Page 621 - Textbook of Pathology, 6th Edition
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ii) Midzonal necrosis is uncommon and involves zone 2 of  Hepatitis B virus (HBV), causing a parenterally transmitted  605
           the hepatic lobule. This pattern of necrosis is seen in yellow  disease that may become chronic.
           fever and viral hepatitis. In viral hepatitis, some of the  Hepatitis C virus (HCV), previously termed non-A, non-B
           necrosed hepatocytes of the mid-zone are transformed into  (NANB) hepatitis virus involved chiefly in transfusion-
           acidophilic, rounded Councilman bodies.             related hepatitis.
           iii) Periportal (peripheral) necrosis is seen in zone 1  Hepatitis delta virus (HDV) which is sometimes associated
           involving the parenchyma closest to the arterial and portal  as superinfection with hepatitis B infection.
           blood supply. Since zone 1 is most well perfused, it is most  Hepatitis E virus (HEV), causing water-borne infection.
           vulnerable to the effects of circulating hepatotoxins e.g. in
           phosphorus poisoning and eclampsia.                    Hepatitis G virus (HGV), is a recently discovered
                                                               transfusion-transmitted hepatotropic virus but is not known
           3. FOCAL NECROSIS. This form of necrosis involves small  to cause hepatitis.
           groups of hepatocytes irregularly distributed in the hepatic  All these human hepatitis viruses are RNA viruses except
           lobule. Focal necrosis is most often caused by microbiologic  HBV which is a DNA virus.
           infections. These include viral hepatitis, miliary tuberculosis,  Though a number of other viral diseases such as infection
           typhoid fever and various other forms of bacterial, viral and  with Epstein-Barr virus (in infectious mononucleosis),
           fungal infections. Focal necrosis may also occur in drug-  arbovirus (in yellow fever), cytomegalovirus, herpes simplex
           induced hepatitis.                                  and several others affect the liver but the changes produced
                                                               by them are nonspecific; the term ‘viral hepatitis’ is strictly
           VIRAL HEPATITIS                                     applied to infection of the liver by the hepatitis viruses.

           The term viral hepatitis is used to describe infection of the  ETIOLOGIC CLASSIFICATION
           liver caused by hepatotropic viruses. Currently there are 5  Based on the etiologic agent, viral hepatitis is currently
           main varieties of these viruses and a sixth poorly-  classified into 6 etiologic types—hepatitis A, hepatitis B,
           characterised virus, causing distinct types of viral hepatitis:
                                                               hepatitis C, hepatitis D, hepatitis E and hepatitis G. The
              Hepatitis A virus (HAV), causing a faecally-spread self-  contrasting features of major types are presented in  CHAPTER 21
           limiting disease.                                   Table 21.6.



             TABLE 21.6: Features of Various Types of Hepatitis Viruses.
              Feature         Hepatitis A   Hepatitis B      Hepatitis C      Hepatitis D          Hepatitis E
            1. Agent          HAV           HBV              HCV              HDV                  HEV
            2. Year identified  1973        1965             1989             1977                 1980
            3. Viral particle  27 nm        42 nm            30-60 nm         35-37 nm             32-34 nm
            4. Genome         RNA, ss, linear  DNA, ss/ds    RNA, ss, linear  RNA, ss, circular    RNA, ss, linear
                                                             circular
            5. Morphology     Icosahedral   Double-shelled,  Enveloped        Enveloped, replication  Icosahedral,
                              non-enveloped  enveloped                        defective            non-enveloped
            6. Spread         Faeco-oral    Parenteral,      Parenteral,      Parenteral, close    Water-borne
                                            close contact    close contact    contact                                 The Liver, Biliary Tract and Exocrine Pancreas
            7. Incubation     15-45 days    30-180 days      20-90 days       30-50 days           15-60 days
              period                                                          (In superinfection)
            8. Antigen(s)     HAV           HBsAg            HCV RNA          HBsAg                HEV
                                            HBcAg            C 100-3          HDV
                                            HBeAg            C 33c
                                            HBxAg            NS5
            9. Antibodies     anti-HAV      anti-HBs         anti-HCV         anti-HBs             anti-HEV
                                            anti-HBc                          anti-HDV
                                            anti-HBe
           10. Severity       Mild          Occasionally severe  Moderate     Occasionally severe  Mild
           11. Chronic        None          Occasional       Common           Common               None
              hepatitis
           12. Carrier state  None          <1%              <1%              1-10%                Unknown
           13. Hepatocellular  No           +                +                ±                    None
              carcinoma
           14. Prognosis      Excellent     Worse with age   Moderate         Acute good; chronic poor  Good
           (ss= single-stranded; ss/ds= partially single-stranded partially double-stranded)
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