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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 199 records · Page 11Linked to original sources
PubMed1992

A longitudinal study of Junin virus activity in the rodent reservoir of Argentine hemorrhagic fever.

We monitored Junin virus (JV) activity in rodent populations for 30 months at seven mark-recapture grids located in agricultural fields and adjacent roadsides and fence lines in endemic and nonendemic areas of Argentine hemorrhagic fever. Blood and oral swabs taken from rodents captured at five-week intervals were analyzed by enzyme-linked immunosorbent assay for JV antigen (Ag). Calomys laucha and C. musculinus were the most frequently captured rodents, making up 47% and 22% of captures, respectively. Of 41 Ag-positive captures, 37 were C. musculinus and four were C. laucha; 34 were from two trapping grids in the same locality. Antigen-positive Calomys were more frequently male (76%), and were found significantly more frequently among the oldest animals and the largest body mass classes. These patterns, combined with the greater mobility and higher frequencies of wounds among males than females, implicated horizontal transmission as the primary route of JV transmission between rodents. Seasonal maximum levels in JV prevalence (up to 25% of captured Ag-positive C. musculinus) occurred during periods of maximal population densities of Calomys. Spatial distribution of Ag-positive rodents reflected habitat preferences; most Ag-positive C. musculinus were captured from border habitats (roadsides and fence lines), and all Ag-positive C. laucha were captured in crop fields. These distinct, but previously undocumented, habitat preferences suggest that the disease in humans may be related to exposures to the primary reservoir species, C. musculinus, in border habitats rather than in crop fields.

Age Factors↗
PubMed1992

Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys.

Simian hemorrhagic fever (SHF) virus and a new strain of Ebola virus were isolated concurrently in recently imported cynomolgus monkeys (Macaca fascicularis) being maintained in a quarantine facility. Ebola virus had never been isolated in the U.S. previously and was presumed to be highly pathogenic for humans. A chronology of events including measures taken to address the public health concerns is presented. The clinicopathologic features of the disease were abrupt anorexia, splenomegaly, marked elevations of lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, with less prominent elevations of blood urea nitrogen, creatinine, and other serum chemistry parameters. Histologically, fibrin deposition, hemorrhage, and necrosis of lymphoid cells and reticular mononuclear phagocytes were present in the spleens of SHF and of Ebola virus-infected animals. Intravascular fibrin thrombi and hemorrhage were also present in the renal medulla and multifocally in the gastrointestinal tract. Necrosis of lymphoid and epithelial cells was occasionally noted in the gastrointestinal tract. The histopathologic findings considered specific for Ebola virus infection include hepatocellular necrosis, necrosis of the zona glomerulosa of the adrenal cortex, and interstitial pneumonia, all of which were generally associated with the presence of 1 to 4 mu intracytoplasmic amphophilic inclusion bodies. The disease spread within rooms despite discontinuation of all direct contact with animals, and droplet or aerosol transmission was suspected. Antibody to Ebola virus developed in animal handlers but no clinical disease was noted, suggesting a less virulent strain of virus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Increased platelet-activating factor (PAF) concentrations in hearts and lungs of Pichinde virus-infected guinea pigs.

Platelet-activating factor (PAF) has been implicated as a cause of cardiopulmonary disturbances in certain diseases. In the present study, concentrations of PAF in hearts, lungs, whole blood, and other organs of control and Pichinde virus-infected guinea pigs on post-inoculation days (PID) 10 and 14 were measured by radioimmunoassay. Results were further confirmed by bioassay after separation and purification with thin-layer chromatography. PAF concentration in the hearts and lungs of virus-infected animals increased significantly on PID 10 and 14, as compared with control levels. PAF level in the blood of infected guinea pigs also significantly increased on PID 14. There was little change of PAF levels in liver and kidney after viral inoculation. Increased PAF concentrations in both hearts and lungs of infected strain 13 guinea pigs suggest that this lipid mediator may play an important role in the development of cardiopulmonary disturbances.

Animals↗
PubMed1992

Filovirus contamination of cell cultures.

The filoviruses Marburg and Ebola comprise a newly recognized family of viruses. The first filovirus to be isolated was Marburg virus in 1967. This virus was imported in shipments of African green monkeys from Uganda and infected several cell-culture technicians, with serious illness resulting. The rarity of Marburg and Ebola virus transmission, decreasing use of imported African monkeys, and quarantine efforts have presumably been responsible for the lack of additional episodes until 1989, when a new filovirus related to Ebola was isolated from quarantined monkeys in Reston, Virginia. This virus was imported on multiple occasions from a Philippine supplier of cynomolgus macaques as a consequence of an epidemic of acute infections in the foreign holding facility. While quarantine procedures prevented the use of any of these animals in research and the three human infections that occurred were asymptomatic, this episode emphasizes that these little understood viruses have considerable potential for mischief. The finding of antibodies reacting with Ebola viruses in many biomedically important Old World primates, including colonized monkeys in the U.S., emphasizes the need for more research to understand the specificity of the antibodies, spectrum of filovirus strains in nature, potential hosts, and true distribution of the family. The filoviruses grow well in primary and established cell strains and cell lines, and cytopathogenic effects may be absent or require several days to be manifest, leading to the possibility of occult contamination. The known viruses are readily detected by polyclonal and monoclonal antibody staining of cells and by electron microscopy; nucleic acid probes exist to develop more sensitive techniques if warranted.

Animals↗
PubMed1991

Further evaluation of a mutagen-attenuated Rift Valley fever vaccine in sheep.

A previous study demonstrated that a mutagen-attenuated Rift Valley fever virus (RVFV) vaccine, RVF MP-12, was immunogenic and non-abortogenic when ewes, 90-110 days pregnant, were inoculated with 5 x 10(5) plaque-forming units (p.f.u.) of the virus strain. The ewes delivered live, healthy lambs that had no neutralizing antibody to RVFV until after they had ingested colostrum. To assess further the safety and protective capability of this candidate vaccine, six pregnant ewes were inoculated with 5 x 10(3) p.f.u. of RVF MP-12 and challenged with 5 x 10(5) p.f.u. of virulent ZH-501 strain of RVFV 30 days later. No viraemia was detected after vaccination or challenge and all six ewes delivered live, healthy lambs. Those lambs tested before their nursing did not have neutralizing antibody to RVFV but quickly acquired antibody titres of 1:320 to greater than or equal to 1:10,240 after ingesting colostrum. To test the safety of the RVF MP-12 immunogen in neonates, lambs less than or equal to 7 days old, born to unvaccinated ewes, were inoculated with 5 x 10(5) p.f.u. of RVF MP-12. With the exception of brief pyrexia in 18 of 26 lambs, and a transient low-titred viraemia in 16 of 26 lambs after inoculation, no untoward effects were observed. Serum-neutralizing antibody to RVFV was detected 5-7 days after inoculation. Lambs vaccinated with either 5 x 10(5) or 5 x 10(3) p.f.u. of RVF MP-12 were protected against virulent RVFV challenge at 14 days postvaccination.

Animals↗
PubMed1991

Recombinant human interferon-gamma modulates Rift Valley fever virus infection in the rhesus monkey.

Prophylactic treatment of rhesus macaques with 10(4)-10(6) U/kg of recombinant human interferon-gamma (rHuIFN-gamma) modulated Rift Valley fever (RVF) virus infection. IFN was given intramuscularly at 24 h prior to infection and daily thereafter for a total of five doses. After infection, treated monkeys showed no evidence of clinical disease; some had no detectable viremia; when viremia was observed, peak virus titers were decreased compared to control infected monkeys; and only minor and transient perturbations in hematologic and clinical chemistry values were seen. Untreated infected control monkeys developed high-titered viremia, mild to severe clinical disease, and moderate to severe changes in hemostatic parameters and clinical laboratory measurements. No evidence of synergism was noted when RVF virus-infected monkeys were treated prophylactically with combined low doses of rHuIFN-gamma and rHuIFN-alpha A.

Animals↗
PubMed1991

Venezuelan equine encephalomyelitis virus infection in and transmission by the tick Amblyomma cajennense (Arachnida: Ixodidae).

To assess a possible role of ticks as the maintenance host for epizootic strains of Venezuelan equine encephalomyelitis (VEE) virus, laboratory experiments were conducted to determine if ticks could become infected, maintain, and transmit the virus. Larval and nymphal Amblyomma cajennense (F.) and larval Dermacentor nitens Neumann ticks were exposed to epizootic VEE virus (Trinidad donkey strain) by allowing them to feed on viremic guinea pigs (strain 13). In A. cajennense, transstadial transmission was observed from larvae to nymphs and adults. Horizontal viral transmission to a mammalian host was accomplished by nymphs. Infection rates in nymphs and adults were 2% (42/2,750) and 4% (9/244), respectively, afer ingestion of virus as larvae. Virus was detected in A. cajennense adult ticks for up to 171 d after infection in the larval stage. A cajennense, exposed as nymphs, ingested virus but did not become infected (0/164 after 10 d after taking an infective bloodmeal). No virus was detected in D. nitens 7 d after exposure. These findings suggest that A. cajennense potentially could be involved in an interepizootic maintenance cycle of epizootic VEE viral strains.

Animals↗
PubMed1991

Infection of inbred rat strains with Rift Valley fever virus: development of a congenic resistant strain and observations on age-dependence of resistance.

A congenic rat strain (WF.LEW) was derived from the susceptible Wistar-Furth (WF) (background strain) and the resistant LEW (donor strain) inbred strains and was used to evaluate the phenotypic expression of a dominant Mendelian gene that confers resistance to fatal hepatic disease caused by the ZH501 strain of Rift Valley fever virus (RVFV). Resistance to hepatic disease developed gradually with age, with full expression at approximately 10 weeks in the WF.LEW and LEW rat strains. The ZH501 strain caused fatal hepatitis in WF rats regardless of age. However, resistance to the SA75 RVFV strain (relatively non-pathogenic for adult rats), was age- and dose-dependent in both WF and LEW rats. The resistance gene transferred to the newly derived WF.LEW congenic rat strain appears to amplify age-dependent resistance of adult rats, resulting in protection against fatal hepatic disease caused by the virulent ZH501 strain. The congenic rat strain will be a valuable asset in elucidating the mechanism of resistance to Rift Valley fever virus governed by the dominant Mendelian gene.

Aging↗
PubMed1991

Junin virus activity in rodents from endemic and nonendemic loci in central Argentina.

Small mammals were trapped during a 21-month period at 27 farm sites in 15 localities within and beyond the known endemic area for Argentine hemorrhagic fever (AHF). Prevalence of Junin virus (JV) was assessed by antigen-capture enzyme immunoassay (ELISA) on samples of body fluids and/or organs from 3, 282 captured rodents. Infection in rodent populations was variable (0-3.7%) among localities but, in all cases, was lower than previously reported rates. Overall prevalence was 1.4% in the AHF epidemic area, 0.6% in the historic (currently low incidence of AHF) area, and 0.4% in two localities beyond the previously defined endemic area. These low values underestimate the actual prevalence of JV, as ELISA validation by virus isolation indicated a sensitivity of 30% and a specificity of 99%. Of 37 positive rodents, 28 (76%) were of two species: Calomys musculinus (23 animals) and C. laucha (5 animals). Antigen also was found in three Akodon azarae, four Bolomys obscurus, one Mus musculus, and one Oxymycterus rufus, and JV was isolated from two Oligoryzomys flavescens. Three of these rodent species (B. obscurus, O. flavescens, and O. rufus) have heretofore not been implicated in JV maintenance in the field. Evidence suggests that the AHF endemic area may continue to expand northward.

Animals↗
PubMed1991

Demonstration of yellow fever and dengue antigens in formalin-fixed paraffin-embedded human liver by immunohistochemical analysis.

Two immunohistochemical techniques to determine the presence of yellow fever and dengue antigens in fixed tissue samples were developed for the purpose of making retrospective diagnoses of these viral diseases in humans. A horseradish peroxidase label was used for one technique and an alkaline phosphatase label for the other. In the former technique, acid hematin was removed from the tissues, iron-containing pigments were counterstained with Prussian blue, and the product of the diaminobenzidine reaction was enhanced with a dilute solution of osmium tetroxide that differentiated antigen from lipofuscin. In the latter technique, alkaline phosphatase was used as the enzyme labeling system with a red chromogen that contrasted nicely with the pigments in the tissues, as mentioned above. Thus, pigment removal or differentiation from antigen was not required. Replicate sections were cut and mouse polyclonal antibodies for yellow fever and all dengue types were applied to individual sections. On samples positive for dengue antigen, monoclonal antibodies were applied to additional replicate sections to demonstrate antigen of dengue types 1 and 4. In order to test the assay, samples of formalin-fixed liver tissue from Brazilian and Peruvian individuals who had died from a variety of causes as long as eight years earlier were received in a blinded fashion for immunohistochemical analysis. The techniques appeared to be highly reliable for yellow fever diagnosis; however, not enough cases were observed to adequately evaluate the procedures for dengue diagnosis. Both procedures appeared to have similar sensitivity.

Adolescent↗
PubMed1991

[New findings on Junin virus infection in rodents inside and outside the endemic area of hemorrhagic fever in Argentina].

In conjunction with field trials for a vaccine against Argentine Hemorrhagic Fever (AHF), small mammals were trapped during a 28-month period (1 November 1987 to 13 March 1990) in 3 epidemiologically defined areas of the central Argentine pampas: northern and central Buenos Aires provinces were included in the AHF "historic" area, where the disease was common 15-20 years ago, but case rates are currently low; southern Santa Fe province is the current high-incidence area for AHF; the nonendemic area was represented by two localities 60-90 km beyond the northernmost extension of human disease. Animals were live-trapped for 3 days per month in permanent "mark-recapture" grids in each of the 3 areas. Samples of blood, sera, and oral swabs were taken from these animals before they were marked and released at the site of capture. In addition, "removal" traplines provided animals from 16 localities in these 3 areas which were sacrificed to obtain samples of organs in addition to the aforementioned samples. Samples were tested for the presence of Junin virus (JV) antigen by enzyme immunoassay (ELISA). In this assay, a pool of 13 mouse anti-JV glycoprotein and nucleocapsid monoclonal antibodies adsorbed to the surface of microtiter plates was used to capture JV antigen in sample suspensions. A polyclonal rabbit anti-JV antiserum was added as a detector antibody, and an anti-rabbit antibody conjugated to horseradish peroxidase applied with substrate to complete the sandwich.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Preliminary report: isolation of Ebola virus from monkeys imported to USA.

An epizootic caused by an Ebola-related filovirus and by simian haemorrhagic fever virus began among cynomolgus monkeys in a US quarantine facility after introduction of monkeys from the Philippines. This incident, the first in which a filovirus has been isolated from non-human primates without deliberate infection, raises the possibility that cynomolgus monkeys could be a reservoir of Ebola virus infection.

Animals↗
PubMed1990

Pathogenesis of a phleboviral infection (Punta Toro virus) in golden Syrian hamsters.

The hamster, Mesocricetus auratus, was examined as a possible model for investigating the poorly defined pathogenesis of the family Bunyaviridae, genus Phlebovirus. Punta Toro virus (PTV) isolates from Eastern Panama were highly virulent for two outbred and five inbred hamster strains, while isolates from western Panama were of low virulence. The Adames strain (eastern Panama) of PTV (LD50 approximately 1 PFU, sc) caused an acute fatal disease (average survival time, 3.8 days) in 10-week-old Lak: LVG (SYR) hamsters. Severe necrosis of the liver, spleen, and small intestine was associated with extensive expression of viral antigen in these organs. The Balliet strain (western Panama) of PTV (LD50 greater than 6 log10 PFU, subcutaneously) caused a mild hepatocellular infection with peak viral liver titers of 3-4 log10 PFU/g compared to 8-9 log10 PFU/g for the Adames strain. We observed histological lesions in the red pulp of the spleen or the lamina propria of the small intestine with the Adames strain. Lesions in the hamsters had characteristics of disseminated intravascular coagulation (DIC). The PTV-hamster model shares similarities to Rift Valley fever (phleboviral disease), which causes fatal disease in man and domesticated ruminants.

Animals↗
PubMed1990

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

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 12 h 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.

Analysis of Variance↗
PubMed1990

Protection of guinea pigs against experimental Argentine hemorrhagic fever by purified human IgG: importance of elimination of infected cells.

Antibody-containing plasma from patients recovered from Argentine hemorrhagic fever (AHF) is of proven value in treatment of the acute disease, but the possibility of transmitting blood-borne organisms such as HIV and hepatitis virus detracts from this approach. Purified human immune plasma fractions IgG1,2,4, IgG1,2,3,4 and F(ab')2 neutralized Junin virus in vitro. IgG1,2,3,4 and IgG1,2,4 lysed (in the presence of complement) cells infected with Junin virus, and protected infected guinea pigs from AHF. However, large quantities of the immune F(ab')2 fraction from the same plasma pool failed to protect guinea pigs from death, to increase the mean time to death, and to diminish virus load in target organs of infected guinea pigs. This suggests that elimination of infected cells rather than virus neutralization may play a critical role in protection against Junin virus.

Animals↗
PubMed1989

Delayed type-hypersensitivity response of inbred strains of Syrian golden hamsters (Mesocricetus auratus) to lethal or non-lethal lymphocytic choriomeningitis virus (LCMV) infections.

In adult Syrian golden hamsters (Mesocricetus auratus), intraperitoneal or footpad inoculation of the lymphocytic choriomeningitis virus (LCMV) strains, WE or Armstrong (ARM), caused systemic infection and induced serum LCMV-antibody. Hamster and virus strain-dependent lethal disease also occurred. With WE, MHA and PD4 inbred hamsters failed to eliminate infection and died of wasting disease. LSH and CB inbred hamsters resisted lethal WE-disease and cleared infection. LVG hamsters and inbred LHC hamsters were intermediate in WE-susceptibility; some died of wasting, while others survived with little illness. Resistance to lethal WE-disease directly correlated with a delayed-type hypersensitivity (DTH) response to live-virus footpad inoculation. In WE-resistant LSH and CB hamsters, DTH-responses were induced by intraplantar WE-inoculation; footpad edema began by 5 days, reached maximum thickness by 7 to 9 days, and subsided thereafter. In the other hamster strains, DTH to WE could not be elicited. Unlike WE, ARM was hamster-avirulent; infections were self-limited and did not induce DTH. All survivors of primary LCMV (WE or ARM)-infection resisted secondary WE-challenge, and did not develop DTH to LCMV. Immunosuppressive treatments, abrogating DTH and antibody responses to LCMV, rendered all hamsters susceptible to lethal WE-infection. Hamster DTH most likely mediated resistance to virulent LCMV-infection.

Animals↗
PubMed1989

Junin virus monoclonal antibodies: characterization and cross-reactivity with other arenaviruses.

Twenty-one monoclonal antibodies reactive with Junin virus structural proteins were produced and characterized. Using radioimmunoprecipitation and Western blot assays, 13 were found to react with the nucleoprotein, seven with the surface glycoprotein and one failed to react, but showed a fluorescent antibody staining pattern consistent with other glycoprotein-specific antibodies. In radioimmunoprecipitation assays, glycoprotein-specific monoclonal antibodies reacted not only with the 35K structural glycoprotein, but also with what is presumed to be the glycoprotein precursor. Four of seven glycoprotein-specific antibodies neutralized Junin virus to high titres. Cross-reactivity with other arenaviruses was found to be restricted to nucleoprotein-specific monoclonal antibodies and occurred only with New World arenaviruses. Cross-reactivity also shows the Junin virus to be most closely related to Machupo and Tacaribe viruses.

Animals↗