Pathogenesis of viral hemorrhagic fevers

Rift Valley fever and Lassa fever contrasted.

C. J. Peters, C. T. Liu, G. W. Anderson, J. C. Morrill, P. B. Jahrling

Research output: Contribution to journalArticle

81 Citations (Scopus)

Abstract

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.

Original languageEnglish (US)
JournalReviews of Infectious Diseases
Volume11 Suppl 4
StatePublished - May 1989
Externally publishedYes

Fingerprint

Lassa Fever
Viral Hemorrhagic Fevers
Rift Valley Fever
Lassa virus
Rift Valley fever virus
Disseminated Intravascular Coagulation
Interferons
Pichinde virus
Phlebovirus
Arenavirus
Viruses
Contractile Proteins
Leukotrienes
RNA Viruses
Myocarditis
Virus Diseases
Pulmonary Edema
Infection
Neutralizing Antibodies
Cell Communication

ASJC Scopus subject areas

  • Microbiology (medical)

Cite this

Peters, C. J., Liu, C. T., Anderson, G. W., Morrill, J. C., & Jahrling, P. B. (1989). Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted. Reviews of Infectious Diseases, 11 Suppl 4.

Pathogenesis of viral hemorrhagic fevers : Rift Valley fever and Lassa fever contrasted. / Peters, C. J.; Liu, C. T.; Anderson, G. W.; Morrill, J. C.; Jahrling, P. B.

In: Reviews of Infectious Diseases, Vol. 11 Suppl 4, 05.1989.

Research output: Contribution to journalArticle

Peters, CJ, Liu, CT, Anderson, GW, Morrill, JC & Jahrling, PB 1989, 'Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted.', Reviews of Infectious Diseases, vol. 11 Suppl 4.
Peters CJ, Liu CT, Anderson GW, Morrill JC, Jahrling PB. Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted. Reviews of Infectious Diseases. 1989 May;11 Suppl 4.
Peters, C. J. ; Liu, C. T. ; Anderson, G. W. ; Morrill, J. C. ; Jahrling, P. B. / Pathogenesis of viral hemorrhagic fevers : Rift Valley fever and Lassa fever contrasted. In: Reviews of Infectious Diseases. 1989 ; Vol. 11 Suppl 4.
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