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Biomedical subjects

J L Hardy

Publications and source records attributed to J L Hardy.

At least 55 records · Page 3Linked to original sources

Effect of the anesthetizing agent triethylamine on western equine encephalomyelitis and St. Louis encephalitis viral titers in mosquitoes (Diptera: Culicidae).

Triethylamine (TEA) is a chemical compound that provides an effective means to anesthetize mosquitoes. The mosquitoes remain alive but are incapacitated for several hours; they do not recover following treatment. There was no effect on the titers of infectious virus recovered from western equine encephalomyelitis or St. Louis encephalitis virus-infected Culex tarsalis Coquillett and Aedes dorsalis (Meigen) that were anesthetized with TEA prior to storage at -70 degrees C. Furthermore, TEA had no effect on isoenzyme profiles of uninfected Cx. tarsalis.

Aedes↗

Distribution of neutralizing antibodies to California and Bunyamwera serogroup viruses in horses and rodents in California.

Neutralization tests were done on sera from 141 horses from high elevation regions of California. Antibody prevalences to Jamestown Canyon, snowshoe hare, and California encephalitis viruses in the California serogroup and Northway virus in the Bunyamwera serogroup were 55%, 43%, 18%, and 46%, respectively. In 51 horses from rural low elevation regions, seroprevalences were 31%, 35%, 35%, and 37%, respectively. Twenty-four horses from a suburban lowland area were seronegative, except for a single horse with a low titer to snowshoe hare virus. Seroprevalence to Jamestown Canyon and snowshoe hare viruses was associated with increasing age. Only 2 of 177 rodents from the Sierra Nevada had antibodies to Northway virus; none had antibodies to Jamestown Canyon or snowshoe hare viruses.

Animals↗

Temporal variations in the susceptibility of a semi-isolated population of Culex tarsalis to peroral infection with western equine encephalomyelitis and St. Louis encephalitis viruses.

A semi-isolated population of Culex tarsalis in Kern County, CA was found to vary significantly in its seasonal and yearly susceptibility to peroral infection with western equine encephalomyelitis (WEE) and St. Louis encephalitis (SLE) viruses during the breeding seasons of 1975-1981. Female cohorts of the population were significantly more resistant to WEE virus from 1975 through 1977 than from 1978 through 1981. On the average, females were 40 times more susceptible to WEE virus during May than during August. Increases in resistance correlated significantly with the number of days accrued from April through June, when daily ambient air temperatures equaled or exceeded 26.7 degrees C or 32.2 degrees C, respectively. Analyses of data on WEE viral susceptibility, temperature, and rainfall for the 7 year period suggested that Cx. tarsalis should be most susceptible to infection in years with wet winter-early spring periods followed by cool springs. However, inconsistencies in the expression of WEE viral susceptibility during mid- to late summer of some years indicated that other unidentified extrinsic factors, in addition to temperature and rainfall, may induce changes during preimaginal development that affect the peroral susceptibility of adult females. Seasonal and yearly changes in the susceptibility of the Cx. tarsalis population to per os infection with SLE virus did not necessarily occur at the same time as those observed with WEE virus and did not appear to correlate with changes in ambient air temperature. Thus, extrinsic factors that affect the expression of viral susceptibility of Cx. tarsalis, and perhaps the genetic basis of viral susceptibility, apparently differ for WEE and SLE viruses.

Animals↗

Persistence of mosquito-borne viruses in Kern County, California, 1983-1988.

The persistence of arboviruses was studied from 1983 to 1988 in mixed agriculture, marsh, riparian, and foothill habitats in Kern County, CA. Western equine encephalomyelitis (WEE) virus was isolated frequently during 1983 from Culex tarsalis and Aedes melanimon and was detected by the seroconversion of sentinel chickens. WEE virus then disappeared, even though vector competence studies during 1984-1986 showed that Cx. tarsalis was able to transmit WEE virus. St. Louis encephalitis (SLE) virus was detected sporadically in 3 of the 6 years of the study by isolation from Cx. tarsalis and/or by sentinel chicken seroconversion. When mosquito pools were screened for virus in suckling mice, Turlock (TUR) and Hart Park (HP) viruses were isolated from Cx. tarsalis during each summer. Vertical transmission of HP was indicated by the isolation of virus from a pool of male Cx. tarsalis. California encephalitis (CE) virus was isolated repeatedly from host-seeking Ae. melanimon females, males, and adults reared from field-collected immatures, verifying vertical transmission in nature. Horizontal transmission of CE virus among both jackrabbits (Lepus californicus) and desert cottontails (Sylvilagus auduboni) appeared to amplify Ae. melanimon infection rates during the summer of 1985, but elevated herd immunity depressed infection rates during 1986. Thus, CE, HP, and TUR viruses persisted in Kern County, while WEE virus appeared to become extinct and required reintroduction. The sporadic occurrence of SLE virus activity remains unexplained, but its persistence may require both vertical transmission and reintroduction.

Aedes↗

Prevalence of neutralizing antibodies against California and Bunyamwera serogroup viruses in deer from mountainous areas of California.

Plaque reduction-serum dilution neutralization was used to evaluate the status of bunyavirus activity in deer in mountainous areas of California. Antibodies against 9 bunyaviruses were measured in 337 mule deer (Odocoileus hemionus hemionus, O. hemionus californicus, and O. hemionus inyoensis) and black-tailed deer (O. hemionus columbianus). More deer from high mountainous areas had neutralizing antibodies against Jamestown Canyon virus than did deer from low mountainous areas (23% vs. 9%; P less than 0.01). This finding is consistent with transmission by snow pool Aedes mosquitoes. Results for Jerry Slough virus were nearly identical to those for Jamestown Canyon virus, which is further evidence that these are strains of the same virus. Neutralizing antibodies against Northway virus were present in 26% of deer from high mountainous areas and 23% of deer from low mountainous areas, suggesting the involvement of a widespread vector, such as Culiseta inornata. Northway virus is not known to occur outside of Alaska and northwestern Canada. Low prevalences of antibodies were detected in deer to California encephalitis, La Crosse, and snowshoe hare viruses of the California serogroup; and Cache Valley, Lokern, and Main Drain viruses of the Bunyamwera serogroup.

Animals↗

Characterization of the mesenteronal infection with Western equine encephalomyelitis virus in an incompetent strain of Culex tarsalis.

Interactions of western equine encephalomyelitis (WEE) virus are compared with mesenterons of 2 genetically selected susceptible (WS) and refractory (WR) lines of Culex tarsalis. Both WS and WR females had similar susceptibility when parenterally inoculated with virus, thus it was initially thought that resistance in WR Cx. tarsalis was associated with a mesenteronal infection barrier. Present data on viral growth in mesenterons dissected from females fed on virus-soaked pledgets suggest that virus infected and multiplied in some WR mesenterons, but to significantly lower titers than in WS mesenterons. The proportion of WR females with infected mesenterons varied depending on the time after feeding, incubation temperature, and whether mesenterons were incubated with WEE viral antibody before viral assay. The percentage of WR mesenterons infected did not increase significantly when diethylaminoethyl dextran was added to the infectious bloodmeal, the pH of the infectious bloodmeal was altered, or virus was introduced by intrathoracic inoculation into the hemocoel. It was concluded that the low titers of virus detected in both WR mesenterons and whole mosquitoes were influenced by the genetic ability of WR Cx. tarsalis to modulate WEE viral titers to low or undetectable levels after peroral or parenteral infection. These findings make it difficult to determine what proportion of the WR mesenterons are resistant to infection with WEE virus. WS and WR Cx. tarsalis were equally susceptible to peroral infection with the flavivirus St. Louis encephalitis and the bunyavirus Turlock.

Animals↗

Atypical depression: is there a need for a better definition.

This paper attempts to delineate subgroups from the heterogeneous group labeled "Atypical Depression," in order to interpret various clinical studies which used varied diagnostic criteria. From the resultant working definition some treatment guidelines are suggested.

Depressive Disorder↗

Establishment and characterization of St Louis encephalitis virus persistent infections in Aedes and Culex mosquito cell lines.

Persistent infections with St Louis encephalitis (SLE) virus were established in three mosquito cell lines (Aedes albopictus, A. dorsalis and Culex tarsalis) and were maintained for over 2 years. All three persistently infected cell cultures shared two features: (i) no overt cytopathic effect and (ii) a relatively high proportion of cells infected (41 to 85%). The Aedes persistently infected cultures were resistant to superinfection with the homologous virus but not heterologous viruses. Two significant differences were observed between the Aedes and C. tarsalis persistently infected cell cultures: (i) viral titres in the A. albopictus and A. dorsalis cell cultures decreased slowly over time (the decrease was particularly marked in the A. albopictus cell cultures), whereas titres in the C. tarsalis cell cultures remained relatively constant and (ii) the addition of anti-SLE virus antibody led to decreased virus production in the C. tarsalis cell cultures (one of two cultures was cured of infection), whereas antibody had no effect on the persistently infected Aedes cell cultures. These results suggest that there may be significant differences in the regulation of viral replication and the maintenance of flavivirus persistent infections in mosquito cell lines of different origins.

Aedes↗

Phenotypes of St Louis encephalitis virus mutants produced in persistently infected mosquito cell cultures.

Viral mutants that appeared during long-term persistent infections of mosquito cell cultures (Aedes albopictus, A. dorsalis and Culex tarsalis) with St Louis encephalitis virus were characterized. Evidence was obtained for the presence of temperature-sensitive mutants in the A. dorsalis and C. tarsalis persistently infected cultures, and small plaque mutants were predominant in all cultures except one of two cell cultures of C. tarsalis. Virus from persistently infected A. albopictus cell cultures was growth-restricted in Vero and C. tarsalis cells. One of two persistently infected A. dorsalis cell cultures also produced viral mutants that were growth-restricted in C. tarsalis cells. Further, Western blots of persistently infected A. albopictus cell extracts showed an overproduction of capsid (C) and envelope (E) structural proteins and reduced production of an Mr 27K protein (p27) which was immunologically related to the E protein. In contrast, the production of E and C proteins in persistently infected C. tarsalis cultures was consistent with the amount of infectious virus present, whereas p27 was relatively overproduced. These observations suggest that the host cell has an important influence on both the types and relative quantities of viral mutants that accumulate during long-term persistent infections.

Aedes↗

Acid phosphatases of the mosquito Culex tarsalis coquillett.

1. Spectrophotometric and isoelectric focusing (IEF) electrophoretic characterization of the acid phosphatases (ACP) of the mosquito, Culex tarsalis, are presented. 2. ACP hydrolysis of P-nitrophenylphosphate (Pnp) was optimal at 37 degrees C, pH 5.25 in the presence of 15 mM MgCl2 and 0.1% (w/v) polyvinylpyrollidone (PVP). Vmax and Km values varied significantly between the various mosquito strains examined. 3. Several divalent cations (i.e. Mn2+, Ca2+, Ba2+ and Co2+), either the chloride or sulphate salts, were stimulatory for ACP. Both Cu2+ and Fe2+ (15 mM) were inhibitory. 4. Slight inhibition (i.e. 10%) of ACP activity was observed with dithiothreitol (100 mM) and 50% inhibition by cysteine (100 mM). 5. ACP activity was cyclic during the 15-day post-adult emergence period of the study. No significant differences were noted between the ACP specific activities of males and females nor between geographic strains. 6. IEF electrophoresis revealed three alpha-naphthyl phosphate hydrolytic ACP isozymes within the pH 4.5-5.5 range (i.e. ACP4.8, ACP5.3 and ACP5.5). 7. IEF ACP isozymes were stimulated by PVP, Mg2+, Zn2+ and inhibited by cysteine, EDTA (except ACP5.3) and NaFl. 8. IEF detection of ACP with Pnp revealed an ACP isozyme (ACP4.3) distinct from those ACP isozymes capable of alpha-naphthyl phosphate hydrolysis.

Acid Phosphatase↗

Abdominal proptosis: a case report.

A case history of abdominal swelling of psychological origin is described. The clinical presentation and psychogenic pathogenesis of the disorder provide a differentiation from pseudocyesis. The psychodynamics of this case are discussed emphasizing the conflict involving strong elements of pre-oedipal aggressivity towards the father image.

Abdomen↗

The ecology of western equine encephalomyelitis virus in the Central Valley of California, 1945-1985.

Reeves' concept of the summer transmission cycle of western equine encephalomyelitis virus in 1945 was that the virus was amplified in a silent transmission cycle involving mosquitoes, domestic chickens, and possibly wild birds, from which it could be transmitted tangentially to and cause disease in human and equine populations. Extensive field and laboratory studies done since 1945 in the Central Valley of California have more clearly defined the specific invertebrate and vertebrate hosts involved in the basic virus transmission cycle, but the overall concept remains unchanged. The basic transmission cycle involves Culex tarsalis as the primary vector mosquito species and house finches and house sparrows as the primary amplifying hosts. Secondary amplifying hosts, upon which Cx. tarsalis frequently feeds, include other passerine species, chickens, and possibly pheasants in areas where they are abundant. Another transmission cycle that most likely is initiated from the Cx. tarsalis-wild bird cycle involves Aedes melanimon and the blacktail jackrabbit. Like humans and horses, California ground squirrels, western tree squirrels, and a few other wild mammal species become infected tangentially with the virus but do not contribute significantly to virus amplification.

Aedes↗

An interspecific mosquito model for the mesenteronal infection barrier to western equine encephalomyelitis virus (Culex tarsalis and Culex pipiens).

Culex tarsalis, a putative mosquito vector of western equine encephalomyelitis (WEE) virus, is susceptible to peroral infection by WEE virus. The nonvector mosquito, Culex pipiens, has a very high peroral threshold of infection and is considered to be refractory. By parenteral inoculation, both mosquito species are equally susceptible. Thus, Cx. tarsalis and Cx. pipiens represent an excellent model system to examine the mechanisms for the mesenteronal infection barrier to WEE virus. Diethylaminoethyl (DEAE)-dextran (1.6 mg/ml), when added to a pledget bloodmeal that contained high concentrations of WEE virus, enhanced peroral infection rates of Cx. pipiens. In Cx. tarsalis, a reduction in infection rates was observed when low WEE concentrations of virus were ingested. DEAE-dextran had no apparent effects on the dissemination of WEE after infection of either mosquito species. It is suggested that the peroral enhancement of WEE viral infection observed with Cx. pipiens may be related to random, nonspecific mechanisms of infection, since it requires high titers of ingested WEE virus. Interference with specific binding of WEE virus to cellular receptor sites is suggested to explain the reduction in WEE viral infection rates in Cx. tarsalis. Altering the pH of the ingested infectious bloodmeal did not affect the WEE viral infection rate of Cx. pipiens, within the range of 6.0-8.5. Cx. tarsalis was optimally infected when the infectious bloodmeal was pH 8.0, and the infection rate was significantly reduced when the infectious blood was at either extreme of the pH range tested. This is again interpreted to indicate that different mechanisms control the peroral infection of Cx. tarsalis and Cx. pipiens with WEE virus. The mesenteronal infection barrier to WEE virus in Cx. pipiens is associated with an inability of the virus to adsorb and/or penetrate mesenteronal epithelial when administered perorally. The barrier is not related to an inability of the Cx. pipiens mesenteronal epithelial cells to support viral multiplication since these cells become infected when the virus is administered parenterally.

Animals↗

Mesenteronal epithelial cell surface charge of the mosquito, Culex tarsalis Coquillett. Binding of colloidal iron hydroxide, native ferritin and cationized ferritin.

The binding of positive and negative colloids of iron hydroxide, native ferritin and cationic ferritin to the mesenteronal epithelial cell surface of the mosquito, Culex tarsalis, was examined electronmicroscopically. The major anionic groups contributing to the negative character of the microvillar surface appear to be the gamma-carboxyls of aspartic and glutamic acids with some contribution from uronic acids. These same anionic groups are expressed along the basolateral membranes and the basal lamina along with the much more acidic sulfates. These specific groups were implicated through an evaluation of the binding of our surface probes at various pH's from 0.8 through 7.2.

Binding Sites↗

Western equine encephalomyelitis virus: in vivo infection and morphogenesis in mosquito mesenteronal epithelial cells.

The infection and morphogenetic events associated with the replication of Western equine encephalomyelitis (WEE) virus within the mesenterons of Aedes dorsalis and three strains of Culex tarsalis are compared and contrasted. WEE virus apparently penetrates mesenteronal epithelial cells in vivo through membrane fusion. Profiles of apparent membrane fusion events were observed between virus particles and the microvillar surface of the mesenteron and naked nucleocapsids are observed intracellularly along the apical margin of the mesenteronal epithelial cell within 3 h of ingestion of the bloodmeal. Further, no viral particles were found in association with endocytotic nor lysosomal vacuoles during the initial phases of infection. In those strains of Cx. tarsalis that supported viral replication and in Ae. dorsalis, accumulations of nucleocapsids and maturation of WEE virus were evident along basolateral membranes of the mesenteron by 22-24 h after ingestion of the blood-meal. Maximal extracellular nascent virus occurred between 30-36 hrs. The Knights Landing strain of Cx. tarsalis revealed no subcellular morphological alteration in response to infection throughout the period of study. However, distinct morphological structures associated with the infection were observed in strains or species with enhanced susceptibility compared to Knights Landing (i.e., Cx. tarsalis WS-3 and Ae. dorsalis). In both, apical accumulations of nucleocapsids were apparent by 29 h post infection. These nucleocapsids were most often embedded in a rather amorphous matrix and occasionally in association with membrane profiles; presumably endoplasmic reticulum. Ae. dorsalis also demonstrated some alterations in response to WEE viral infection that were unique relative to Cx. tarsalis and some of these may be considered cytopathological. First, progeny virions were observed repeatedly within lysosomal figures. Second, extensive cytoplasmic vacuolization was noted and occasionally it appeared that these vacuolated cells were being sloughed off into the lumen of the mesenteron.

Aedes↗