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Hepatitis E Virus (HEV) – Hepeviruses

by Sean Elliott, MD

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    00:01 Hepeviridae viruses.

    00:04 The hepeviridae include and especially are the hepatitis E virus.

    00:10 This is a small, nonenveloped, icosahedral capsule, which contains a linear, single-stranded, positive-sense RNA genome.

    00:18 So, again, able to function like messenger RNA.

    00:21 This resembles the Norwalk virus and in fact, if you've seen that session already, we talked about the hepatitis E virus within the caliciviridae family.

    00:30 However, this session will be important to compare and contrast the different hepatitis viruses.

    00:37 This slide we see a transmission electron micrograph which depicts numerous spheroid shaped hepatitis E viruses.

    00:44 Transmission of hepatitis C virus mostly is via the fecal oral route, especially with genotypes one and two.

    00:51 And this might be via contaminated water or food with a significant high lifetime risk in endemic areas, especially in low income countries.

    01:00 However, there can also be transmission via and rarely via blood transfusions, mother to child vertical transmission or via breast milk.

    01:09 And infants who are nursing zoonotic transmission also can occur, especially with hepatitis E, genotypes three and four, and this would be via exposure to or consumption of shellfish, occupational exposure to animals such as swine pigs, deer, internal organs, etc..

    01:28 In China, a cases of transmission via cow's milk have been documented even in pasteurised cow's milk.

    01:35 However, unlike hepatitis A virus, the hepatitis E virus can be quite severe, especially in pregnant women.

    01:43 And in those individuals, specifically, it can cause fulminant hepatitis, along with a hepatic encephalopathy, typically over a period of 8 weeks or so.

    01:53 The electron microscopy picture you see in front of you shows the hepatitis E virus in small form and it clusters just like that in real life So, let's now do that hepatitis virus comparison, starting with hepatitis A.

    02:10 So just like we talked about with hepatitis E, hepatitis A is a fecal-oral transmission, short incubation.

    02:17 Many times, it is completely asymptomatic.

    02:21 But in those patients in whom disease develops, it is an acute onset with rapid progression to fulminant hepatitis, but then rapid resolution as well.

    02:31 The mortality rate, the death rate is very low, and there's no carrier state.

    02:36 Also, hepatitis A because it is so short lived and relatively non-acute, doesn't have any extra-hepatic manifestations or other diseases associated Hepatitis B acquired via parenteral, so blood borne or blood and body fluid exposure, so parenteral, sexual transmission, perinatal transmission to infants born to mothers who are actively infected with hepatitis B.

    03:04 The incubation period for hepatitis B is long; months to get to the potential for acute disease, and potentially years if one has a chronic infection with hepatitis B to eventually go to either hepatitis or serotic disease.

    03:21 In patients who develop the acute hepatitis, so after a month- long or even longer incubation period, they'll develop fever along with arthralgias, a rash, and then the acute onset of the hepatitis.

    03:35 Those patients then may go into a complete recovery if they develop antibody protection, or a chronic carrier state, which may ultimately lead to hepatic carcinoma.

    03:46 The immediate and medium-term mortality rate is quite low, but those patients developing hepatic carcinoma, of course, have a much higher mortality rate.

    03:57 Yes, there is a carrier status, a prolonged carrier state, and it's during this time that blood and body fluid transmission can still occur to other partners.

    04:07 Associated diseases.

    04:09 Hepatic carcinoma, as mentioned before, and cirrhosis; long-term, progressive, slowly-onset form of cirrhosis and liver failure.

    04:19 And then extra-hepatic manifestations: aplastic anemia, kidney disease with glomerulonephritis, and then even an inflammatory disease of mall and large blood vessels called polyarteritis nodosa.

    04:33 Hepatitis C, also transmitted via blood and also body fluid exposure, although blood transmission via transfusion is perhaps the currently most likely acquisition in blood which has not been properly screened.

    04:48 A long transmission or a long incubation period just like hepatitis B, and also like Hepatitis B, there can be an acute hepatitis with liver disease and/or a long progression to cirrhosis and carcinoma.

    05:04 So, think of hepatitis B and C in a very similar fashion, similar exposure, similar incubation, similar potential for long-term progression.

    05:13 Mortality rate for both is quite low, and the carrier state is quite common in hepatitis C as well.

    05:20 And also, the same progression to hepatic cirrhosis and hepatic carcinoma.

    05:26 There are fewer known extra-hepatic manifestations in hepatitis C there are for hepatitis B.

    05:34 Hepatitis D.

    05:36 This is an interesting one because it's only been more recently described and its pathogenesis has yet to be completely understood or flushed out.

    05:45 It can be thought of in the same lines as hepatitis B, in that it is a parenteral, you know, so blood and body fluid exposure, so parenteral, sexual, perinatal transmission.

    05:57 But it only appears to cause disease in combination with hepatitis B.

    06:03 So, if a patient has previously been infected with and developed disease from hepatitis B, and then gets hepatitis D as a second exposure, they have a very rapid progression to fulminant hepatitis with liver failure.

    06:19 However, if hepatitis B and D are co-infected, so acquired at the same time, , then, just like hepatitis B, it's a very long incubation period.

    06:30 And then the clinical course, very much like I described, just now with hepatitis B.

    06:35 High mortality rate, especially when hepatitis D is a second infection.

    06:40 Yes, there's a carrier state.

    06:42 Yes, there is association with cirrhosis, and then the fulminant hepatitis.

    06:47 And very much like we described with the hepatitis B there are additional extra-hepatic manifestations, such as you see in the slide.

    06:55 So, hemolytic anemia, again, the glomerulonephritis for kidney failure, inflammatory vasculitis, very much like polyarteritis nodosa and then skin lesions with lichen planus, and even in association with diabetes mellitus.

    07:11 And then our friend hepatitis E in comparison sounds very mild and minor after what we've just described for B, C, and D.

    07:20 So, just like hepatitis A, hepatitis E, fecal-oral transmission, short incubation, is very -- well, I should say, relatively mild in comparison to the others, unless the infection occurs in pregnant women in which there can be a 10% attack rate, 10% risk of fulminant hepatitis.

    07:41 So, in those pregnant women only, the mortality is high.

    07:45 Otherwise, this is a mild, self-resolving disease with no associated additional major impact.

    07:52 So, that is our friend hepatitis E in comparison to the other viral hepatitises.

    07:56 Think of this session as a important review of the hepatitis viruses as it covers several of the other sessions that you may already have watched.


    About the Lecture

    The lecture Hepatitis E Virus (HEV) – Hepeviruses by Sean Elliott, MD is from the course Viruses.


    Included Quiz Questions

    1. Fecal-oral route
    2. Blood transfusion
    3. Sexual contact
    4. Vector-borne
    5. Droplet transmission
    1. Caliciviridae
    2. Hepadnaviridae
    3. Picornaviridae
    4. Flaviviridae
    5. Coronaviridae
    1. ...10%.
    2. ...20%.
    3. ...30%.
    4. ...40%.
    5. ...50%.
    1. Hepatitis B virus
    2. Hepatitis A virus
    3. Hepatitis C virus
    4. Hepatitis D virus
    5. Hepatitis E virus

    Author of lecture Hepatitis E Virus (HEV) – Hepeviruses

     Sean Elliott, MD

    Sean Elliott, MD


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