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The elusive hepatitis C virus.

Specific laboratory tests are generally available now for three hepatitis viruses: hepatitis A (infectious or epidemic hepatitis), hepatitis B (previously referred to as serum hepatitis), and hepatitis D (the delta virus). A fourth virus, which causes enterically transmitted non-A, non-B hepatitis (or epidemic non-A hepatitis) has been seen by electron microscopy and has morphological and biophysical characteristics that suggest that it is a member of the calicivirus group. Serological tests are under development, and molecular cloning of this virus is in progress. Other viruses that cause an acute hepatitis include the Epstein-Barr virus, cytomegalovirus, yellow fever virus, and the more exotic haemorrhagic fever viruses such as Lassa fever virus, the Marburg agent, Ebola virus, and Rift Valley fever virus, but the diseases caused by these viruses are not generally included in the term viral hepatitis. As specific diagnosis of the different types of viral hepatitis became possible some 10 years ago it became apparent that there was one form, previously unrecognised and unrelated to hepatitis A, B, or D, that was transmitted principally by the parenteral route. This became known as non-A, non-B hepatitis. Results obtained from several carefully conducted surveys of posttransfusion hepatitis in the United States and elsewhere provided strong epidemiological evidence of "guilt by association." This form of non-A, non-B hepatitis has been found in every country in which it has been sought; and it shares several features with hepatitis B. In countries where all blood donations are screened for hepatitis B surface antigen by very sensitive techniques non-A, non-B hepatitis may account for as many as 90% of all cases of posttransfusion hepatitis. Outbreaks of non-A, non-B hepatitis have also been reported after treatment with blood clotting factors VIII and IX. Non-A, non-B hepatitis has occurred in haemodialysis and other specialist units, among drug addicts, and after accidental inoculation with contaminated needles and other sharp objects. Mother to infant transmission has been reported.' In Britain and in several other countries some cases are not associated with transfusion, and such sporadic cases of non-A, non-B hepatitis account for 10-25% of all adult patients with clinical viral hepatitis. The route of infection or the source of infection cannot be identified in many of these patients, but sexual transmission is a strong candidate. Although in general the illness is mild and often subclinical or anicteric, severe hepatitis with jaundice does occur, and non-A, non-B hepatitis accounts for a substantial fraction of all fulminant hepatitis. In many patients the infection may be followed by prolonged viraemia and a persistent carrier state. Studies of the histopathological sequels ofacute non-A, non-B hepatitis infection showed that chronic liver damage, which may be severe, may occur in as many as 40-50% of patients. The virus(es) causing the parenterally transmitted form of non-A, non-B hepatitis have not been fully characterised, and their mode of replication and antigenic composition were not clear until recently despite intensive efforts in many laboratories throughout the world. There is no homology between the viruses causing hepatitis A and B, the delta hepatitis virus, and the enterically transmitted and the parenteral non-A, non-B virus. A claim to have identified the last of these viruses came in the form of a news release by the Chiron Corporation, based in California, followed by a press conference in Washington in May 1988. This described the identification, cloning, and expression of proteins from the virus (Wall Street Journal, 11 May 1988). But, to the intense disappointment of the medical and scientific community, no scientific publication appeared until nearly a year later. Choo et al derived a random primed complementary DNA from infectious plasma known to contain the non-A, non-B agent using a construct in the bacteriophage X gt 11.3 This phage vector permits efficient expression of polypeptides encoded by complementary DNA and was designed originally by Young and Davis to help isolate complementary DNA clones by well characterised antibodies that bind to clones synthesising the polypeptides of interest.4 The infectious plasma was ultracentrifuged to make a pellet from a putative small virus, and nucleic acid was recovered from this. Since the nature of the genome of the virus was not known, the nucleic acid was denatured before synthesising complementary DNA from both RNA and DNA with random primers of reverse transcriptase. About a million clones were screened. One was found to produce a protein that reacted with the serum ofa patient with chronic non-A, non-B hepatitis, which was presumed to contain antibodies to the virus. The 155 base pair insert in this clone was then cut and used as a hybridisation probe to the original library of complementary DNA, and a larger overlapping clone with 353 base pairs was extracted. This double stranded cloned DNA did not hybridise to host cell DNA or to DNA derived from plasma or liver infected with non-A, non-B hepatitis. One of the strands hybridised specifically to RNA from infected liver, however, and was shown to be homologous to a single stranded RNA in the original