Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mortality trends of missionary staff serving in sub-Saharan Africa were tracked for the period 1945-1985. For 1945-1970, when more complete incidence data were available, the missionary death rate was approximately 40% lower, after adjustment, than would be expected in a comparable US population. This trend persisted through 1985. Between 1945 and 1970, the largest number of fatalities was attributable to malignancy, atherosclerosis, accidents, and infectious disease, and the greatest mortality risks, compared with the US experience, were from homicides, the complications of pregnancy, and infections, notably malaria, hepatitis, and polio. Beginning in the late 1950s, motor vehicle accidents became the leading cause of death. Since the 1960s, accidental causes of death have been approximately 50% higher than in the US, and homicides have been four times higher. During this same period, the infectious disease death rate decreased to approximately that within the US. Currently, the leading causes of mortality are motor vehicle accidents, malignancy, and atherosclerosis, followed by other accidental causes, notably aircraft mishaps and drownings. Viral hepatitis is presently the leading infectious disease cause of death. Other contemporary lethal infections include malaria, rabies, typhoid, Lassa fever, and retroviral infection. It was concluded that missionaries in sub-Saharan Africa had a death rate approximately half that expected in a comparable domestic control population. Preventive strategies, particularly relative to accident and infectious disease prevention, could effectively reduce mortality risk further.
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PMID:Mortality trends of American missionaries in Africa, 1945-1985. 162 93

In order to explore the significance of a previous observation that the most important pathologic changes in fatal Lassa fever are hepatic, we have studied postmortem liver biopsies from 19 patients with fatal Lassa fever. We observed a vigorous macrophage response to cellular damage, but we found no evidence of lymphocyte infiltration in infected hepatic tissues. Using semi-quantitative estimates of liver cell damage, we found a wide range in the severity and progression of Lassa virus hepatitis in our fatal cases. We have classified for descriptive purposes three general nosopoeitic phases: active hepatocellular injury (less than 20% necrosis), continued damage and early recovery, and mitotic activity representing hepatic recovery. We conclude that the liver goes through cellular injury, necrosis and regeneration and any or all may be present at death. In no instance was the degree of hepatic damage sufficient to implicate hepatic failure, and all three phases were represented among our cases. We conclude that the hepatitis of Lassa fever in humans is not the primary cause of death.
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PMID:Lassa virus hepatitis: a study of fatal Lassa fever in humans. 395 52

Under continuous observation of several months, 42 patients from the eastern province of Sierra Leone, Liberia (Lofa County), and neighbouring Guinea were identified as Lassa fever cases by indirect immunofluorescent antibody technique, indicating that the disease is endemic in these areas. The clinical course varied from mild disease to severe illness with haemorrhagic disorders. The fatality rate was 14%. The occurrence of only two possible secondary cases suggests that person-to-person spread of the disease is unimportant epidemiologically. There was a wide range of patients' ages, tribes, and occupations, including a 2 months old baby and a white US citizen. Clinical, laboratory, and histopathological investigations demonstrated the panorganotropism of Lassa virus. Haematological tests in few selected haemorrhagic cases with Lassa fever did not support coagulation disorders or thrombocytopenia as causing the bleeding tendency. The histopathologic changes bear resemblance to those observed in Argentinian and Bolivian haemorrhagic fever, both being caused by viruses of the Arena group. However, Lassa virus hepatitis may be differentiated from liver lesions occurring in yellow fever, Marburg virus disease, and Ebola (Maridi) haemorrhagic fever.
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PMID:Clinical observations in 42 patients with Lassa fever. 723 35

Callitrichid hepatitis is an arenavirus infection that recently emerged as a highly fatal disease of New World primates in the Callitrichidae family. As we previously reported, these primates develop hepatitis after contact with mice that are infected with variants of LCMV (LVMCCH), recently determined to have 86% identity with GC-P gene of the Armstrong and Western strains of LCMV. Here, we describe the histopathological lesions and tissue localization of viral antigens in confirmed cases of callitrichid hepatitis from recent outbreaks in two U.S. zoos. The liver in marmosets and tamarins with fatal infections consistently showed degeneration, necrosis, and inflammation, with variable involvement of the spleen, lymph nodes, adrenal glands, intestine, pancreas, and central nervous system. Lymphocytic choriomeningitis virus antigens were identified immunohistochemically in necrotic foci in these organs as well as in nondegenerating areas in lungs, kidney, urinary bladder, brain, and testes. The multi-organ tropism and histological pattern of LCMV infection in marmosets and tamarins are similar to those reported for the highly virulent arenavirus that causes Lassa fever in humans. Comparative studies of callitrichid hepatitis and Lassa fever would therefore be mutually beneficial for human and nonhuman primate medicine.
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PMID:Pathology and immunohistochemistry of callitrichid hepatitis, an emerging disease of captive New World primates caused by lymphocytic choriomeningitis virus. 748 6

The high density of populations and insufficient sanitary conditions increases the risk to acquire viral diseases in tropical areas. This holds true for ubiquitous as well as for regional viral infections. Hepatitis and AIDS are found worldwide, but play a dominant role in tropical areas. Classical tropical viral infections are zoonoses. They are primarily infections of nonhuman vertebrates (e.g. rodents) and of arthropod vectors and can be transmitted to man. According to the clinical outcome these viral infections can be divided into three groups: influenza-like disease with arthralgia, encephalitis and hemorrhagic fevers. The majority of infections belong to the first group, followed by encephalitis cases. Viral hemorrhagic fevers are rare in visitors of tropical areas. Antibody detection is the method of choice in the diagnosis of tropical viral infections. In special situations (e.g. Lassa fever) the direct detection of the virus by PCR can be helpful. Tests for the detection of arboviruses, filoviruses and arenaviruses are only performed at a few centers worldwide.
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PMID:[Virus diseases in patients returning from the tropics]. 794 Apr 15

This study describes an RT-PCR assay targeting the L RNA segment of arenaviruses. Conserved regions were identified in the polymerase domain of the L gene on the basis of published sequences for Lassa virus, lymphocytic choriomeningitis virus (LCMV), Pichinde virus and Tacaribe virus, as well as 15 novel sequences for Lassa virus, LCMV, Ippy virus, Mobala virus and Mopeia virus determined in this study. Using these regions as target sites, a PCR assay for detection of all known Old World arenaviruses was developed and optimized. The concentration that yields 95% positive results in a set of replicate tests (95% detection limit) was determined to be 4290 copies of Lassa virus L RNA per ml of serum, corresponding to 30 copies per reaction. The ability of the assay to detect various Old World arenaviruses was demonstrated with in vitro transcribed RNA, material from infected cell cultures and samples from patients with Lassa fever and monkeys with LCMV-associated callitrichid hepatitis. The L gene PCR assay may be applicable: (i) as a complementary diagnostic test for Lassa virus and LCMV; (ii) to identify unknown Old World arenaviruses suspected as aetiological agents of disease; and (iii) for screening of potential reservoir hosts for unknown Old World arenaviruses.
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PMID:RT-PCR assay for detection of Lassa virus and related Old World arenaviruses targeting the L gene. 1790 72

Viral hemorrhagic fevers (VHFs) encompass a group of diseases with cardinal symptoms of fever, hemorrhage, and shock. The liver is a critical mediator of VHF disease pathogenesis and high levels of ALT/AST transaminases in plasma correlate with poor prognosis. In fact, Lassa Fever (LF), the most prevalent VHF in Africa, was initially clinically described as hepatitis. Previous studies in non-human primate (NHP) models also correlated LF pathogenesis with a robust proliferative response in the liver. The purpose of the current study was to gain insight into the mechanism of liver injury and to determine the potential role of proliferation in LF pathogenesis. C57Bl/6J mice were infected with either the pathogenic (for NHPs) strain of lymphocytic choriomeningitis virus (LCMV, the prototypic arenavirus), LCMV-WE, or with the non-pathogenic strain, LCMV-ARM. As expected, LCMV-WE, but not ARM, caused a hepatitis-like infection. LCMV-WE also induced a robust increase in the number of actively cycling hepatocytes. Despite this increase in proliferation, there was no significant difference in liver size between LCMV-WE and LCMV-ARM, suggesting that cell cycle was incomplete. Indeed, cells appeared arrested in the G1 phase and LCMV-WE infection increased the number of hepatocytes that were simultaneously stained for proliferation and apoptosis. LCMV-WE infection also induced expression of a non-conventional virus receptor, AXL-1, from the TAM (TYRO3/AXL/MERTK) family of receptor tyrosine kinases and this expression correlated with proliferation. Taken together, these results shed new light on the mechanism of liver involvement in VHF pathogenesis. Specifically, it is hypothesized that the induction of hepatocyte proliferation contributes to expansion of the infection to parenchymal cells. Elevated levels of plasma transaminases are likely explained, at least in part, by abortive cell cycle arrest induced by the infection. These results may lead to the development of new therapies to prevent VHF progression.
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PMID:Novel mechanism of arenavirus-induced liver pathology. 2582 3