Transmission of Non-a Non-B Hepatitis to Chimpanzees by Factor-Ix Concentrates After Fatal Complications in Patients With Chronic Liver Disease

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Toga virus-like particles (typically 60-70 nm: enveloped with small surface spikes) were detected in the native hepatectomy specimens in 7 of 18 patients grafted for acute liver failure attributed to sporadic non-A, non-B hepatitis and in 2 patients grafted for fulminant hepatitis attributed to anti-epileptic drug hepatotoxicity. These particles were not detected in the hepatectomies from 12 other patients grafted for other causes of acute liver failure, 12 for various chronic liver diseases, and 2 histologically normal livers. Acute hepatic failure, characterized histologically by severe haemorrhagic necrosis, developed 7 days after grafting in 5 patients, all in the non-A, non-B group with toga virus-like particles in native liver. Similar virus-like particles were detected in all grafts and were in greater abundance than in the native livers. The agent may be novel because pre- and post-grafting sera were negative for antibodies against representative panels of arboviruses and in first and second generation antibody tests for hepatitis C virus.

Section: Discussionsupporting

confidence: 78%

Toga virus‐like particles in acute liver failure attributed to sporadic non‐A, non‐B hepatitis and recurrence after liver transplantation

Fagan

Ellis

Tovey

et al. 1992

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“…5 ) . These were similar to the type 11 and 111 CTS structures found in chimpanzees with posttranstusion types of N A N B IShimizu et al, 1979;Bradley et al, 1981;Yoshizawa et al 1981;Gravelle et al 1982;Karayiannis et al 19831. Abundant bacteria.…”

Section: Electron Microscopysupporting

confidence: 76%

Microbial Structures in a Patient With Sporadic Non‐A, Non‐B Fulminant Hepatitis Treated by Liver Transplantation

Fagan¹,

Ellis

Portmann³

et al. 1987

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Double-shelled virus-like particles (60 nm) and long cytoplasmic tubular structures were found in the cytoplasm of hepatocytes from areas of collapsed and regenerating areas of hepatectomised liver in a 13-year-old boy who received a liver graft for fulminant hepatitis attributed to sporadic non-A, non-B hepatitis. The patient died on the ninth postoperative day from acute graft failure. Although virus-like particles were not found, instead, gram-negative rods were identified in the necrotic graft and the most likely cause of death was a gram-negative septicaemia with a Shwartzman-like reaction localized to the liver.

“…Hepatic necrosis attributed to NANB infection occurring after such a short incubation period has been reported following administration of Factor IX [Wyke et al, 1979;Iwatsuki et al, 19851 and in a single case of sporadic NANB hepatitis [Wall et al, 19851.…”

Section: Discussionmentioning

confidence: 99%

Toga‐Like virus as a cause of fulminant hepatitis attributed to sporadic non‐a, non‐b

Fagan¹,

Portmann²,

Williams³

et al. 1989

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Virus-like particles (60-70 nm) with spiked surfaces budding into cell vacuoles and rod-shaped inclusions were detected in nuclei of hepatocytes from a British patient transplanted for sporadic non-A, non-B fulminant hepatitis (NANB-FHF), probably contracted in Kenya. Identical particles were seen in two successive grafts (days 2 and 10) at regrafting for recurrent FHF. Ultrastructural features resembled those of the RNA-containing arbovirus, Rift Valley fever virus, but serological markers against a representative panel for arboviruses (Togaviruses) and transmission in mice proved negative. The particles shared features with the different arboviruses seen in the hepatectomy specimen of a second patient with NANB-FHF, and in both patients an insect vector was implicated in the clinical history. The particles were identical in size to those of a third patient with NANB-FHF, who had remained in the United Kingdom. These findings, together with the recent report of isolation of an RNA-containing virus resembling the Togaviridae, in parenteral NANB, suggest that several exotic virus-like agents resembling the arboviruses may be involved in the aetiology of NANB, including in the sporadic forms of FHF in the United Kingdom.