Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of arenavirus infection is considered separately for the haemorrhagic fever (HF) syndrome and for lymphocytic choriomeningitis (LCM) virus infection of rodents. Experimental models of HF have received only limited study, mainly because of the virulence of the causal agents. Two useful models (Junin virus in guinea-pigs and Machupo virus in rhesus monkeys) are now available and an attempt is made to delineate crucial questions for future studies, including the physiology of shock, disseminated intravascular coagulation, immune mediation of disease, efficacy of antibody in treatment, and relative utility of attenuated and inactivated vaccines. Immunobiologic problems currently under investigation in LCM virus infection include the mechanism of immune destruction of infected tissues, the H-2 restriction of in vitro T-cell-mediated lysis of infected target cells, the transient immunodepression that accompanies acute primary LCM virus infection, and the mechanism of T-cell-mediated clearance of virus from infected tissues following adoptive immunization of persistently infected carrier mice.
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PMID:Directions for future research on the pathogenesis of arenaviral infections. 108 29

The salient abnormalities of blood coagulation found in the acute phase of Argentine hemorrhagic fever (AHF) were thrombocytopenia, prolonged partial thromboplastin time activated with kaolin, low factor VIII:C activity concurrent with high levels of von Willebrand factor, and increased values of factor V. No evidence of disseminated intravascular coagulation (DIC) was observed. Therefore, the hemostatic abnormalities detected in patients with AHF could not be attributed to DIC. There was no correlation between severity of the disease and occurrence of impairment of coagulation. Complement activation was observed during the acute phase of AHF. There was reduction of total complement and C2 activity. Antigenic levels of C1q, C3, and C5 were low; level of C4 antigen was high. Degradation products of C3 and B were demonstrated before day 11. Experimental models of AHF were developed (guinea pigs, Callitrix jacchus). These models may be useful, but they reproduced only some of the features of blood coagulation and complement abnormalities described in human AHF.
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PMID:Hemostasis and the complement system in Argentine hemorrhagic fever. 266 12