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Biomedical subjects

C G Hayes

Publications and source records attributed to C G Hayes.

84 records · Page 5Linked to original sources

Comparison of vector competence for West Nile virus of colonized populations of Culex tritaeniorhynchus from southern Asia and the Far East.

Seven colonized stocks of Cx. tritaeniorhynchus from different geographic areas of Southern Asia and the Far East were assayed for susceptibility to WN virus infection by membrane feeding and by intrathoracic inoculation. Infected females also were tested for their ability to transmit virus to baby mice. No geographic pattern of differential susceptibility to WN virus infection was apparent from the experiments; however, the per os ID50 of one strain from Khulna, Bangladesh was over 10-fold greater than the ID50's of stocks from Karachi, Pakistan and Sendai, Japan. No difference in susceptibility was found by parenteral inoculation of virus. Likewise, greater than or equal to 90% of infected females from all the colonies were able to transmit virus.

Animals↗

Exploratory monitoring of air pollutants for mutagenicity activity with the Tradescantia stamen hair system.

The Tradescantia genetic system developed by the late Dr. Arnold H. Sparrow for the study of effects of ionizing radiation is applicable to chemical mutagen detection. Early radiobiological data demonstrated that the stamen hairs were sensitive to as little as 0.25 rad of x-rays and that the number of cells showing a phenotypic change in pigmentation from blue to pink plateaus after approximately 21 days of chronic, low-level irradiation. Exposures to the air pollutants SO(2), NO(2), and O(3) and to vapors of mutagens such as 1,2-dibromoethane (DBE) and ethyl methanesulfonate (EMS) demonstrated the usefulness of the system as a detector of chemical mutagens. A significant number of phenotypic changes was observed following exposures to as little as 0.14 ppm of DBE. The maximum sensitivity of the system is obtained with long-term or chronic exposures because the response increases linearly in proportion to the duration of exposure up to 21 days. To monitor industrial sites for atmospheric mutagens a mobile laboratory was designed to support plant culture in the field. Environment-controlled growth chambers were installed in a trailer so that both ambient air fumigations and concurrent clean-air control exposures could be made. Sites monitored by the mobile laboratory were: Elizabeth, N. J.; Charleston, W. Va.; Birmingham, Ala.; Baton Rouge, La.; Houston, Tex.; Upland, Calif.; Magna, Utah; and Grand Canyon, Ariz. The latter site at Grand Canyon served as a clean air control study. Atmospheric contaminants from petroleum and chemical processing plants generated a significant number of phenotypic pigment changes that were 17 to 31% above the control levels; contaminants from steel and copper smelters, automotive combustion products and photochemical compounds were negative. Chemical analyses are underway to identify the atmospheric mutagens at the sites that showed a positive response.

Air Pollutants↗

Variations in biological properties of geographic strains of western equine encephalomyelitis virus before and after passage in Culex tarsalis and Culiseta melanura.

Western equine encephalomyelitis (WEE) virus strains from the eastern and western United States were compared using two biological markers: antigenic properties measured by cross complement fixation (CF) tests and the size of plaques produced in Vero cell cultures. Slight antigenic differences were discernible on a geographic basis, and all of the virus strains from the West produced significantly larger plaques than the eastern isolates. One virus strain from each region was serially passaged in Culex tarsalis and Culiseta melanura by intrathoracic inoculation. No change in plaque size was detected as a result of mosquito passage. After passage of the eastern strain of WEE virus in C. tarsalis, its mouse brain CF antigen titer was increased to resemble the high CF antigen titer produced by the western strain. However, the antisera titers did not change when tested with this antigen. A cross plaque reduction neutralization test (PRNT) with the two virus strains before and after passage in mosquitoes failed to reveal any antigenic changes.

Animals↗

A nationwide survey of heavy metal absorption in children living near primary copper, lead, and zinc smelters.

Arsenic, lead, and cadmium absorption levels were determined in 1774 children 1-5 years old living in 19 USA towns with primary nonferrous metal smelters. Results were compared with data on 258 children of the same age in three communities without smelters. Increased systemic absorption of arsenic, as reflected by urine arsenic content, was noted in children near 10 of 11 copper smelters. Blood lead levels were also modestly elevated near two copper smelters. Near lead and zinc smelters, elevated levels of lead and cadmium in hair provided evidence of external exposure to these elements. Levels of lead in blood were not, however, elevated near any of three lead smelters and were elevated near only two of five zinc smelters. Blood cadmium levels were high near one lead and two zinc smelters. The apparent sources of exposure (except in one community with elevated levels of arsenic in drinking water) were air, soil, and dust contaminated by smelting operations. While the full biologic significance of these findings is not known exposure of children to toxic heavy metals emitted by smelters should be reduced to a minimum.

Arsenic↗

Evaluation of the epidemic potential of western equine encephalitis virus in the northeastern United States.

The problem of evaluating the epidemic potential of western equine encephalitis in the northeastern United States is presented and possible reasons are discussed for the present lack of human and horse cases of this disease even though increased numbers of isolations of the virus have been obtained in the East during recent years. Epidemiologic factors of vector bionomics and virus strain variations are considered. It is concluded that while this virus strain can no longer be regarded as uncommon in the Northeast, the evidence indicates there is little potential for epidemic expression of this agent in the human and horse population. This appears to be due to differences in the bionomics of the mosquito Culiseta melanura, which serves as the primary enzootic vector in the northeastern United States and in the bionomics of Culex tarsalis that is the vector in the western region of the United States. Other limiting factors in the epidemic potential may be variations between virus strains located in the East and West.

Animals↗

Molecular characterization of a hepatitis E virus isolate from Namibia.

Hepatitis E virus (HEV) causes sporadic and epidemic acute viral hepatitis in many developing countries. In Africa, hepatitis E has been documented by virus detection (reverse transcriptase polymerase chain reaction, RT-PCR) in Egypt, Chad, Algeria, Morocco and Tunisia. Cases of presumptive hepatitis E also have been documented by detection of antibody to HEV in the Sudan, Kenya, Ethiopia, Somalia, Djibouti and South Africa. Recently, we reported the recovery of 9 isolates of HEV from feces collected during an outbreak of jaundice in Namibia. These specimens were stored frozen for many years at the South African Institute for Medical Research awaiting new methods to determine the etiology of jaundice. HEV genomic sequences were detected by antigen-capture RT-PCR with primers that amplified 2 independent regions of the HEV genome (ORF-2 and ORF-3). To further characterize the HEV 83-Namibia isolates, we determined the nucleotide (nt) sequence of the 3' end of the capsid gene (296 of 1, 980 nt in ORF-2) and ORF-3 for 1 isolate. The capsid gene sequence shared 86% identity with the prototype Burma strain and up to 96% identity with other African strains at the (nt) level, and 99% identity with Burma or other Africa strains at the amino acid level. A 188 (nt) fragment amplified from ORF-3 was also highly homologous to other HEV but was too short for meaningful comparison. Phylogenetic analysis indicated that HEV 83-Namibia is closely related to other African isolates, and differs from Burmese, Mexican and Chinese HEV. These data link the HEV causing the 1983 Namibia outbreak to more recent HEV transmission in northern and sub-Saharan Africa, suggesting this subgenotype of HEV is firmly established throughout the continent.

Capsid↗

Hepatitis E virus DNA vaccine elicits immunologic memory in mice.

Injection of an expression vector pJHEV containing hepatitis E virus (HEV) structural protein open reading frame 2 gene generates a strong antibody response in BALB/c mice that can bind to and agglutinate HEV. In this study, we tested for immunologic memory in immunized mice whose current levels of IgG to HEV were low or undetectable despite 3 doses of HEV DNA vaccine 18 months earlier. Mice previously vaccinated with vector alone were controls. All mice were administered a dose of HEV DNA vaccine to simulate an infectious challenge with HEV. The endpoint was IgG to HEV determined by ELISA. Ten days after the vaccine dose, 5 of 9 mice previously immunized with HEV DNA vaccine had a slight increase in IgG to HEV. By 40 days after the vaccine dose, the level of IgG to HEV had increased dramatically in all 9 mice (108-fold increase in geometric mean titer). In contrast, no control mice became seropositive. These results indicate that mice vaccinated with 3 doses of HEV DNA vaccine retain immunologic memory. In response to a small antigenic challenge delivered as DNA, possibly less than delivered by a human infective dose of virus, mice with memory were able to generate high levels of antibody in less time than the usual incubation period of hepatitis E. We speculate that this type of response could protect a human from overt disease.

Animals↗

Longitudinal studies of children born to HIV-1 antibody positive Filipino commercial sex workers (CSW): diagnostic dilemmas.

Fifteen term babies born to 12 HIV-1 antibody positive Filipino CSW have been monitored for signs and symptoms of HIV-1 infection. Eleven babies were enrolled in the study within the first 6 months after birth; 4 others were enrolled at 4, 9, 11 and 21 months of age respectively. Every 3 months after enrolment, each baby received a physical examination, serum was tested for HIV-1 antibodies and p24 antigen and peripheral blood mononuclear cells were cultured for isolation of virus. After a mean follow-up period of 39.3 months (range 7-72 months), virus isolation and serum p24 antigen assays confirmed that 2 babies have been infected with HIV-1. If the 4 babies less than 18 months of age were excluded, the vertical transmission rate was 18.2%. Seven babies who have been monitored for a minimum of 25 months (range 31-60 months) lost their maternal antibodies but 6 of them subsequently developed indeterminant Western blots (WB); reactivity to p24 and/or gp120/ 160 but no reactivity to gp41. Of the remaining 6 babies, still less than 25 months of age (range 7-24 months), 2 lost their maternal antibodies within one year. The other 4 continued to recognize either p24 or gp120/160 well after the accepted 15-month period for loss of maternal antibody. Although a diagnosis could not be established upon the basis of these laboratory findings, clinical observations (failure to thrive, anergy, persistent generalized lymphadenopathy and recurrent pneumonias) mimicked HIV-1 infection. However, because these clinical features are common among many babies in the developing world, their usefulness in supporting a diagnosis of perinatal HIV-1 infection is limited.

Adolescent↗