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Biomedical subjects

J C Morrill

Publications and source records attributed to J C Morrill.

At least 37 records · Page 2Linked to original sources
PubMed1988

A study of viral and rickettsial exposure and causes of fever in Juba, southern Sudan.

Patients presenting at the Juba Teaching Hospital, either with fever of undetermined origin or with a clinical cause of fever, gave evidence of exposure to a wide range of viral and rickettsial agents. Serological tests showed high antibody levels to flaviviruses (56.9%) and alphaviruses (29.2%), with lesser levels of bunyamweraviruses (3.8%), Rift Valley fever (2.3%), and sandfly fever (0.75%). Flavivirus exposure was significantly associated with clinical evidence of liver disease; repeated exposure to flaviviruses was particularly prevalent in those with poor sanitation and who had received previous injections. A significant focus of Ebola and Marburg exposure in Juba has been identified. Clinical evidence of liver disease was evident in 37% of patients studied, and 24.6% were HBsAg positive. The first 2 HIV-positive individuals from the southern Sudan are reported, including one with clinical AIDS. A high prevalence of positive antibodies to Rickettsia typhi in the population indicated that murine typhus was common locally. This study indicates the need for further public health measures in the southern Sudan to control the spread of these infections.

Adolescent↗
PubMed1988

Solid-phase immunosorbent technique for rapid detection of Rift Valley fever virus immunoglobulin M by hemagglutination inhibition.

A solid-phase immunosorbent technique (SPIT) was adapted to detect Rift Valley fever (RVF) virus-specific immunoglobulin M (IgM) in serum samples from humans vaccinated with Formalin-inactivated RVF vaccine. Microdilution plates coated with goat anti-human IgM were successively incubated with serum samples from human vaccinees, RVF virus hemagglutinating antigen, and goose erythrocytes. The RVF virus-specific IgM in the serum samples from vaccinees bound to the RVF virus antigen and inhibited hemagglutination of goose erythrocytes. SPIT was compared to the IgM capture enzyme linked immunosorbent assay (ELISA) and the indirect immunofluorescent-antibody (IFA) assay and was found to be sensitive in detecting RVF virus-specific IgM antibody, with high correlations between SPIT and the other two tests (Pearson's correlation coefficient [r] = 0.9 and 0.6, respectively). Results of SPIT were obtained within 5 h, offering speed over ELISA (8 h). In addition, SPIT does not require sophisticated equipment or expensive reagents. Serum rheumatoid factor did not produce false-positive reactions in SPIT as in the indirect immunofluorescent-antibody assay and IgM capture ELISA.

Antibodies, Viral↗
PubMed1988

Rift Valley fever in Egypt 1986. Surveillance of sheep flocks grazing in the northeast Nile Delta.

From October 1985 through November 1986, 1714 presumably unvaccinated sheep in 13 nomadic flocks located in four provinces in Dakahliya Governorate, in the northeast Nile Delta, were ear tagged and monitored for acquisition of Rift Valley fever virus (RVFV) antibodies. Sheep were bled at approximately 3 month intervals and sera were tested for haemagglutination inhibition (HI) antibodies to RVFV. HI reactors were tested for RVFV specific IgM antibody by enzyme-linked immunosorbent assay (ELISA) and neutralizing antibody to RVFV by plaque reduction neutralization (PRN) tests. Base line results showed 1.2% prevalence of HI antibody to RVFV with titres from 1:20 to 1:320. All HI positive sera were PRN positive through PRN titres were generally higher than HI titres. No RVFV specific IgM antibody was detected in the HI and PRN positive sera. Throughout the study, no initially seronegative sheep became positive and no HI positive sheep showed an appreciable increase above initial antibody titre. These data indicate absence of RVFV transmission to sheep in Dakahliya Governorate during the period of the study.

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

Pathogenicity and immunogenicity of a mutagen-attenuated Rift Valley fever virus immunogen in pregnant ewes.

A mutagenized clone of Rift Valley fever virus (RVFV; MV P12) used in inoculation of 3 pregnant ewes was immunogenic, nonpathogenic, and nonabortogenic. In contrast, inoculation of a matched group of 3 pregnant ewes with parent RVFV induced clinical disease and abortions. Ewes given MV P12 delivered healthy lambs that had RVFV antibody titers of less than 1:10 at birth, increasing to greater than or equal to 1:80 after ingestion of colostrum. Ewes inoculated with parent RVFV developed marked viremia, followed by RVFV antibody titers greater than or equal to 1:1,280; ewes inoculated with MV P12 developed low viremia titers and RVFV antibody titers of 1:80 to 1:320. Postpartum challenge exposure of the previously MV P12-inoculated ewes with virulent Zagazig human 501 strain RVFV indicated that the ewes were protected from clinical disease. The RVFV-susceptible female Culex pipiens that fed on the MV P12-inoculated ewes failed to transmit RVFV to hamsters; mosquitoes that fed on the parent RVFV-inoculated ewes became infected and transmitted RVFV to hamsters.

Animals↗
PubMed1985

An electron microscopic study of blood cells from calves experimentally infected with bluetongue virus.

Cellular elements from blood samples of calves experimentally inoculated with a quadrivalent mixture of bluetongue virus (BTV) types 10, 11, 13 and 17 were examined by transmission electron microscopy (TEM). Virus-like particles were observed within cytoplasmic vacuoles of infected agranular leukocytes from inoculated calves on postinoculation day (PID) 14. No virus-like particles were seen associated with other cellular blood elements nor were they observed in blood samples obtained prior to virus inoculation. The intravacuolar viral particles were 60nm in diameter, had a cockleburr appearance and lacked the outer polypeptide coats of mature virions. Increased cytoplasmic vacuolation was the most noticeable change in the infected cells. BTV infection was confirmed by viral isolation and serological testing. Pyrexia was the only consistent clinical sign seen in the viremic calves.

Animals↗
PubMed1985

Use of a quadrivalent modified-live bluetongue virus vaccine in wildlife species.

Three hundred and twenty-seven animals comprised of deer, mouflon sheep and bighorn sheep were vaccinated with an experimental quadrivalent, modified-live, bluetongue virus (BTV) vaccine. No untoward effects due to the vaccine were noted nor were abortions observed in vaccinated pregnant mouflon sheep. Precipitating antibodies to BTV and epizootic hemorrhagic disease (EHD) virus were identified in the serum of several animals prior to vaccination. Virus neutralizing antibodies to 3 of the 5 serotypes of BTV which exist in the US were identified in the serum of 2 peninsular bighorn sheep.

Animals↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Replication of hemorrhagic fever viruses in monocytic cells.

Monocytes play a central role in protection against many viruses. In some infections they are target cells for viral replication. There is increasing evidence that these cells may also be important in regulation of hemostasis. The part played by monocytic cells in the pathogenesis of hemorrhage in the viral hemorrhagic fevers is presently uncertain. Monocytes and monocytic cell lines have been used to investigate the ability of viruses to infect these cells in vitro. Several factors may affect the ability of a particular virus to infect monocytic cells, including specific antiserum to virus and the degree of cellular maturation. The effect of cellular maturation on the replication of Rift Valley fever virus in the U937 cell line is discussed in light of studies on the infectivity of other viruses for monocytic cells. Data supporting the ability of specific antibody to enhance the infectivity of Pichinde virus and Lassa fever virus for U937 cells are presented.

Antibodies, Viral↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗