Hepatitis e virus vaccine

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Since discharge from hospital our patient remains well and liver biochemistry has continued to improve on a tapering course of prednisolone Fig. There are a number of similarities between the previously described cases and our own.

Firstly, there was a short interval between vaccination and symptom onset in all cases. In response to the first case, Capecchi et al. It is indeed short when compared to established causatives agents of drug-induced autoimmune liver disease such as immune checkpoint inhibitors where a latency period of 2 to 24 weeks has been described. Secondly, histological appearances are similar between our case and that described by Bril et al.

Both cases had an eosinophil infiltration which is more typical of a drug-induced liver injury. This raises the possibility that this is a vaccine-related drug-induced liver injury with features of AIH rather than the vaccine causing immune dysregulation. Unlike the other cases, our patient had no confounding risk factors for developing autoimmune liver disease such as other autoimmune conditions or recent pregnancy and she received a different mRNA vaccine, Moderna rather than Pfizer-BioNTech.

These findings raise the question as to whether COVID mRNA vaccination can, through activation of the innate immune system and subsequent non-specific activation of autoreactive lymphocytes, lead to the development of autoimmune diseases including AIH or trigger a drug-induced liver injury with features of AIH. The trigger, if any, may become more apparent over time, especially following withdrawal of immunosuppression. As with other autoimmune diseases associated with vaccines the causality or casualty factor will prove difficult to tease apart and should not distract from the overwhelming benefits of mass COVID vaccination.

The authors received no financial support to produce this manuscript. Dr Jonathan Rigby — interpreted histology and involved with writing of manuscript. The authors declare no conflicts of interest that pertain to this work. National Center for Biotechnology Information , U. People living in crowded camps or temporary housing, including refugees and people who are internally displaced, are at particularly high risk. HEV is unique, in that it has a different clinical and epidemiologic profile depending on where the infection is acquired.

This can be attributed largely to the viral genotypes circulating in different parts of the world. Four genotypes of HEV cause illness in humans, each displaying different epidemiologic and clinical characteristics in developing and developed countries.

Cases of hepatitis E typically present in one of two ways: either as large outbreaks and sporadic cases in areas where HEV is endemic genotype 1 in Asia and Africa, genotype 2 in Mexico and west Africa, and genotype 4 in Taiwan and China or as isolated cases in developed countries like the United States genotype 3.

Recently, a new genotype genotype 7 was identified in a liver-transplant recipient from UAE with chronic hepatitis E virus infection who frequently consumed camel meat and milk 4. HEV is usually spread by the fecal-oral route. In developing countries, where HEV genotypes 1 and 2 predominate, the most common source of HEV infection is contaminated drinking water.

Consumption of shellfish was a risk factor in a recently described outbreak that occurred among cruise ship passengers 5. HEV genotype 4, detected in China, Taiwan, and Japan, has also been associated with foodborne transmission 6. When they occur, the signs and symptoms of hepatitis E are similar to those of other types of acute viral hepatitis and liver injury.

They include:. Many people with hepatitis E do not have symptoms of acute infection. In developing countries, symptomatic hepatitis E commonly occurs among older adolescents and young adults i.

Pregnant women are more likely to experience severe illness, including fulminant hepatitis and death 8. The specific period of infectiousness for HEV has not been determined, but virus excretion in stool has been demonstrated from 1 week prior to onset to 30 days after the onset of jaundice 9.

Chronically infected persons shed virus as long as they remain infected. Most people with hepatitis E recover completely. Hepatitis E can also pose serious health threats to people with preexisting chronic liver disease and organ-transplant recipients on immunosuppressive therapy, resulting in decompensated liver disease and death.

To date, there is no report of progression of acute hepatitis E to chronic hepatitis E in developing countries, where HEV genotypes 1 and 2 are the predominant causes of illness. However, increasing numbers of hepatitis E genotype 3 infections acquired in developed countries are progressing to cause chronic hepatitis and chronic liver disease. These chronic cases occur mainly among solid-organ transplant recipients receiving immunosuppressive treatment.

HEV infection should be considered in any person with symptoms of viral hepatitis who tests negative for serologic markers of hepatitis A, hepatitis B, hepatitis C, other hepatotropic viruses, and all other causes of acute liver injury.

Any symptomatic person who has traveled either to or from an hepatitis E-endemic area or outbreak-afflicted region should also be evaluated for HEV infection.

A detailed history regarding travel, sources of drinking water, uncooked food, and contact with jaundiced persons should be obtained from these patients to aid in diagnosis. Because domestically acquired cases of hepatitis E are occurring in the United States, HEV infection also should be considered in any person with unexplained symptoms of liver injury, regardless of travel history.

Because cases of hepatitis E are not clinically distinguishable from other types of acute viral hepatitis, diagnosis can be confirmed only by testing for the presence of antibody against HEV or HEV RNA.