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PubMed1992

Inactivated Lassa virus elicits a non protective immune response in rhesus monkeys.

We attempted to protect three rhesus monkeys from Lassa fever by vaccination with a preparation of purified whole Lassa virus which had been inactivated by gamma irradiation. The vaccinated monkeys developed antibodies against the three major viral proteins of Lassa virus demonstrated by radioimmunoprecipitation. When the three vaccinated monkeys and two unvaccinated control monkeys were challenged all five became severely ill and died. Prior to death a secondary, high-titer antibody response to Lassa virus was observed in the three vaccinated monkeys, whereas the two unvaccinated monkeys developed a primary, low-titer antibody response. Though titers of Lassa virus in serum reached peak levels earlier following challenge in the non vaccinated, at the time of death serum and organ virus titers did not differ significantly. Changes in platelet aggregation, leukocyte counts, and liver enzymes, abnormalities of which have been associated with severity of Lassa fever, were found to be comparable in the two groups. The humoral antibody response measured in these animals following vaccination, although of the same magnitude as found in humans recovered from Lassa fever, was insufficient to protect the animals from this fatal disease. Evidence is now accumulating that the cell-mediated immune response must be activated in order to protect against challenge with arenaviruses.

Animals↗

PubMed1992

Current progress towards vaccines for arenavirus-caused diseases.

The arenaviruses are primarily viruses of rodents, but some members of the group cause severe disease (Argentine and Bolivian haemorrhagic fevers and Lassa fever) when transmitted to humans in the specific areas of the world where they are enzootic. Current research of relevance to the provision of vaccines against these diseases, which highlights many of the problems encountered generally in the development of vaccines, is reviewed here. Although one of the classical approaches to vaccine production, the use of inactivated preparations of virus of varying degrees of purity, has produced no results of promise, attenuation of a virulent strain of Junin virus by passage in cultured cells has yielded a vaccine strain currently being tested for efficacy in protecting against Argentine haemorrhagic fever in the human population at risk. The experimental evidence for protection in animal model systems by related, apparently non-pathogenic, viruses and by recombinant vaccinia viruses expressing arenavirus proteins is discussed, together with some of the potential difficulties of these approaches.

Animals↗

PubMed1987

Viral diseases involving the liver.

Even though HAV, HBV and HNANB viruses are responsible for most of the viral hepatitis cases, many other viruses have been reported to cause hepatic injury. These viruses may involve the liver, either as part of a systemic illness (e.g. EBV, CMV, HSV) or as the primary target organ (e.g. yellow fever virus, Lassa fever virus, Ebola virus). Clinically overt hepatocellular dysfunction is rare in such viral infections. Biochemical disturbance of hepatic functions shown, for example, by rises in AST and ALT, is a frequent event and indicates hepatic damage. Morphological changes of the liver include varying degrees of hepatic necrosis with a paucity of inflammatory activities. Intranuclear or cytoplasmic inclusion bodies may be characteristic findings in these diseases. Laboratory diagnosis depends upon serology and liver histology. Treatment is still largely supportive in most of these diseases, although recent trials of antiviral agents show promise against some viruses. Chronic sequelae, such as cirrhosis or hepatocellular cancer, are not encountered. More work is needed to elucidate the pathogenesis of hepatic injury in these illnesses.

Hemorrhagic Fevers, Viral↗

PubMedDate not supplied

[Viral haemorrhagic fevers--evolution of the epidemic potential].

In this review modern data on dangerous and particularly dangerous viral haemorrhagic fevers caused by a group of viruses belonging to the families of phylo-, arena-, flavi-, bunya- and togaviruses are presented. Morbidity rates and epidemics caused by Marburg virus, Ebola fever virus, Lassa fever virus, Argentinian and Bolivian haemorrhagic fever viruses, dengue haemorrhagic fever virus, Crimean haemorrhagic fever virus, Hantaviruses are analyzed. Mechanisms of the evolution of the epidemic manifestation of these infections are considered. The importance of the development of tools and methods of diagnosis, rapid prevention and treatment of exotic haemorrhagic fevers is emphasized.

Disease Outbreaks↗

PubMed2005

[Countermeasure against viral hemorrhagic fever at the border in Japan].

Human have struggled against many infectious diseases such as cholera, plague, dysentery and yellow fever for a long time. And we have spent a lot of energy to control these infectious diseases and developed various tool for them. One of these efforts was Quarantine system that was established in 14th century in Europe. But during recent days, we are suffering from newly emerged diseases. These new infectious diseases are zoonosis and most of them are serious and highly infectious. Viral hemorrhagic fever such as Ebola hemorrhagic fever, Marburg hemorrhagic fever and Lassa fever are typical these emerging serious diseases, and these outbreak always have occurred in Africa and neighboring countries. Fortunately we have never experienced any case, but as these diseases are so serious, we are so nervous diseases entering in Japan. Against these serious diseases, in Japan, Quarantine Station are doing screening examination at airport and port by questionnaire and measuring body temperature, because these viral hemorrhagic fever patients show high fever. If people were suspected viral hemorrhagic fever at Quarantine Station at the border, they will be leaded to hospital for further examination and treatment as soon as possible.

Animals↗

PubMed1982

Experimental infection of rhesus monkeys with Lassa virus and a closely related arenavirus, Mozambique virus.

As a model for the pathogenesis of Lassa fever in humans, nine rhesus monkeys were inoculated with Lassa virus. Three monkeys had had a previous asymptomatic experimental infection with Mozambique virus, a closely related arenavirus; these monkeys were protected from illness and viremia and manifested only mild pathologic lesions. The other animals developed severe disease and viremia. At necropsy, hepatocellular necrosis, interstitial pneumonia, a unique pulmonary arteritis, adrenal gland necrosis, encephalitis, and uveitis were prominent pathologic lesions which correlated with the organ titers of virus. One animal infected with Lassa virus developed prolonged viremia, a typical immune response, and sudden onset of lower limb paralysis after recovery; at necropsy chronic proliferative arteritis of the spinal cord, brain, and heart was evident. Similarities and differences in the pathologic lesions in this model and Lassa fever in humans indicate that care must be taken in interpreting the results of experiments concerning immune prophylaxis, pathogenesis, and treatment in rhesus monkeys.

Animals↗

PubMed2000

[Is MBSL-level ward needed for the treatment of viral hemorrhagic diseases and pest?].

The recently revised Japanese Law on Infectious Diseases designates pest, Lassa, Marburg, Ebola and Crimean-Congo hemorrhagic diseases should be treated in an MBSL-level ward and that it should be constructed in each prefecture. However, pest can be treated with several antibiotics easily in an ordinary infectious disease ward. Lassa, Marburg and Ebola virus diseases are endemic in tropical Africa and only Lassa fever was imported into Japan in 1987. The probability of its importation to each prefecture is calculated on an assumption that a Lassa fever patient may be imported into Japan once in 10 years. Its incidence was calculated in comparison with the incidence of imported malaria from the African continent. Its probability P is calculated as follows. Corrected number of imported malaria patients from the African continent per year for each prefecture CN is divided by 445. 445 is the number of imported malaria patients from the African continent in ten years. Finally 445/CN is the number of years needed for each prefecture to import one case of Lassa fever. The results indicate that it takes 37 years for Metropolitan Tokyo where the largest number of malaria patients are imported annually. Other prefectures need more than 100 to 10,000 years, with an average of 1,017 years, for importation of one patient of Lassa fever. It is concluded that construction of an MBSL-level ward in each prefecture is unnecessary. The reports that the above mentioned viral hemorrhagic diseases can be treated safely in the ordinary infectious disease ward should be carefully reviewed.

Hemorrhagic Fevers, Viral↗

PubMed1984

Detection of Lassa virus antigens and Lassa virus-specific immunoglobulins G and M by enzyme-linked immunosorbent assay.

Rapid diagnosis of Lassa fever is desirable for the timely therapeutic intervention and implementation of strict quarantine procedures both in West Africa field hospitals where the disease is endemic and at international crossroads. An enzyme-linked immunosorbent assay (ELISA) to measure Lassa virus antigens in viremic sera was developed in which experimentally infected monkeys were used as a model for the human disease. In this test, Lassa virus antigens in test sera were captured in wells of microtiter plates by monkey anti-Lassa virus immunoglobulin. Guinea pig anti-Lassa virus immunoglobulin was then added, and binding of specific immunoglobulin was quantitated by the addition of rabbit anti-guinea pig immunoglobulin followed by alkaline phosphatase-labeled anti-rabbit immunoglobulin. This test detected viremia titers as low as 2.1 log10 PFU/ml in experimentally infected monkey sera, a titer often exceeded in patients with Lassa fever. Inactivation of infectious virus by beta-propiolactone or gamma-irradiation did not diminish reactivity. Antigen-ELISA concentrations increased with infectivity for the first 10 days after infection but then declined while infectivity titers remained high, suggesting that the presence of humoral antibody in viremic sera diminishes the sensitivity of the antigen ELISA. Lassa virus-specific immunoglobulin M (IgM) titers measured in an IgM capture ELISA were detectable within 10 days of infection and peaked after 36 days but remained detectable for 1.5 years. The Lassa virus-specific IgG ELISA response was slightly delayed, peaking on day 73 but declining only slightly thereafter. These studies in a realistic primate model suggest that the antigen detection ELISA or the IgM capture ELISA described, in which beta-propiolactone-inactivated sera are used, should be useful for the rapid diagnosis of human Lassa fever.

Animals↗

PubMed2004

Mucosal arenavirus infection of primates can protect them from lethal hemorrhagic fever.

Arenaviruses are transmitted from rodents to human beings by blood or mucosal exposure. The most devastating arenavirus in terms of human disease is Lassa fever virus, causing up to 300,000 annual infections in West Africa. We used a model for Lassa fever in which Rhesus macaques were infected with a related virus, lymphocytic choriomeningitis virus (LCMV). Our goals were to determine the outcome of infection after mucosal inoculation and later lethal challenge, to characterize protective immune responses, and to test cross-protection between a virulent (LCMV-WE) and an avirulent (LCMV-ARM) strain of virus. Although intravenous infections in the monkey model were uniformly lethal, intragastric infections recapitulated the spectrum of clinical outcomes seen in human exposure to Lassa fever virus: death, recovery from disease, and most often, subclinical infection. Plaque neutralization, ELISA, lymphocyte proliferation, and chromium-release assays were used to monitor humoral and cellular immune responses. Cross protection between the two strains was observed. The three out of seven monkeys that experienced protection were also the three with the strongest cell-mediated immunity.

Animals↗

PubMedDate not supplied

Mucosal immunization with Salmonella typhimurium expressing Lassa virus nucleocapsid protein cross-protects mice from lethal challenge with lymphocytic choriomeningitis virus.

OBJECTIVES: Lassa fever virus (LAS) is transmitted to man by rodent carriers and is fatal in a third of untreated cases. Our goal is to provide immune protection from Lassa fever by mucosal vaccination. STUDY DESIGN/METHODS: Mice were vaccinated intragastrically with control vectors or with vectors (vaccinia or Salmonella) expressing LAS nucleocapsid protein (NP). Mice were challenged intracranially with a lethal dose of the related arenavirus, lymphocytic choriomeningitis virus (LCMV), as a measure of the vaccine's ability to elicit cross-protection. RESULTS: Salmonella and vaccinia vectors expressing LAS NP each protected a third of the mice from lethal challenge with LCMV. All mice vaccinated with a vector expressing LCMV NP were protected as expected. CONCLUSIONS: The LAS recombinant Salmonella vector is comparable to the LAS recombinant vaccinia vector in its ability to cross-protect mice from lethal challenge. Nucleocapsid protein is an inadequate immunogen on its own, but provides sufficient cross-protection to make it a useful component of a broadly reactive arenavirus vaccine.

Animals↗

PubMed1994

Cardiovascular and pulmonary responses to Pichinde virus infection in strain 13 guinea pigs.

In fatal human Lassa fever, severe hypotension, circulatory shock, and pulmonary edema develop as terminal events. We examined cardiovascular and respiratory functions in strain 13 guinea pigs infected with Pichinde virus, an animal model for studying human Lassa fever. Cardiovascular functions were studied in anesthetized and conscious guinea pigs, whereas pulmonary functions were measured only on animals under anesthesia. In anesthetized animals, cardiovascular disturbances were severe and progressive from postinoculation day (PID) 10. Cardiac output, measured by thermodilution, decreased 28 to 53% below baseline values from PID 10 to 12 and was accompanied by a gradual reduction of mean arterial blood pressure and heart rate. Although left ventricular systolic pressure decreased significantly, the left ventricular +dp/dtmax and -dp/dtmax decreased only slightly on PID 12. Similar depressed cardiovascular responses were observed in conscious animals infected with Pichinde virus. Changes included decreased cardiac output, heart rate, cardiac work, cardiac power, and stroke volume, as well as increased total peripheral resistance and prolonged mean transit time. We postulate that a global cardiovascular dysfunction with the involvement of right and left sides of the heart may be the main cause of irreversible circulatory deterioration and death during Pichinde virus infection in strain 13 guinea pigs.

Animals↗

PubMed1982

Pathogenesis of Lassa virus infection in guinea pigs.

A rodent model for human Lassa fever was developed which uses inbred (strain 13) and outbred (Hartley) guinea pigs. Strain 13 guinea pigs were uniformly susceptible to lethal infection by 2 or more PFU of Lassa virus strain Josiah. In contrast, no more than 30% of the Hartley guinea pigs died regardless of the virus dose. In lethally infected strain 13 guinea pigs, peak titers of virus (10(7) to 10(8) PFU) occurred in the spleen and lymph nodes at 8 to 9 days, in the salivary glands at 11 days, and in the lung at 14 to 16 days. Virus reached low titers (10(4) PFU) in the plasma and brain and intermediate titers in the liver, adrenal glands, kidney, pancreas, and heart. In moribund animals, the most consistent and severe histological lesion as an interstitial pneumonia. In contrast, the brain was only minimally involved. The immune response of lethally infected strain 13 guinea pigs, as measured by the indirect fluorescent antibody test, was detectable within 10 days of infection and was similar in timing and intensity to the fluorescent antibody test response of both lethally infected and surviving outbred animals. In contrast to the fluorescent antibody response, neutralizing antibody developed late in convalescence and was thus detected only in surviving outbred guinea pigs. The availability of a rodent model for human Lassa fever in uniformly susceptible strain 13 guinea pigs should facilitate detailed pathophysiological studies and efficacy testing of antiviral drugs, candidate vaccines, and immunotherapy regimens to develop control methods for this life-threatening disease in humans.

Animals↗

PubMed1996

Hunting of peridomestic rodents and consumption of their meat as possible risk factors for rodent-to-human transmission of Lassa virus in the Republic of Guinea.

In this population-based study, we correlated possible risk factors for rodent-to-human transmission of Lassa virus with markers of Lassa fever in two different regions of the Republic of Guinea (Prefectures of Pita and Gueckedou). Antibody prevalence was 2.6% (6 of 232) in Pita compared with 14.0% (105 of 751) in Gueckedou, with up to 35.0% seropositivity in selected villages of the higher prevalence area. We observed three major risk factors in Gueckedou favoring Lassa virus transmission: rodent infestation was much higher, food was more often stored uncovered and most strikingly, peridomestic rodents were hunted as a protein source by 91.5% of the population as opposed to 0% in Pita. To control for the confounding effects of differences in rodent infestation and food storage, rodent consumption was analyzed as a risk factor for transmission of Lassa virus comparing rodent consumers (RC) and nonconsumers (NC) in Gueckedou only: 14.6% of RC had Lassa virus antibodies versus 7.4% of NC (P = 0.1) and 23.0% of RC reported a history of a febrile illness with hearing loss (the most common sequel of Lassa fever) versus 6.1% of NC (P = 0.003).

Adolescent↗

PubMed2002

Management of viral haemorrhagic fever in the Netherlands.

Two cases of Lassa fever have been reported in the Netherlands since viral haemorrhagic fevers became notifiable diseases in 1978. In 1980, an expatriate from Burkina Faso who was not seriously ill was confirmed by laboratory tests after his discharge from hospital. The second case occurred in 2000: the patient died on the 11th day of admission to hospital. The problems we faced in the management of this case and the contact investigation--more than one hundred contacts - highlighted the need for national recommendations in the Netherlands.

Contact Tracing↗

PubMed1997

[Viral haemorrhagic fever].

Viral haemorrhagic fever denotes various kinds of febrile illness caused by certain viruses which often presents with bleeding tendency and occasionally shock. Out of these, the four maladies, Lassa fever, Ebola haemorrhagic fever, Marburg haemorrhagic fever and Crimean-Congo haemorrhagic fever which are endemically present in Africa or eastern Europe, are known to be such diseases with high man-to-man communicability. These four haemorrhagic fevers are, therefore, designated as special conditions requiring isolation during the period when the infected patients are shedding the viruses, not only in Japan but also in many other countries. We have so far only one such case of Lassa fever who returned to Japan from Sierra Leone in 1987. Some haemorrhagic fevers including dengue (haemorrhagic) fever and hantavirus infections (e.g. haemorrhagic fever with renal syndrome) are not known to be man-to-man transmissible and requiring no isolation. We have a number of dengue and dengue haemorrhagic fevers here in Japan today among imported febrile cases from tropical or subtropical countries. Every physician should take viral haemorrhagic fevers into consideration as one of the possibilities in diagnosing patients returning from overseas travel.

Adult↗

PubMed1995

Pathology and immunohistochemistry of callitrichid hepatitis, an emerging disease of captive New World primates caused by lymphocytic choriomeningitis virus.

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.

Animals↗

PubMedDate not supplied

Imported viral haemorrhagic fever with a potential for person-to-person transmission: review and recommendations for initial management of a suspected case in Belgium.

Viral haemorrhagic fevers are caused by a wide range of viruses. There are 4 types of viruses well known to spread from person to person and able to cause nosocomial outbreaks with a high case fatality rate: an arenavirus (Lassa fever and more exceptionally the Junin and Machupo virus), a bunyavirus (Crimean-Congo haemorrhagic fever) and the Filoviridae (Ebola and Marburg viruses). So far there have been only a limited number of imported cases of viral haemorrhagic fever in industrialized countries. In recent years an increasing number of outbreaks of filovirus infections have occurred in Africa and in 2000 5 cases of Lassa fever were brought from Sierra Leone to Europe. Therefore European physicians should consider the possibility of a viral haemorrhagic fever in an acutely ill patient just returning from Africa or South-America with fever for which there is no obvious cause. Such patients should be questioned for risk factors for viral haemorrhagic fever. Using universal precautions for handling blood and body fluids and barrier nursing techniques there is little risk that if a patient with viral haemorrhagic fever arrives in Belgium there will be secondary cases.

Belgium↗

PubMed2002

Management of viral haemorrhagic fevers in Switzerland.

Over the past years, there have been very few imported cases of VHF in Switzerland: one confirmed and four suspected cases of Ebola fever in Basel in 1994, two suspected cases of Ebola and Lassa fevers in Lausanne in 2000, and in the same year, six suspected cases of Lassa fever in Geneva. Given the considerable diversity in the management of patients with suspected or confirmed VHF, national guidelines are needed, as well as the establishment of a national reference centre.

Communicable Disease Control↗