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Biomedical subjects

W F Scherer

Publications and source records attributed to W F Scherer.

At least 55 records · Page 3Linked to original sources

Studies of possible movement of Venezuelan encephalitis virus from an enzootic focus in Guatemala during 1971-1974.

During the wet seasons of 1972 and possibly 1971, sentinel horses became infected by Venezuelan encephalitis (VE) virus in a temporally and geographically progressive manner inland from an enzootic marsh focus of virus on the Pacific couast of southeastern Guatemala. During the wet seasons of 1972 and 1973, VE virus was detected by sentinel horses (and a sentinel hamster in 1972) in a small woods 10 km north of the marsh, but virus was undetectable there during the dry seasons of 1973 and 1974 and the wet season of 1974. Culex (Melanoconion) mosquitoes were found in this woods and at the marsh during August 1973. These observations are compatible with movement of VE virus from the marsh habitat during some wet seasons. However, virus activity in this region adjacent to the marsh was quantitatively unpredictable on a yearly basis and occurred in only very focal habitats during 1971 to 1974. Mechanisms of VE virus movement from the marsh are currently unknown, but bats are under study as a likely possibility.

Animals↗

Vector competence of mosquitoes as a marker to distinguish Central American and Mexican epizootic from enzootic strains of Venezuelan encephalitis virus.

Two epizootic strains of Venezuelan encephalitis (VE) virus from Central America and Mexico were transmitted by a colonized epizootic vector mosquito, Aedes taeniorhynchus, at higher rates than were two enzootic strains when the mosquitoes were infected by intrathroacic inoculation or feeding of virus. Differences in transmission rates also occurred with colonized Aedes aegypti, but were less marked. Following intrathoracic inoculation of A. taeniorhynchus or A. aegypti, epizootic strains grew to slightly higher concentrations in the mosquitoes than did enzootic strains. Intestinal thresholds of infection for A. taeniorhynchus were slightly lower for epizootic than for enzootic virus strains, but were essentially equal for A. aegypti. Only a small percentage of individual Culex pipiens quinquefasciatus mosquitoes supported growth of epizootic VE virus, and only 1 of 6 tested C. p. quinquefasciatus transmitted virus by bite. Thus, transmission and growth of virus in these Aedes mosquitoes distinguished between these epizootic and enzootic strains of VE virus.

Aedes↗

Ecologic studies of Venezuelan encephalitis virus in Peru during 1970-1971.

Venezuelan encephalitis (VE) virus has intermittently produced epidemics and equine epizootics on the dry Pacific coastal plain of Peru since at least the 1930's. However, evidence that the virus exists in the Amazon region of Peru to the east of the Andes mountains was not obtained until antibodies were found in human sera collected in 1965, and 10 strains of the virus were isolated in a forest near the city of Iquitos, Peru during February and March 1971. Eight strains came from mosquitoes and two from dead sentinel hamsters. Three hamsters exposed in forests near Iquitos developed VE virus antibodies suggesting that hamster-benign strains also exist there. Antibody tests of equine sera revealed no evidence that VE virus was actively cycling during the late 1950's or 1960's in southern coastal Peru, where equine epizootics had occurred in the 1930's and 1940's. In northern coastal Peru bordering Ecuador, antibodies were present in equine sera, presumably residual from the 1969 outbreak caused by subtype I virus, since neutralizing antibody titers were higher to subtype I virus than to subtypes III or IV. No VE virus was detected in this northern region during the dry season of 1970 by use of sentinel hamsters. The possibility is considered that VE epidemics and equine epizootics on the Pacific coast of Peru are caused by movements of virus in infected vertebrates traversing Andean passes or in infected vertebrates or mosquitoes carried in airplanes from the Amazon region.

Animals↗

Antigenic and biologic characteristics of Venezuelan encephalitis virus strains including a possible new subtype, isolated from the Amazon region of Peru in 1971.

Nine strains of Venezuelan encephalitis (VE) virus isolated from the Amazon region of Peru in 1971 were identified as antigenic subtype I based on plaque-reduction neutralization tests with four and 20 units of antibody. A tenth strain, 71D1252, was possibly a new subtype, but was related to subtypes I and III. Hemagglutinins of each strain made from infected mouse brains had optimals pHs of 6.2 and 6.4. Nine strains were pathogenic for adult hamsters and adult mice, but strain 71D1252 inapparently infected some adult hamsters and mice inoculated peripherally. Plaques of nine strains in Vero African green monkey kidney cell cultures were intermediate in size between representative epizootic and enzootic strains, but plaques of strain 71D1252 were small like epizootic strains.

Animals↗

The first isolations of eastern encephalitis, group C, and Guama group arboviruses from the Peruvian Amazon region of western South America.

Two strains of eastern encephalitis (EE) virus were isolated in the Amazon region of Peru near Pucallpa, Loreto Department, using sentinel hamsters. EE virus antibodies were found in healthy horses at both Pucallpa and Iquitos in the same Department. Fourteen group C and four Guama group arboviruses were recovered from sentenel hamsters and mosquitoes near Iquitos. The group C agents were Caraparu-Ossa, Marituba, and Oriboca-Itaqui viruses, and the Guama group agents were Bimiti virus. Besides providing a detailed account of these investigations, this article includes a current list of known arboviruses of the American tropics that can be detected with sentinel hamsters.

Animals↗

Homegeneity of Venezuelan encephalitis virion populations of hamster-virulent and benign strains, including the attenuated TC83 vaccine.

A hamster-virulent strain of Venezuelan encephalitis virus (BeAn8, subtype III) and a benign strain (BeAr35645, subtype IV) each yielded 100 clones with virulence properties like those of the parental virion population. Another hamster-virulent strain (63U2, subtype I, variety E) was heterogeneous since 2 out of 100 clones were less virulent for hamsters than the other 98 clones or the parental virus population. The attenuated TC83 vaccine strain, (a derivative of subtype I, variety A), although over 99% homogeneous with respect to hamster virulence, was unstable since virulent virions could be selected from the parental population by passage through hamsters.

Age Factors↗

Growth curves and clearance rates of virulent and benign Venezuelan encephalitis viruses in hamsters.

Four virulent strains of Venezuelan encephalitis virus attained higher concentrations of infectious virus in bloods of adult hamsters than two benign strains when given subcutaneously. One benign virus, the attenuated TC83 vaccine strain, reached higher concentrations in bone marrow and Peyer's patches than virulent subtype I strains, and another benign virus, subtype IV, grew to lower levels. When inoculated intracranially, the two benign viruses attained high concentrations in brain, but did not significantly alter in lethality although morbidity was increased. Intracardiac inoculation failed to increase virus concentrations of two benign viruses in blood or hematopoietic tissues above those found after subcutaneous inoculation, nor did it increase lethalities to those of virulent virus. Three benign virus strains were cleared more rapidly from hamster plasmas than six virulent strains. Differences in clearance rates were apparently not due to destruction of benign viruses by blood or tissue components. Thus viral concentrations in blood correlated directly and clearance rates inversely with hamster virulence, whereas the rate and extent of growth of a VE virus in hematopoietic or brain tissues did not correlate with ability to kill hamsters.

Animals↗