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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 217 records · Page 12Linked to original sources
PubMed1989

Inhibition of Crimean-Congo hemorrhagic fever viral infectivity yields in vitro by ribavirin.

Ribavirin was evaluated as a potential therapeutic for Crimean-Congo hemorrhagic fever (CCHF). Viral yields for strains of CCHF virus from Europe, Asia, and Africa in African green monkey kidney (Vero) cells were markedly reduced by this drug. Some CCHF viral strains appeared more sensitive than others, but in general, ribavirin doses as low as 5 micrograms/ml caused a transient reduction of viral yields. A further reduction in viral yields was induced by a dose of 25 micrograms/ml, and evidence of viral replication was not demonstrated in cells treated with 50 or 250 micrograms/ml. In contrast, a dose of ribavirin at least 9 times greater was required to induce a comparable inhibitory effect on the yields of Rift Valley fever virus, for which the drug has been shown to inhibit replication in monkeys and rodents.

Animals↗
PubMed1989

A comparison of early and delayed induction of labor with spontaneous rupture of membranes at term.

The management of women with spontaneous rupture of membranes at term in the absence of labor and with a cervix unfavorable for induction of labor is controversial. In this randomized study of 182 patients, we report the effects of delayed versus early induction of labor on maternal and neonatal outcome. Qualifying patients not in labor at 6 hours after spontaneous rupture of membranes were randomized to either immediate oxytocin induction (86 women) or expectant management with oxytocin induction at 24 hours if labor had not occurred spontaneously (96 women). The cesarean section rate did not differ between the two groups. Women in the delayed group had significantly longer hospitalization (P less than .003), and their infants were significantly more likely to receive antibiotics (P = .006). Infectious morbidity (positive cultures or x-ray-documented pneumonia) occurred in five of the neonates in the delayed group, all of whose mothers had an initial digital cervical examination, but in none of the neonates in the early group, a difference that did not reach statistical significance (P = .061). Five (28%) of 18 infants from the delayed group whose mothers had received an initial digital cervical examination became infected, compared with none of the 78 infants from the delayed group whose mothers did not have digital examinations (P less than .001). We conclude that there is no advantage to delaying induction of labor when women present at term with spontaneous rupture of membranes.

Adult↗
PubMed1988

The gerbil, Meriones unguiculatus, a model for Rift Valley fever viral encephalitis.

The gerbil, Meriones unguiculatus, was investigated as a model for the encephalitic form of Rift Valley fever. Resistance to necrotizing encephalitis was age-dependent with 100% mortality at 3 weeks, decreasing to approximately 20% by 10 weeks of age in outbred gerbils inoculated subcutaneously. Fatal encephalitis in the 10-week-old adults was dose-independent [1.0-7.0 log10 plaque forming units (PFU), subcutaneously]. Viral replication and histological lesions were followed serially throughout the course of the infection in young (4 week) and adult (10 week) gerbils. Viral replication was evident in the brain tissue of young gerbils from day 4 (3.0 log10 PFU/g) through day 7 (6.0 log10 PFU/g), the last day the young gerbils survived. Virus was only detected in the brain tissue of a single adult gerbil (day 7, 4.0 log10 PFU/g) of 26 studied in the sequential survey. In contrast, two moribund adult gerbils had approximately 7.0 log10 PFU/g of virus in the brain tissue on days 8 and 11. When young and adult gerbils were inoculated with a low dose (50 PFU) of virus intracranially, there were no detectable differences in the course of infection with all animals succumbing to fatal necrotizing encephalitis approximately 7 days postinoculation. The young gerbil becomes the first animal model in which uniformly fatal RVFV-induced encephalitis is produced without significant extraneural lesions.

Aging↗
PubMed1988

Experimental Rift Valley fever in rhesus macaques.

Rift Valley fever (RVF) is a major cause of human morbidity and mortality in endemic areas of sub-Saharan Africa and has the potential to cause epidemic disease in receptive areas world-wide. In this study, a RVF viral isolate from the 1977 Egyptian epidemic (ZH-501) inoculated intravenously into rhesus macaques caused a benign viremic infection in most, but resulted in the hemorrhagic fever syndrome in 20 per cent (3 of 15). Serious disease of this type has not previously been observed in nonhuman primates inoculated with RVF virus and may be a consequence of the viral strain used or the route of inoculation. Severe disease was accompanied by extensive liver necrosis, disseminated intravascular coagulation, and microangiopathic hemolytic anemia. We also attempted to prevent RVF by passive transfer of serum from vaccinated rhesus monkeys (plaque-reduction neutralization test titer 1:2,560). As little as 0.025 ml/kg prevented the development of viremia in naive rhesus monkeys after subcutaneous inoculation of virus. The monkey model should be helpful in understanding the pathogenesis and prevention of human RVF.

Animals↗
PubMed1988

Viral determinants of virulence for Rift Valley fever (RVF) in rats.

Rift Valley fever viral strains or variants (RVFV) were compared with respect to (a) virulence for Wistar-Furth rats; (b) in vitro sensitivity to rat and human interferon; (c) ability to form plaques in primary hepatocyte cultures from genetically resistant or susceptible rat strains, and (d) replicative potential in continuous rat cell lines. Egyptian strains were highly virulent for Wistar-Furth rats; relatively resistant to rat interferon-alpha/beta; capable of producing plaques in primary hepatocyte monolayers; and, in general, replicated more rapidly than the low-virulent, sub-Saharan strains. Virtually all strains from sub-Saharan Africa were sensitive to rat interferon and did not form plaques in rat hepatocyte monolayers. An exception was the 2269/74 strain from Zimbabwe, which had characteristics of the Egyptian strains including increased virulence for Wistar-Furth rats. The relative virulence of RVFV strains for rats did not correlate with interferon sensitivity when human recombinant interferon-alpha was tested on A-549 cells. Thus, several in vitro phenotypic characteristics of RVFV strains tend to correlate with virulence for Wistar-Furth rats and with geographical origin of the viral strains.

Animals↗
PubMed1988

Susceptibility and resistance of inbred strains of Syrian golden hamsters (Mesocricetus auratus) to wasting disease caused by lymphocytic choriomeningitis virus: pathogenesis of lethal and non-lethal infections.

In different strains of inbred Syrian golden hamsters (Mesocricetus auratus), the lymphocytic choriomeningitis virus (LCMV) strains WE and Armstrong (ARM) produced systemic infection with infective virus and viral antigens detected predominantly in reticuloendothelial organs. Host and virus strain-dependent fatal wasting disease also occurred. After infection with WE, all MHA and PD4 hamsters died of a progressive wasting disease and infectivity persisted in organs at relatively high titres. LSH and CB strain hamsters resisted lethal disease and totally eliminated infection. LVG and LHC strain hamsters were intermediate in susceptibility to WE; some died of wasting and had persistently infected organs, while others cleared infection and survived. ARM was avirulent causing an inapparent infection in all hamsters. LCMV antibody responses were temporally comparable for all hamsters with either lethal or non-lethal infection. Histologically, lymphoid hyperplasia and low-grade systemic perivascular mononuclear leukocyte infiltration were found in all LCMV-infected hamsters. However, non-necrotic segmental ileal changes, which included vascular congestion, minimal haemorrhage and crypt epithelial growth extension into the intestinal wall, were found in susceptible hamsters when infected with the lethal WE strain.

Animals↗
PubMed1988

Viral strain dependent differences in experimental Argentine hemorrhagic fever (Junin virus) infection of guinea pigs.

Guinea pigs infected with low-passage Junin virus of human origin showed viral strain dependent differences in mortality, LD50, time to death, and in viral spread and distribution. Different Junin strains appeared to cause at least two broad patterns of Argentine hemorrhagic fever in guinea pigs. A number of strains of Junin virus caused a viscerotropic type of illness in which virus replicated predominantly in lymph nodes, spleen, and bone marrow. With the most severe visceral forms of Argentine hemorrhagic fever, the guinea pigs became viremic, developed necrosis of spleen, lymph nodes, and bone marrow, showed gastric hemorrhages, and all animals died within 13-15 days. Other Junin strains induced a neurological type of illness with transient viral replication in and lymphocyte depletion of spleen and lymph nodes, with no detectable viremia or viral replication in bone marrow. Subsequently, virus was found in the brain with varying severities of polioencephalitis, and the guinea pigs frequently showed rear leg paralysis before death occurred 28-34 days after inoculation. Not all animals infected with a neurotropic strain developed all these signs. One viral strain induced some signs characteristic of both patterns of illness. Although the disease forms in the guinea pig model did not strictly correlate with those observed in the humans from which these strains were obtained, the different strains of Junin virus consistently caused very different patterns of illness in infected guinea pigs.

Animals↗
PubMed1988

Isolation of a newly recognized Bunyamwera serogroup virus from a febrile human in Panama.

A virus, strain 86MSP18, was isolated from the acute phase serum of a U.S. soldier with a febrile illness. He was stationed at Fort Sherman in the Republic of Panama when the onset of his illness occurred. A rise in neutralizing antibody to the viral isolate was observed between the patient's acute and convalescent-phase serum samples. Virus strain 86MSP18 has been shown by plaque reduction neutralization to be closely related to but distinct from Cache Valley virus and known subtypes. It appears to be a newly recognized subtype of Cache Valley virus and is believed to be the second isolation of a Cache Valley virus subtype from a human with a febrile illness. The name "Fort Sherman" virus for strain 86MSP18 is proposed.

Animals↗
PubMed1988

Experimental infection of Phlebotomus papatasi with sand fly fever Sicilian virus.

Experimental studies were conducted to evaluate humans as hosts infecting the sand fly Phlebotomus papatasi with sand fly fever Sicilian (SFS) virus. Viral antigen and infectious virus circulated in the blood of infected volunteers on days 4 and 5 after intravenous inoculation with SFS virus. Viremia levels during the latter period were high enough to infect feeding sand flies, but only 13% (9/69) of the flies became infected. One out of every 3 infected sand flies that survived to feed a second time transmitted SFS to a hamster. These results confirm a vertebrate-sand fly-vertebrate transmission cycle for SFS virus, and demonstrate that horizontal transmission may contribute to the maintenance of this virus in nature.

Animals↗
PubMed1987

Virus-specific factors in experimental Argentine hemorrhagic fever in rhesus macaques.

A nonhuman primate model for Argentine hemorrhagic fever has been developed that closely mimics the human clinical syndrome. Parenteral infection of adult Macaca mulatta with low-passage isolates of two Junin viral strains resulted in distinctive hemorrhagic or neurological disease in rhesus macaques that correlated with clinical illness patterns present in the humans from whom the viral strains were obtained. Transient leukopenia, together with thrombocytopenia and secondary bacterial septicemia, were documented among animals infected with both viral strains. In contrast, differing patterns of viremia, oropharyngeal viral shedding, and antibody response occurred in the two virus-infected groups. These results, together with postmortem virologic and histopathologic findings, suggest that viral-strain-specific factors are important determinants of clinical disease patterns in this model system.

Animals↗
PubMed1987

Differentiation of a human monocytic cell line associated with increased production of Rift Valley fever virus by infected cells.

Rift Valley fever (RVF) virus is a cause of significant human and animal disease in many parts of Africa. In some cases, it causes a hemorrhagic fever, which is frequently fatal. Prior studies have shown that RVF virus productively infects peritoneal macrophages from susceptible rat strains. The U937 human monocytic cell line was used to determine the effect of monocytic cell differentiation on the degree of viral production by cell cultures infected with RVF virus. Differentiation of U937 cells to more mature monocytic cells by phorbol ester resulted in production of 10 times more infectious virions in comparison with undifferentiated cells. These studies imply that monocytic cell differentiation increases permissiveness for RVF virus production.

Bunyaviridae↗
PubMed1987

Immunosuppression-induced susceptibility of inbred hamsters (Mesocricetus auratus) to lethal-disease by lymphocytic choriomeningitis virus infection.

The role of the immune response in the pathogenesis of lethal and non-lethal lymphocytic choriomeningitis virus (LCMV)-infections of young adult Syrian golden hamsters (Mesocricetus auratus) of different strains was examined using immunosuppressive treatment with cyclophosphamide or with whole-body gamma-irradiation. In all hamsters, the LCMV strains, WE and Armstrong (ARM), caused systemic infections and induced comparable serum LCMV-antibody titers. However, lethal wasting-disease occurred which was hamster-strain and virus-strain dependent. With WE-inocula, MHA and PD4 inbred hamsters were all susceptible to lethal-disease and failed to completely eliminate infection. All LSH and CB inbred hamsters resisted lethal-disease and totally cleared WE-infection. Random colony-bred LVG hamsters and inbred LHC hamsters were intermediate in WE-susceptibility; some died with wasting, while others survived with minimal to no illness. ARM was avirulent for all hamsters and infections were totally cleared. By immunosuppressive treatment, all hamsters were rendered completely susceptible to lethal-disease by WE, and had unresolved infections and diminished serum LCMV-antibody titers. Immunosuppression also rendered all hamster strains partially susceptible to lethal infection by ARM. The hamster immune response was thus shown to suppress LCMV-infection and protect against lethal illness.

Animals↗
PubMed1987

Pathogenesis of Rift Valley fever virus (RVFV) in inbred rats.

The pathogenesis of Rift Valley fever in adult rats from 3 inbred strains (LEW, MAXX, WF) was investigated. WF rats all died by day 2 postinoculation with viral tissue titers reaching 9 log10 PFU/g. LEW and MAXX rats were resistant to liver disease, but fatal necrotising encephalitis developed in 16 and 44% of the rats, respectively. Detection of serum neutralising antibody on day 3 coincided with clearance of virus from serum and liver, although infectious virus was detected in spleen homogenates as late as day 19 postinfection. Viral titers in LEW and MAXX rats did not exceed 4.5 log10 PFU/g. Cyclophosphamide immunosuppression of LEW rats led to death 5-9 days postinfection; early patterns of viral replication were not affected, but continued growth in the liver resulted in fatal hepatitis. These animals could be protected by passive antibody therapy administered on days 2-5 postinfection to mimic the serum neutralising antibody pattern seen in unmanipulated infected LEW rats. Thus, RVF virus replication and spread is rapid in the WF rats tissues, whereas in LEW and MAXX rats viral growth is less due to an intrinsic mechanism which allows sufficient time for an immune response to terminate infection. A slightly diminished immune response may lead to the development of encephalitis more frequently in MAXX than LEW rats. These rat strains should be useful in elucidating those mechanisms of resistance which limit RVFV-induced hepatitis and encephalitis.

Animals↗
PubMed1987

Rift Valley fever: a sero-epidemiological survey among pregnant women in Mozambique.

Rift Valley fever (RVF) causes abortion in sheep and cattle. However, the teratogenic and abortogenic potential of RVF in humans is not known. Sera from a total of 1163 pregnant women in Mozambique were tested for RVF virus antibodies by ELISA and 28 (2%) were found to be positive. Mothers experiencing fetal death or miscarriage (155) had the same RVF virus antibody prevalence as those with normal deliveries. Analysis of maternity histories showed some indication of increased fetal wastage among women positive for RVF virus antibody. The ELISA used in this study was compared with a plaque reduction neutralization test and found to be equally sensitive and specific for the detection of RVF virus IgG antibodies.

Abortion, Spontaneous↗
PubMed1987

Susceptibility of inbred Syrian golden hamsters (Mesocricetus auratus) to lethal disease by lymphocytic choriomeningitis virus.

An acutely lethal LCMV disease model has been established in the Syrian golden hamster (Mesocricetus auratus) in which lethality and disease are dependent upon both the inbred hamster strain and the LCMV strain. Young adult inbred, male and female, hamsters were tested for lethal-disease susceptibility by lymphocytic choriomeningitis virus (LCMV) strains, WE or Armstrong (ARM). With WE inocula, PD4 and MHA inbred hamsters were highly susceptible to a wasting disease. LVG and LHC inbred hamsters were intermediate in susceptibility; some of these animals died of wasting illness, and others exhibited minimal disease and survived. CB and LSH hamsters were highly resistant to any disease by WE. Mean survival times of susceptible hamsters given lethal WE inocula approximated 2.5 weeks and were not dependent on virus dose. By 1.5 weeks after WE inoculation wasting disease signs were notable and consisted of lethargy, progressive body weight loss, and diarrhea. The LCMV strain, ARM, was avirulent for all hamster strains, causing neither death nor disease. Hamsters surviving WE or ARM inoculation appeared healthy, produced LCMV antibody, and acquired resistance to further lethal WE challenge. Despite hamster-lethality differences. WE and ARM appeared comparably immunogenic for all hamster strains, based on host antibody titers. A number of other differences between the LCMV strains were, however, noted which could be relevant to virus virulence and lethality for hamster hosts. These included guinea pig lethality, temperature sensitivity, and plaque morphology.

Animals↗