Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response

J. C. Morrill, G. B. Jennings, A. J. Johnson, T. M. Cosgriff, P. H. Gibbs, C. J. Peters

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.

Original languageEnglish (US)
Pages (from-to)195-212
Number of pages18
JournalArchives of Virology
Volume110
Issue number3-4
DOIs
StatePublished - Sep 1990
Externally publishedYes

Fingerprint

Rift Valley Fever
Macaca mulatta
Interferons
Haplorhini
Rift Valley fever virus
Viremia
Infection
Vomiting
Serum
Skin
Epistaxis
Purpura
Disseminated Intravascular Coagulation
Macaca
Anorexia
Blood Coagulation
Virus Diseases
Transferases
Neutralizing Antibodies
Fever

ASJC Scopus subject areas

  • Applied Microbiology and Biotechnology
  • Genetics

Cite this

Morrill, J. C., Jennings, G. B., Johnson, A. J., Cosgriff, T. M., Gibbs, P. H., & Peters, C. J. (1990). Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response. Archives of Virology, 110(3-4), 195-212. https://doi.org/10.1007/BF01311288

Pathogenesis of Rift Valley fever in rhesus monkeys : role of interferon response. / Morrill, J. C.; Jennings, G. B.; Johnson, A. J.; Cosgriff, T. M.; Gibbs, P. H.; Peters, C. J.

In: Archives of Virology, Vol. 110, No. 3-4, 09.1990, p. 195-212.

Research output: Contribution to journalArticle

Morrill, JC, Jennings, GB, Johnson, AJ, Cosgriff, TM, Gibbs, PH & Peters, CJ 1990, 'Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response', Archives of Virology, vol. 110, no. 3-4, pp. 195-212. https://doi.org/10.1007/BF01311288
Morrill JC, Jennings GB, Johnson AJ, Cosgriff TM, Gibbs PH, Peters CJ. Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response. Archives of Virology. 1990 Sep;110(3-4):195-212. https://doi.org/10.1007/BF01311288
Morrill, J. C. ; Jennings, G. B. ; Johnson, A. J. ; Cosgriff, T. M. ; Gibbs, P. H. ; Peters, C. J. / Pathogenesis of Rift Valley fever in rhesus monkeys : role of interferon response. In: Archives of Virology. 1990 ; Vol. 110, No. 3-4. pp. 195-212.
@article{79a1db61bd88456ab3cc829f5c185f35,
title = "Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response",
abstract = "Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18{\%}) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.",
author = "Morrill, {J. C.} and Jennings, {G. B.} and Johnson, {A. J.} and Cosgriff, {T. M.} and Gibbs, {P. H.} and Peters, {C. J.}",
year = "1990",
month = "9",
doi = "10.1007/BF01311288",
language = "English (US)",
volume = "110",
pages = "195--212",
journal = "Archives of Virology",
issn = "0304-8608",
publisher = "Springer Wien",
number = "3-4",

}

TY - JOUR

T1 - Pathogenesis of Rift Valley fever in rhesus monkeys

T2 - role of interferon response

AU - Morrill, J. C.

AU - Jennings, G. B.

AU - Johnson, A. J.

AU - Cosgriff, T. M.

AU - Gibbs, P. H.

AU - Peters, C. J.

PY - 1990/9

Y1 - 1990/9

N2 - Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.

AB - Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.

UR - http://www.scopus.com/inward/record.url?scp=0025308252&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025308252&partnerID=8YFLogxK

U2 - 10.1007/BF01311288

DO - 10.1007/BF01311288

M3 - Article

C2 - 1690534

AN - SCOPUS:0025308252

VL - 110

SP - 195

EP - 212

JO - Archives of Virology

JF - Archives of Virology

SN - 0304-8608

IS - 3-4

ER -