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PubMed1980

[Lassa letter].

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History, 20th Century↗
PubMedDate not supplied

Tropical diseases.

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Animals↗
PubMed2006

Combinatorial ribavirin and interferon alfacon-1 therapy of acute arenaviral disease in hamsters.

Several arenaviruses endemic to South America (Junin, Machupo, and Guanarito) and Africa (Lassa) are known to cause frequently fatal haemorrhagic fever. With the exception of ribavirin, which has demonstrated efficacy in cases of Lassa fever, there is no other effective therapeutic for the treatment of arenaviral haemorrhagic fever. We have recently reported that consensus interferon-a (IFN alfacon-1) can protect hamsters from lethal Pichinde virus (PCV) infection, which serves as a model for acute arenaviral disease in humans. Here we demonstrate highly effective therapy through the combined use of ribavirin with IFN alfacon-1 for the treatment of PCV infection in hamsters. Ribavirin was given orally, twice per day for 7 days, and IFN alfacon-1 was administered intraperitoneally once per day for 10 days. Treatments were initiated 1-5 days post-virus challenge using various dose combinations, many of which were less than optimal when the drugs were given independently. Combining suboptimal doses of ribavirin (5-10 mg/kg/day) with IFN alfacon-1 (5-10 microg/kg/day), we were able to demonstrate increased protection from mortality, reduced viral burden and liver disease, and greatly extended survival times as compared to treatments where drugs were administered alone. Our data indicate that combination therapy results in synergistic activity that may slow down the progression of the disease and decrease fatality rates associated with severe arenaviral infections in humans. Further, combination therapy reduces the effective dosage of ribavirin, which would serve to limit its toxicity.

Acute Disease↗
PubMed1988

Construction of a recombinant vaccinia virus expressing the Lassa virus glycoprotein gene and protection of guinea pigs from a lethal Lassa virus infection.

A cloned cDNA (1.65 kb) containing the complete glycoprotein gene of the Josiah strain of Lassa virus was inserted into the thymidine kinase (TK) gene of the New York Board of Health (WYETH) strain of vaccinia virus. The Lassa virus glycoprotein precursor, GPC, and the posttranslational cleavage products, G1 and G2, were shown by Western blot analysis to be properly expressed in cells infected with the recombinant virus. Northern blot hybridization of total cytoplasmic RNA extracted from recombinant virus infected cells demonstrated the presence of RNA transcripts of appropriate size considering the site of transcription initiation from the vaccinia P7.5 promoter, the size of the Lassa glycoprotein gene, and the presumed location of the transcription terminator in the vaccinia thymidine kinase gene. All guinea pigs vaccinated with the recombinant virus survived a lethal challenge infection with Lassa virus, whereas 80% of control animals died. The vaccinated guinea pigs did, however, develop transient, low-grade, fevers and detectable viremias following infection with Lassa virus, indicating that protection was not complete.

Animals↗
PubMed1981

Preparation of polyvalent viral immunofluorescent intracellular antigens and use in human serosurveys.

A method is described for preparation of polyvalent antigens for use in rapid screening for immunofluorescent antibodies to Lassa, Marburg, and Ebola viruses. The technique uses mixtures of specifically infected Vero cells placed on Teflon-templated microscopy slides. It was found to be as sensitive as the use of monovalent antigens for detection and quantitation of antibodies to these highly hazardous human pathogens.

Animals↗
PubMed1978

[Recent Lassa, Marbourg and Ebola viruses in African tropical viruses. I. Semiology--physiopathology--diagnosis--treatment (author's transl)].

Three new viruses have been identified in Africa during the present decade. They may cause sporadic cases or limited outbreaks, and they are probably endemic in areas which are still ill-defined. Severe forms of infection lead to the haemorrhagic syndrome or to hypovolemic shock, the physiopathology of which is being studied. The case-fatality ratio of severe cases is between 30 and 85 per cent. Nosocomial outbreaks have been observed, but they can be avoided if appropriate barrier nursing measures are carried out for the treatment of patients or adequate protection measures for sampling and examination of laboratory specimens. As such cases may be transferred outside the endemic zone, this implies that countries receiving travellers from Africa should have hospitals with specialized units for strict isolation and treatment of these patients.

Africa↗
PubMed1978

Viral infections in travellers from tropical Africa.

Examination of sera from 86 travellers to Britain from tropical Africa disclosed evidence of past infection with 10 identifiable viruses, of which the most important were O'nyong-nyong, dengue, chikungunya, and Ntaya. The findings indicate that infection with O'nyong-nyong may be acquired sporadically in Nigeria, Ghana, and Sierra Leone, where it has not previously been identified. Chikungunya infection had not been recorded in West Africa other than Nigeria and Senegal. Patients from Sierra Leone and contiguous Liberia had antibodies to this infection. An outbread of dengue fever in the Seychelles in early 1977 was confirmed. Ntaya virus, though known in Uganda, Cameroon, and Zaire, appears also to be transmitted in Kenya, Nigeria, and Zambia. Clinical studies indicated that chikungunya infection may present with alimentary features, possibly with jaundice. The clinical features of Ntaya infection may include kizarre neurological manifestations in addition to fever. The absence of Lassa antibodies among these travellers suggested that this infection is not a common hazard among such persons.

Adult↗
PubMed1983

Detection of viral antigens in formalin-fixed specimens by enzyme treatment.

Enzyme treatment (protease or trypsin) was applied to formalin-fixed paraffin-embedded materials and virus-infected cultured cells to detect viral antigens by immunofluorescence. The viral antigens were demonstrated in several organs of autopsy or biopsy cases of which diagnoses had been established by immunofluorescence or virus isolation using frozen materials, or suspected on the basis of serology and/or histopathological findings. These included herpes simplex, varicella-zoster, cytomegalo, subacute sclerosing panencephalitis, progressive multifocal leukoencephalopathy, Japanese B encephalitis, measles, acute hemorrhagic conjunctivitis, Lassa and Korean hemorrhagic fever. Antigen could be recovered also in virus-infected cells (herpes simplex, measles, Lassa, Ebola, Marburg, Rift Valley, Congo and Korean Hemorrhagic fever) by enzyme treatment after periods of formalin fixation of four weeks and storage of three months. In herpes simplex virus-infected mouse brain, antigen was detected after fixation for three months in formalin.

Adolescent↗
PubMed2001

Risks and prevention of nosocomial transmission of rare zoonotic diseases.

Americans are increasingly exposed to exotic zoonotic diseases through travel, contact with exotic pets, occupational exposure, and leisure pursuits. Appropriate isolation precautions are required to prevent nosocomial transmission of rare zoonotic diseases for which person-to-person transmission has been documented. This minireview provides guidelines for the isolation of patients and management of staff exposed to the following infectious diseases with documented person-to-person transmission: Andes hantavirus disease, anthrax, B virus infection, hemorrhagic fevers (due to Ebola, Marburg, Lassa, Crimean-Congo hemorrhagic fever, Argentine hemorrhagic fever, and Bolivian hemorrhagic fever viruses), monkeypox, plague, Q fever, and rabies. Several of these infections may also be encountered as bioterrorism hazards (i.e., anthrax, hemorrhagic fever viruses, plague, and Q fever). Adherence to recommended isolation precautions will allow for proper patient care while protecting the health care workers who provide care to patients with known or suspected zoonotic infections capable of nosocomial transmission.

Animals↗
PubMed2003

Arenavirus-mediated liver pathology: acute lymphocytic choriomeningitis virus infection of rhesus macaques is characterized by high-level interleukin-6 expression and hepatocyte proliferation.

Lymphocytic choriomeningitis virus (LCMV) and Lassa virus can cause hemorrhagic fever and liver disease in primates. The WE strain of LCMV (LCMV-WE) causes a fatal Lassa fever-like disease in rhesus macaques and provides a model for arenavirus pathogenesis in humans. LCMV-WE delivered intravenously or intragastrically to rhesus macaques targets hepatocytes and induces high levels of liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis factor receptors (sTNFRI and -II) in plasma during acute infection. Proinflammatory cytokines TNF-alpha and IL-1beta were not detected in plasma of infected animals, but increased plasma gamma interferon was noted in fatally infected animals. Immunohistochemistry of acute liver biopsies revealed that 25 to 40% of nuclei were positive for proliferation antigen Ki-67. The increases in IL-6, sIL-6R, sTNFR, and proliferation antigen that we observe are similar to the profile of incipient liver regeneration after surgical or toxic injury (N. Fausto, Am. J. Physiol. 277:G917-G921, 1999). Although IL-6 was not directly induced by virus infection in vitro, peripheral blood mononuclear cells from acutely infected monkeys produced higher levels of IL-6 upon lipopolysaccharide stimulation than did healthy controls. Our data confirm that acute infection is associated with weak inflammatory responses in tissues and initiates a program of liver regeneration in primates.

Alanine Transaminase↗
PubMed1999

Lassa and Mopeia virus replication in human monocytes/macrophages and in endothelial cells: different effects on IL-8 and TNF-alpha gene expression.

Cells of the mononuclear and endothelial lineages are targets for viruses which cause hemorrhagic fevers (HF) such as the filoviruses Marburg and Ebola, and the arenaviruses Lassa and Junin. A recent model of Marburg HF pathogenesis proposes that virus directly causes endothelial cell damage and macrophage release of TNF-alpha which increases the permeability of endothelial monolayers [Feldmann et al. , 1996]. We show that Lassa virus replicates in human monocytes/macrophages and endothelial cells without damaging them. Human endothelial cells (HUVEC) are highly susceptible to infection by both Lassa and Mopeia (a non-pathogenic Lassa-related arenavirus). Whereas monocytes must differentiate into macrophages before supporting even low level production of these viruses, the virus yields in the culture medium of infected HUVEC cells reach more than 7 log10 PFU/ml without cellular damage. In contrast to filovirus, Lassa virus replication in monocytes/macrophages fails to stimulate TNF-alpha gene expression and even down-regulates LPS-stimulated TNF-alpha mRNA synthesis. The expression of IL-8, a prototypic proinflammatory CXC chemokine, was also suppressed in Lassa virus infected monocytes/macrophages and HUVEC on both the protein and mRNA levels. This contrasts with Mopeia virus infection of HUVEC in which neither IL-8 mRNA nor protein are reduced. The cumulative down-regulation of TNF-alpha and IL-8 expression could explain the absence of inflammatory and effective immune responses in severe cases of Lassa HF.

Arenaviridae↗