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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 307 records · Page 17Linked to original sources
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A survey for antibodies to Lassa virus among health workers in Nigeria.

A study was conducted among 552 health workers at 6 health facilities in Nigeria. Lassa virus immunoglobulin (Ig) G antibody was detected in 12.3%, using an enzyme-linked immunosorbent assay. Antibody prevalence in the 6 health centres ranged from 1.2% to 27.3%. Prevalences were higher in primary and secondary health facilities than in tertiary centres. Seroprevalences ranged from 1.7% to 23.7% among different occupational groups of health workers; the highest observed antibody prevalence was among ward aids. Lassa virus IgM antibody, indicating recent infection, was present in 6 of the health workers, 5 of whom were ward aids and one was a nurse. All of the health workers with specific IgM came from a single facility in Lafia, sampled during an outbreak of Lassa fever.

Antibodies, Viral↗
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Virologic investigation of a case of suspected haemorrhagic fever.

After travelling in subSaharan Africa, an area known for sporadic cases of Marburg virus infection, a young Swedish man presented with a classical picture of severe viral haemorrhagic fever complicated by disseminated intravascular coagulation and septicaemia. Serum samples examined by electron microscopy revealed particles of a size compatible with filovirions. Indirect fluorescent antibody tests indicated transient seroconversion to Marburg virus. In lymphocyte transformation assays of cells isolated from the patient 11 months after the onset of acute disease, Marburg viral antigen was able to stimulate lymphocyte proliferation 3.9-fold; however, exhaustive attempts to isolate virus from acute phase blood cultured in vitro or in vivo from guinea pigs and monkeys failed. Data suggest that this patient may have been infected with a filovirus. This case demonstrates the difficulties that may occur in laboratory diagnosis of viral haemorrhagic fevers.

Adult↗
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Isolation of the Rift Valley fever virus by inoculation into Aedes pseudoscutellaris cells: comparison with other diagnostic methods.

The Rift Valley fever epidemic, which arose in the south of Mauritania beginning on October 15, 1987, enabled a comparative study of different diagnostic methods among humans. During the first two weeks of the epidemic, four parallel methods were used: inoculation into Aedes pseudoscutellaris cells, inoculation intracerebrally into suckling mice, tests by immunocapture of the circulating antigen and detection of type IgM gammaglobulins. Of 370 examined sera, 181 showed at least one marker of recent infection. Inoculation into A. pseudoscutellaris cells was by far the most sensitive and easiest method to use. Detection of the antigen by immunocapture was also a useful technique, since it allowed quick aetiological diagnosis or examination of sera conserved under poor conditions. However, its sensitivity was weak, as it could only detect 26% of positive cases. Vero cells used on a limited scale, in this particular case seemed less sensitive than A. pseudoscutellaris cells. Of a total of 991 sera, 221 diagnoses were reported by discovery of the virus and 271 by detection of specific IgM. In every case, A. pseudoscutellaris cells seemed most appropriate as the system of reference.

Aedes↗
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Assessment of an rDNA probe filter hybridization assay for the detection of Rift Valley fever virus RNA in human serum samples from the Mauritanian epidemic.

The Rift Valley fever virus (RVFV) epidemic that occurred in southern Mauritania during the 1987 rainy season provided a unique opportunity to test and evaluate a recently developed, M-segment-specific, nucleic acid filter hybridization assay on a large collection of infected human serum samples. It afforded the opportunity to compare the procedure with two other methods for detecting virus: virus isolation and antigen detection by ELISA. The filter hybridization procedure employed a polyethylene-glycol-precipitation and proteinase-K-digestion sample treatment step developed specifically for preparing serum samples for hybridization. The procedure was less sensitive for detecting RVFV in the Mauritanian human viremic samples than in sera from experimentally infected monkeys used to evaluate this procedure. It was also less sensitive than an antigen detection procedure used to test the Mauritanian samples. However, we were able to detect virus RNA in a significant proportion of the virus-isolation-positive samples. Advances in sample preparation, labelling and detection procedures, and hybridization methods will improve the sensitivity, precision and ease of use of this assay and increase its value as a diagnostic tool.

Antibodies, Viral↗
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Rapid diagnosis of Rift Valley fever: a comparison of methods for the direct detection of viral antigen in human sera.

Human sera collected during the 1987 Rift Valley fever (RVF) epidemic in the Senegal River basin were analysed using three enzyme immunoassays to establish the best method for rapid diagnosis of RVF. A biotin-avidin-enhanced antigen detection method utilizing monoclonal antibodies proved most sensitive. Eighty-two viremic human sera were tested, and this assay detected antigen in 29.3% of the samples.

Africa, Western↗
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Rift Valley fever among domestic animals in the recent West African outbreak.

Severe haemorrhagic disease among the human population of the Senegal River Basin brought the Rift Valley fever virus (RVFV) outbreak of 1987 to the attention of science. As in previous RVFV outbreaks, local herdsmen reported a high incidence of abortion and disease in their livestock. Serum samples were obtained from domestic animal populations from areas near Rosso, the best studied focus of human infection, as well as other areas distant from known human disease. Among animals from the area of high incidence of human disease, antibody prevalence was as high as 85%, with approximately 80% of the sera positive for both RVFV IgG- and viral-specific IgM antibodies. In contrast, human populations in the same area had lower RVFV antibody prevalences, 40% or less, with 90% also being IgM-positive. Sera from livestock in coastal areas 280 km south of the epidemic area were negative for RVFV antibodies. Thus, the detection of RVFV specific IgG and IgM antibodies provided evidence of recent disease activity without the requirement to establish pre-disease antibody levels in populations or individuals and without viral isolation. Subsequently, detection of modest levels of IgG and IgM in the Ferlo region, 130 km south of the Senegal River flood plain, established that RVFV transmission also occurred in another area of the basin. Similar serological testing of domestic ungulates in The Gambia, 340 km south of Rosso, demonstrated antibody prevalence consistent with a lower level of recent transmission of RVFV, i.e., 24% IgG-positive with 6% of the positive sera also having RVFV-specific IgM.

Animals↗
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Comparison of in vitro and in vivo systems for propagation of Rift Valley fever virus from clinical specimens.

Several cell cultures and animals were compared for their relative sensitivity as primary isolation systems for Rift Valley fever virus (RVFV) and to determine if virulence characteristics of the isolates were altered in these systems. Eleven human sera from known cases of Rift Valley fever (RVF) were obtained from the 1987 epidemic in Mauritania and served as the source of virus for these studies. Sera were inoculated directly into cell cultures (Vero, C6/36 and DBS-FRhL-2) and animals (ICR suckling mice, Lak:LVG(SYR) hamsters and WF rats) concurrently. The cell lines provided a quick method to propagate, quantitate and identify these specimens without prior adaption. The isolates were highly virulent for suckling mice and hamsters, but not for WF rats, even after cell culture passage, which indicated that the Mauritanian isolates more closely resembled those strains from sub-Saharan Africa than those from the 1977-78 Egyptian epidemic.

Aedes↗
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Rift Valley fever infection of rhesus monkeys: implications for rapid diagnosis of human disease.

Rhesus monkeys inoculated with Rift Valley fever (RVF) virus provide a model in which serial observations of serum viral antigen and antibodies can be made. In 9 non-fatal and 3 fatal infections, either antigen or IgM enzyme-linked immunosorbent assay (ELISA) antibodies were detected in every serum sample during the acute phase. Furthermore, viral nucleic acid could be detected by filter hybridization in most samples taken on days 1 to 3. Circulation of significant quantities of viral RNA provides an additional approach to the diagnosis and study of RVF.

Animals↗
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Isolation of Rift Valley fever virus from human peripheral blood mononuclear cells: Mauritanian epidemic.

During the Mauritanian Rift Valley fever (RVF) epidemic of 1987, peripheral blood mononuclear cells (PBMC) were studied from 78 sick patients. RVF virus (RVFV) was isolated in 5 cases, on Aedes pseudoscutellaris AP61, from both PBMC and serum. Among the 78 cases studied, RVF was proven in 19 cases (24.3%) by specific IgM detection, and in 12 cases (15.3%) by virus isolation from serum, of which 3 also exhibited anti-RVF IgM. Among the 5 PBMC-positive RVFV cases, 2 strains were isolated in the presence of specific IgM from patients presenting with neurologic signs. These observations raised the question as to the role of specific IgM in cellular infection, and suggest that, in certain cases, mononuclear cells may promote RVFV dissemination into brain cells. Further investigations need to be undertaken to determine the RVFV receptor expressed on PBMC membranes.

Antibodies, Viral↗
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Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted.

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.

Animals↗
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Actions of complement on Junin virus.

Fresh sera from normal rhesus monkeys, guinea pigs, and rabbits inactivated 90%-99% of the infectivity of Vero cell-passaged, attenuated strains of Junin virus (JV) within 60 minutes. Selective depletion studies showed that inactivation occurred by the classical complement pathway. Complement had little effect on virulent JV strains. Adsorption of the fresh sera with JV-infected Vero cells showed that inactivation was not mediated by low levels of antibodies in normal sera. The cells used for propagation of the virus affected inactivation: virus passaged in Vero cells (a continuous African green monkey kidney line) was more susceptible than virus passaged in FRhL-2 cells (a diploid strain derived from fetal rhesus monkey lung). Complement was important for in vitro neutralization of virulent JV strains by immune sera but was unnecessary for neutralization of attenuated strains. Thus, complement may be important in host resistance to Argentine hemorrhagic fever in two ways: first, complement activation may contribute to the attenuated phenotype of some strains; and second, complement may be necessary for efficient neutralization of virulent strains.

Animals↗
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Hemostatic derangement produced by Rift Valley fever virus in rhesus monkeys.

Rift Valley fever (RVF) is an important cause of disease in animals and humans in sub-Saharan Africa. In a small percentage of human cases, the disease is complicated by hemorrhage, which often is associated with a fatal outcome. Inoculation of rhesus monkeys with the Zagazig Hospital strain of RVF virus produced a clinical picture similar to illness in humans. Ten of 17 monkeys developed clinical evidence of hemostatic impairment. When coagulation tests were performed, this group of monkeys had significant abnormalities, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the remaining seven monkeys-whose only sign of illness was transient fever-and, in general, they paralleled the level of viremia and the degree of elevation in levels of serum hepatic enzymes. Autopsy of the three monkeys with severe disease revealed hepatic necrosis.

Animals↗
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Prevention of Rift Valley fever in rhesus monkeys with interferon-alpha.

Prophylactic and therapeutic efficacy of recombinant leukocyte A interferon (rIFN-alpha A) and Sendai virus-induced human leukocyte interferon (HuIFN-alpha) administered intramuscularly to Rift Valley fever virus (RVFV)-infected rhesus monkeys was studied. Clinical, virologic, immunologic, and hemostatic parameters were monitored. Five daily inoculations of 5 X 10(5) units of either interferon product per kilogram of body weight, initiated 24 hours before or 6 hours after RVFV infection, prevented or greatly suppressed viremia. No clinical signs of disease or laboratory evidence of impaired hemostasis was observed. Serum neutralizing antibody to RVFV was detected within 6 days of virus inoculation. Prophylactic administration of 5 X 10(4) or 5 X 10(3) units of rIFN-alpha A per kilogram also limited viremia, hepatocellular damage, and hemostatic derangement. Untreated, RVFV-infected, control monkeys developed high-titered viremia, clinical disease, and impaired hemostasis. These data suggest that rIFN-alpha A and HuIFN-alpha are effective in protecting RVFV-infected rhesus monkeys from viremia and hepatocellular damage and may be beneficial in human RVF infection.

Animals↗