Monitoring of clinical and laboratory data in two cases of imported Lassa fever

Schmitz, Herbert; Köhler, Bernhard; Laue, Thomas M.; Drosten, Christian; Veldkamp, Peter; Günther, Stephan; Emmerich, Petra; Geisen, H. P.; Fleischer, K; Beersma, Matthias F. C.; Hoerauf, Achim

doi:10.1016/s1286-4579(01)01508-8

Cited by 119 publications

(111 citation statements)

References 36 publications

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“…The Z protein of LV may be responsible for the lack of cell activation as this protein has been reported to interact with certain host cell translation factors in the LCMV system (35). The lack of proinflammatory cytokine production by LV-infected DC and MP suggests that these cells may not directly be involved in the increase in permeability of the endothelium observed in LV infection, in contrast to previous suggestions (36). Nevertheless, we cannot exclude the possibility that factors other than those analyzed here are produced by infected APC.…”

Section: Discussioncontrasting

confidence: 76%

Lassa Virus Infection of Human Dendritic Cells and Macrophages Is Productive but Fails to Activate Cells

Baize

Kaplon

Faure

et al. 2004

The Journal of Immunology

191

208

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Lassa fever is a hemorrhagic fever caused by Lassa virus (LV), an old-world Arenavirus. Little is known about the immune responses that occur during the disease, but protection seems to be linked to the induction of cellular responses specific for viral glycoproteins. Conversely, severe Lassa fever may be associated with immunosuppression. We studied the infection of human dendritic cells (DC) and macrophages (MP) by LV. Both these cell types are susceptible to LV infection. Viral nucleoprotein was detected in DC and MP, and high and moderate viral titers were obtained with culture supernatants of DC and MP, respectively. LV did not induce apoptosis in DC and MP. These cells were not activated by LV infection. No change was observed in the expression of surface molecules involved in activation, costimulation, adhesion, and Ag presentation following LV infection, or in the functional properties of DC. Inflammatory cytokine production was not detected at the mRNA or protein level after LV infection of DC and MP. Thus, MP, and particularly DC, are crucial targets for LV and are probably involved in the early replication of LV from the initial site of infection. The lack of activation and maturation of cells following infection may be associated with the immunosuppression observed in severe LV infection.

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Section: Discussioncontrasting

confidence: 76%

Lassa Virus Infection of Human Dendritic Cells and Macrophages Is Productive but Fails to Activate Cells

Baize

Kaplon

Faure

et al. 2004

The Journal of Immunology

191

208

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“…The drug ribavirin has been shown to be effective if it is administered early after infection (35). However, several recent cases of Lassa fever in Europe have demonstrated that even state-of-the-art intensive care cannot prevent a fatal outcome (42). In contrast to the highly pathogenic Lassa virus, the related lymphocytic choriomeningitis virus (LCMV), which is carried by Mus musculus, causes only a mild febrile illness and benign meningitis in humans.…”

Section: Lassa Virus Belongs To the Old World Complex Of The Familymentioning

confidence: 99%

Inhibition of Different Lassa Virus Strains by Alpha and Gamma Interferons and Comparison with a Less Pathogenic Arenavirus

Asper

Sternsdorf

Haß

et al. 2004

J Virol

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“…Because of their high mortality and the limited therapeutic repertoire available, hemorrhagic arenaviruses have been classified as Category A pathogens by the Centers for Disease Control and Prevention (5). Apart from the severe humanitarian burden in endemic regions, increased international air traffic has also led to the importation of arenaviral viral hemorrhagic fever cases into metropolitan areas around the globe (6,7).…”

mentioning

confidence: 99%