 28]

Women with HBV infection should receive the appropriate follow-up and counseling to help prevent transmission. Intimate contacts should be notified, tested, and vaccinated if they are susceptible to infection. Condoms should be used to reduce risk of transmission during sexual intercourse and sharing of possible blood-contaminated items should be avoided.


Hepatitis C


HCV is an RNA virus that can lead to significant morbidity and mortality. The incidence of HCV infection has increased over the past decade within the United States, which is thought to coincide with the opioid epidemic. Among pregnant people, the incidence has increased to 1-4%.[29]  Due to this rise, multiple organizations including the CDC, US Preventive Services Task Force, and the Society for Maternal Fetal Medicine have updated their recommendations and guidelines for HCV infection in pregnancy.[30, 29]

Acute and chronic infection

Within the first 6 months after exposure to HCV, nearly 75% of exposed persons will remain asymptomatic.[31]  Others may develop nonspecific abdominal pain, nausea, anorexia, jaundice, or malaise. Without treatment, up to 60% will progress to chronic HCV infection. Chronic HCV infections are a major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma around the world.[32]

HCV infection in pregnancy can lead to a variety of sequelae. During pregnancy, the maternal immune response is dampened, which is believed to offset the immune-mediated hepatocyte damage from HCV. Clinically, this often results in a decrease in serum maternal liver enzymes, such as alanine aminotransferase (ALT), during the second half of pregnancy and a rise in the HCV viral load. Thus, it is not recommended to trend liver function during pregnancy.[29]

Other associations of HCV infection in pregnancy include gestational diabetes, especially in the setting of excessive weight gain in pregnancy. There is also 20 times the odds of developing intrahepatic cholestasis of pregnancy. HCV infection in pregnancy has consistently been associated with poorer fetal outcomes, including fetal growth restriction and low birth weight. A growth scan in the third trimester is recommended for women with HCV infection in pregnancy.[29]

Screening and diagnosis

Screening guidance has changed in recent years including a recommendation for universal HCV screening during pregnancy.[33, 30, 29]  This endorsement stems from the increase in incidence of infection and the fact that risk-based screening misses nearly 50% of infections. It is recommended that all pregnant people are screened with anti-HCV antibody testing at the initial prenatal visit.[30, 29]  If antibody testing is positive, this finding should be reflexed to evaluate for HCV RNA viral load.

No definitive test diagnoses acute HCV infection.[32]  Most patients are identified by a known exposure, documented seroconversion, unexplained increases in liver enzymes, and exclusion of other causes of liver disease.[32]  The only conclusive method to diagnose an acute or recent-onset HCV infection is to demonstrate seroconversion in a previously seronegative individual. Attempting to establish infection based on the presence of antibodies is not a reliable way to confirm the diagnosis, as many individuals may continue to be antibody negative for 6-12 months. Therefore, the absence of antibodies does not preclude infection in the acute setting.[32]  Up to 30% of patients will have delayed seroconversion, especially those who are immunocompromised[34]  Additionally, measuring anti-HCV IgM has not proven to be useful, as its concentrations remain stable in acute and chronic disease.[35]

Management and perinatal considerations

Following diagnosis of active infection in pregnancy, additional laboratory evaluation should be undertaken, including baseline liver function tests (AST, ALT, and bilirubin), albumin, platelet count, prothrombin time, STI screening, and HCV genotype.[29]  The treatment regimens considered for active HCV infection depend on HCV genotype, presence of cirrhosis, and previous treatments.[31, 36, 37]  To date, no antiviral therapies are approved for use during pregnancy outside of clinical trials.[38, 39, 29]  Patients should be referred to a hepatologist or infectious disease specialist during pregnancy to expedite therapy postpartum.

Transmission during pregnancy can occur while in utero or during the peripartum period, leading to a 5% transmission rate.[16, 29]  Vertical transmission is greatly impacted by coinfection with HIV and current maternal HCV viral load.[32, 31, 40, 41, 42]  The risk of transmission at the time of prenatal diagnostic testing is likely low, but the data are limited.[29]  Internal fetal monitors and prolonged rupture of membranes should be avoided when possible, but preterm prelabor rupture of membranes should not be an indication for earlier delivery than usual recommendations.[29]  Cesarean delivery should be reserved for usual indications, as it has not been shown to mitigate transmission rate.[43, 44, 45, 46, 47]  The infected infants tend to do well, and severe hepatitis is rare.[31]


The prevention of HCV transmission and acquisition depends on preventing exposure to infected blood or blood products as well as implementation of universal precautions. It also requires avoidance of high-risk sexual behavior. The most common form of transmission in the United States is through IV drug use.[48]  Needle-exchange programs for injecting drug users may help to limit the spread of HCV infection as well as that of HIV and HBV.[49]  Patients who are HIV positive also have a higher risk of acquiring the disease.[32, 31, 40, 41, 42]  Pregnant people with HCV infection should be vaccinated against hepatitis A and B.[50, 29]

Patients should be educated that HCV is not spread by breastfeeding, sneezing, coughing, hugging, sharing eating utensils or drinking from the same glass, other normal social contact, food, or water.[31]  Testing and counseling for HCV infection should be offered to all women during each pregnancy.[33, 29]  Currently, no pre-exposure prophylaxis, vaccine, or post-exposure prophylaxis is available for HCV infection,[10, 32]  and post-exposure prophylaxis with immunoglobulin is not effective in preventing infection.[31]


Hepatitis D


HDV, also known as delta variant, is a defective RNA virus that relies on the presence of HBV to replicate. It may be acquired simultaneously with HBV as a co-infection or secondarily with chronic HBV infection as a superinfection. Like hepatitis B, hepatitis D is acquired parenterally by exposure to infected blood, serum, semen, or vaginal fluids.[51]  The suspected prevalence of hepatitis D in the United States is low, and most cases are the result of travel to endemic areas, including Eastern Europe, Southern Europe, the Mediterranean region, the Middle East, West and Central Africa, East Asia, and the Amazon Basin in South America.

Acute and chronic infection

Symptoms of acute HDV co-infection may present identically to hepatitis B, but a superinfection of HDV in the setting of chronic HBV infection can lead to fulminant hepatitis, which is fatal in about 80% of cases. Less than 5% of individuals who are co-infected with HDV/HBV will go on to develop chronic infection,[52]  but 80% will develop chronic HDV infection when there is superinfection with chronic hepatitis B.[53]  Chronic HDV superinfection accelerates the liver disease typically seen with HBV infection. As a result, cirrhosis and liver failure occur in 70-80% of individuals within 5-10 years of infection.

Screening and diagnosis

All women with a positive HBsAg test should also undergo testing for HDV with an HDV RNA polymerase chain reaction (PCR) assay.[54]

Management and perinatal considerations

Maternal-fetal transmission of HDV has been described, but the same preventive measures to reduce HBV transmission, including identification with screening, risk stratification and treatment of those at highest risk (high HBV DNA levels and positive HBeAg), and passive-active immunization of the newborn, are all effective at reducing transmission of HDV. Pegylated interferon-alpha has been used to treat HDV/HBV coinfection or superinfection, but the duration of clinical response is short.[53]  Pegylated interferon-alpha is considered Category C in pregnancy and should only be used if benefits outweigh fetal risks; therefore, supportive therapy is the mainstay of treatment.[55]


Because HDV cannot persist in the absence of HBV, prevention of HBV infection as well as resolution of infection with HBV will result in its clearance. There is currently no vaccine against hepatitis D, but it is vaccine-preventable with immunity acquired through hepatitis B vaccination.


Hepatitis E


HEV is a significant cause of viral hepatitis in endemic regions, largely because of poor sanitation. Although it is less common in the United States, endemic areas include Asia, Africa, Mexico, and South America. HEV is a single-stranded RNA virus with four main viral genotypes. HEV genotypes 1 and 2 are transmitted via the fecal-oral route and contamination of water supplies due to poor sanitation.[56]  Genotypes 3 and 4 cause foodborne illnesses acquired by ingestion of undercooked meat, including pork, venison, and shellfish.[20]

Acute and chronic infection

Acute infection with HEV may be asymptomatic or may present with symptoms similar to other viral hepatitides, including fever, fatigue, malaise, loss of appetite, nausea, vomiting, abdominal pain, jaundice, acholic stools, dark urine, and joint pain. Symptoms may occur about 15-60 days following exposure, with a mean of 40 days. The majority of individuals who will be symptomatic are young adults, aged 15-44 years, and special populations including pregnant people may be affected severely.

HEV is very unlikely to cause chronic disease; however, it has been demonstrated to progress to chronic hepatitis in certain individuals, including patients who have undergone solid organ transplantation and are on immunosuppressive therapy.

Screening and diagnosis

The diagnosis of hepatitis E should be considered in patients who have symptoms of hepatitis but other hepatotropic viral testing has been negative; have no other identified cause for liver injury; or have certain risk factors, including recent travel, consumption of undercooked foods, contaminated water sources, or exposure to contacts with hepatitis. Diagnosis can be made based on laboratory testing for IgM and IgG antibodies to HEV or HEV RNA PCR.[57]

Management and perinatal considerations

Treatment of hepatitis E is supportive, as there is no specific antiviral treatment. Hospitalization is indicated for patients with manifestations of liver failure or fulminant hepatitis and should be considered for pregnant people.[58]  Liver transplant may be indicated in the case of fulminant liver failure.

The overall mortality rate associated with hepatitis E is about 1%. In pregnant patients with HEV infection, mortality can reach as high as 30%. The severe disease and fulminant hepatitis seen among pregnant people is attributable to an altered innate immune system that is adaptationally designed to allow tolerance to the developing pregnancy, meanwhile lowering defense to certain infectious pathogens including HEV, influenza virus, ebolavirus, dengue virus, and coronavirus-19.[59]

In a systematic review, data from five studies that included 479 HEV-positive and 490 HEV-negative women were analyzed to evaluate the maternal-fetal outcomes of HEV infection in pregnancy. Maternal HEV infection was significantly associated with low birth weight (odds ratio [OR]: 3.23; 95% CI: 1.71-6.10), small for gestational age (OR: 3.63; 95% CI: 1.25-10.49), prematurity < 32 weeks (OR: 4.18; 95% CI: 1.23-14.20), prematurity < 37 weeks (OR: 3.45; 95% CI: 2.32-5.13), stillbirth (OR: 2.61; 95% CI: 1.64-4.14), intrauterine demise (OR: 3.07; 95% CI: 2.13-4.43), and maternal death (pooled OR: 7.17; 95% CI 3.32-15.47).[60]  Perinatal transmission is unlikely but can lead to neonatal liver injury, impaired glucose regulation, and death in the newborn.[20]  Breastfeeding has not been demonstrated to increase transmission.[11]


There is currently no FDA-approved vaccine for hepatitis E available in the United States. Prevention is largely through improvement of sanitation in developing countries, avoiding drinking of unpurified water in endemic regions, and avoiding consumption of uncooked or undercooked animal meat.


Other hepatitis-causing viruses

Epstein-Barr virus

Epstein-Barr virus (EBV) is a member of the Herpesviridae family of viruses.[61]  It is transmitted via nasopharyngeal and oral secretions. Primary EBV infection occurs most frequently in childhood and adolescence, and more than 90% of adults will have IgG to EBV, indicating prior exposure.[61]  Primary EBV infection leads to infectious mononucleosis, which is classically an upper respiratory tract disease but can be associated with hepatic injury in more than 50% of cases.[62]

The diagnosis should be considered in pregnant people with an unspecified hepatitis with or without the typical accompanying symptoms of infectious mononucleosis. Laboratory testing may reveal elevated transaminases and cholestasis as well as lymphocytosis. The diagnosis can be confirmed with serologic testing for IgM antibodies to EBV or EBV DNA quantification.

Hepatitis secondary to EBV infection in pregnancy is most often mild. More severe cases of EBV-related hepatitis in pregnancy can lead to spontaneous abortion or preterm labor. Liver failure, fulminant hepatitis, and hemophagocytic lymphohistiocytosis are extraordinarily rare but potentially life-threatening complications.[61, 63]

Treatment of EBV infection in pregnancy is generally supportive. However, in severe cases, steroids and acyclovir may be considered.[61, 64]  Breastfeeding is not impacted by EBV infection in pregnancy.[61]


Cytomegalovirus (CMV) is another member of the Herpesviridae family of viruses and leads to lifelong latent infection that remains dormant in myeloid cells. The prevalence of CMV IgG in reproductive-aged women is higher than 90-100%.[65]  The diagnosis is made based on serologic testing of IgM and IgG antibodies to CMV, with the presence of IgM indicating a primary infection. CMV IgG avidity testing can help differentiate between primary and recurrent infections. CMV DNA can also be isolated from urine in the setting of active infection.

Primary CMV infection in pregnancy is usually asymptomatic but can cause flu-like symptoms in about 30% of patients and occasionally can lead to more significant liver injury, including hepatitis or liver failure.[61]  Perinatal transmission of CMV occurs more frequently with infections occurring later in pregnancy, with a 40-70% risk of congenital infection in the third trimester. Congenital CMV infection can lead to hearing loss and neurodevelopmental delay.

Treatment of CMV infection is supportive, and due to limited evidence on the safety of its use in pregnancy, parenteral antiviral therapy including ganciclovir is reserved for extreme cases of immunosuppression or coinfection with HIV.[61]  Breastfeeding is a common route of transmission of CMV. However, due to reduced morbidity associated with postpartum CMV infection, the benefits of breastfeeding outweigh the risks and should be recommended.[66]

Herpes simplex virus

Herpes simplex virus (HSV), HSV-1 and HSV-2, are capable of causing recurrent oropharyngeal or genital outbreaks of mucocutaneous lesions. Very rarely, HSV-1 and HSV-2 can lead to acute hepatitis and can be particularly fatal in pregnancy if left untreated. The diagnosis should be considered in pregnant people with unspecified liver injury and fever. Mucocutaneous herpetic lesions may only be present in less than 50% of individuals with HSV hepatitis. The diagnosis can be made with HSV IgM and IgG serologies, HSV DNA PCR, viral detection on smears, and viral culture. Liver biopsy can also be used to make the diagnosis.

If HSV hepatitis is suspected, empiric antiviral therapy with parenteral acyclovir, 10 mg/kg IV every 8 hours, should be initiated without delay.[67]  Acyclovir is a Category B drug and thus is considered safe for use in pregnancy. Due to the risk of viral transmission during labor and vaginal delivery, cesarean delivery is recommended for any women with active genital lesions or prodromal symptoms at the time of delivery. Infants born to mothers with HSV hepatitis should receive empiric prophylaxis with acyclovir for 2-3 weeks to minimize the risk of neonatal transmission.[61]  Breastfeeding is unlikely to cause transmission of HSV and is therefore encouraged unless lesions are present on the breast or nipple.[68]