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Biomedical subjects

W F Scherer

Publications and source records attributed to W F Scherer.

At least 37 records · Page 2Linked to original sources
PubMed1979

A hamster-attenuated, temperature-sensitive mutant of Venezuelan encephalitis virus.

Pathogenicities of 10 temperature-sensitive mutants of Venezuelan encephalitis virus were studied using the hamster model of human virulence. The parental strain and nine of the temperature-sensitive mutants produced lethal infections in hamsters. Strain ts 126 showed reduced hamster virulence. Deaths with the lethal mutants usually occurred 1 to 3 days later than with parental virus. Nine mutants produced lower levels of viremia than parental virus. Attenuation of ts 126 was related to restriction of viral growth in spleen and probably bone marrow and to absence of the usual pathological lesions in hemopoietic tissues and brain, but was functionally unrelated to temperature sensitivity since temperatures of both normal and infected hamsters remained within the permissive range of the mutant. Deaths did not correlate with titers of the 10 mutants in blood at permissive temperatures or with reversions of four temperature-sensitive mutants to non-temperature-sensitive virus in hamsters.

Animals↗
PubMed1979

Transmission of Venezuelan encephalitis virus by naturally infected Culex (Melanoconion) opisthopus.

During August 1977 two of 975 Culex (Melanoconion) opisthopus collected from an enzootic marsh habitat on the Pacific coast of Guatemala transmitted VE virus to hamsters. Eight VE strains were isolated from Cu. opisthopus. The minimal level of VE infection in this species during July-August 1977 at La Avellana, Guatemala was 1/128 (8/1,021), and the prevalence of Cu. (Mel.) opisthopus transmitting VE virus was 1/487 (2/975). This mosquito was the predominant species attacking humans at that time, suggesting that Cu. opisthopus is a vector of VE virus to man as well as a vector in enzootic cycles in Guatemala. These studies establish Cu. opisthopus as the third proven enzootic vector of VE virus.

Animals↗
PubMed1979

Further observations on infections of guinea pigs with Venezuelan encephalitis virus strains.

Guinea pigs from a Guatemalan colony died after subcutaneous inoculating of moderately small doses of equine-benign strains of Venezuelan encephalitis (VE) virus of hemagglutination-inhibition subtype I-E from enzootic habitats in Mexico and Guatemala. Thus these guinea pigs were unlike English short hair and inbred 13 guinea pigs, which usually survive infections with equine-benign VE strains of subtype I-E. We therefore caution others that not all strains of guinea pigs can be used to evaluate the potential equine virulence of VE viruses.

Animals↗
PubMed1978

Infections of congenitally athymic (nude) and normal mice with avirulent and virulent strains of Venezuelan encephalitis virus.

Two strains of Venezuelan encephalitis virus that are avirulent for normal BALB/c mice inoculated subcutaneously were also avirulent for infected congenitally athymic (nude) mice of the same strain. Viremias were of similar magnitudes and durations in normal and nude mice. Brain concentrations were higher in nude mice with the one avirulent strain tested, although the periods of detectable virus in brains were similar. No lesions were found in brains, spleens, or lymph nodes by ordinary histopathological examination. Viral neutralizing antibody titers in plasmas at 1 to 3 weeks after infection were lower and more transient in nude than in normal mice, and implantations of thymic tissues into nude mice partially restored their neutralizing antibody responses. Concentrations of spleen cells producing antibodies that lysed sheep erythrocytes 4 days after inoculation of erythrocytes and avirulent virus into nude mice were above the levels of uninfected nude mice. These concentrations were similar in infected and uninfected normal mice. In contrast, two mouse-virulent strains of Venezuelan encephalitis virus killed nude mice faster than normal mice after subcutaneous inoculation. Yet concentrations and durations of virus in bloods and brains were not consistently different between nude and normal mice. There were perivascular monocytes in brains and slight architectural alterations of spleens and lymph nodes. Concentrations of spleen cells producing antibodies hemolytic for sheep erythrocytes 4 days after inoculation with erythrocytes were depressed in nude and normal mice by infection with virulent strains.

Animals↗
PubMed1977

Comparisons of Venezuelan encephalitis virus strains by hemagglutination-inhibition tests with chicken antibodies.

Twenty strains of Venezuelan encephalitis (VE) virus inoculated intravenously in large doses into roosters produced hemagglutination-inhibition (HI) antibodies detectable in plasmas within 7 to 10 days. No signs of illness occurred, and there was no evidence of viral growth in tissues since blood concentrations of infectious virus steadily decreased after inoculation. HI antibodies in early plasmas were specific for VE virus and did not cross-react significantly with two other North American alphaviruses, eastern and western encephalitis viruses. VE virus strains could be distinquished by virus-dilution, short-incubation HI, but not by plasma-dilution neutralization tests, by using early rooster antibodies. The distinctions by HI test were similar with some strains to, but different with other strains from, those described by Young and Johnson with the spiny rat antisera used to establish their subtype classifications of VE virus (14, 28). Nevertheless, results of HI tests with rooster antibodies correlated with equine virulence, as did results with spiny rat antibodies, and distinguished the new strains of virus that appeared in Middle America during the VE outbreak of 1969 from preexisting strains.

Animals↗
PubMed1977

Search for subtype I strains of Venezuelan encephalitis virus among isolates from Trinidad, W.I., during 1960-1972.

Twenty-one strains of Venezuelan encephalitis (VE) virus isolated from three habitats in Trinidad, W.I. during 1960 to 1972, were subtype III (Mucambo) VE virus by plaque-reduction neutralization tests. Like prototype Mucambo virus, each strain killed 8- to 15-week-old mice inoculated intraperitoneally. If the subtype I strain of VE virus that caused a major outbreak in Trinidad during 1943 to 1944 persisted on the island into the 1960s and early 1970s, it did not become the dominant VE virus in these three enzootic foci.

Animals↗
PubMed1977

Responses of guinea pigs to infections with strains of Venezuelan encephalitis virus, and correlations with equine virulence.

Five equine-virulent strains of Venezuelan encephalitis (VE) virus consistently killed guinea pigs (strain English short hair) inoculated subcutaneously, whereas ten equine benign strains did not. Two enzootic eastern Panamanian and Colombian strains of hemagglutination-inhibition antigenic subtype I-D and of undetermined virulence for equine animals also killed guinea pigs. This subtype of VE virus may represent an excpetion to a positive correlation between equine virulence and guinea pig lethality since another strain of ts subtype has been reported to be benign in horses inoculated subcutaneously. Within the strains tested, viruses of subtypes I-ABC and I-D were lethal for guinea pigs, and viruses of other subtypes were benign. There was no correlation between guinea pig and human virulence of VE strains.

Animals↗
PubMed1976

Interferon induction and sensitivity as correlates to virulence of Venezuelan encephalitis viruses for hamsters.

Venezuelan encephalitis (VEE) virus strains, which differ in virulence for adult hamsters, were compared with respect to (a) sensitivity to hamster interferon (IF) in vitro and in vivo and (b) induction of IF in plasma and target tissues (spleen, bone marrow and brain) following subcutaneous inoculation. In vitro, in cultures of a continuous line of hamster kidney cells, hamster interferon inhibited the replication of a benign VEE strain (BeAr 35,645) more than another benign strain (TC-83 vaccine) or two hamster-virulent strains (68 U 201 and Trinidad donkey). In vivo, in hamsters given poly I: poly C 24 hours before virus to induce interferon formation, BeAr 35,645 and TC-83 virus infections were prevented more frequently than infections with virulent strains Trinidad donkey and 68U201. Benign VEE strains BeAr 35,645 and TC-83 induced only slightly lower concentrations of IF in plasma, bone marrow, spleen and brain than virulent strains Trinidad donkey, 63Z21 and 68U201. However, concentrations of infectious BeAr 35,645 virus were significantly lower in these tissues than virulent strains, resulting in higher ratios of IF: invectious virus, suggesting efficient interferon induction. Benign strain TC-83 showed irregular relationships between IF and infectious virus in plasma or blood and tissues, Splenectomy significantly depressed plasma plasma IF responses to TC-83 virus 20 to 30 hours after inoculation. Interferon appears to be a factor that influences virulence of VEE viruses for hamsters.

Animals↗
PubMed1976

Search for epizootic-like Venezuelan encephalitis virus at enzootic habitats in Guatemala during 1969-1971.

Seventy-four strains of Venezuelan encephalitis (VE) virus recovered from sentinel hamsters or mosquitoes at enzootic habitats in Guatemala in the two years following the 1969 epidemic-equine epizootic were examined for ability to produce small plaques in Vero African green monkey kidney cell cultures, like isolates obtained during the epizootic. (a) One strain recovered from a sentinel hamster in late October 1969 at an enzootic habitat near the epicenter of the hemagglutination-inhibition (HI) and equine-virulence properties like epizootic virus; this strain retained its small plaque characteristic after inoculation and recovery from bloods of three horses. (b) None of the other 73 strains produced uniformly small plaques, but 31 formed a few small plaques among large ones. Virions from small plaques of five strains were cloned twice in Vero cell cultures. Four clones produced uniformly small plaques after one more passage in Vero cells; three had hemagglutination-pH properties compatible with epizootic virus or intermediate between epizootic and enzootic virus, but HI tests with these three hemagglutinins or with antibody to the fourth cloned strain showed them to be like Central American enzootic virus. One of three cloned strains tested in horses produced encephalitis and death in one of four horses; another strain produced encephalitis with recovery in one of two horses. (c) Thus these small Vero plaque clones resembled Central American enzootic strains of VE virus in HI and equine-virulence tests, and the small Vero plaque characteristic was not a satisfactory marker for consistently isolating equine-virulent, epizootic VE virions. Nevertheless, this technic led to recognition of one epizootic strain isolated at an enzootic habitat in Guatemala at the end of 1969 outbreak. Whether this strain was there before the outbreak or subsequently penetrated the habitat is uncertain. During the next two years, this strain did not become dominant in that enzootic focus.

Animals↗
PubMed1976

Search for persistent epizootic Venezuelan encephalitis virus in Guatemala, El Salvador and Nicaragua during 1970-1975.

Evidence was sought during 1970-1975 of persistence of equine-virulent Venezuelan encephalitis (VE) virus in regions of Central America that were heavily involved in the epidemic-equine epizootic of 1969. (a) Four sentinel horses were exposed in an arid, upland region of the Atlantic drainage of Guatemala during August-October 1970, but no horse became infected. (b) The epicenter region of the 1969 outbreak, in southwestern Guatemala and southwestern El Salvador, was studied during July 1970-February 1974; no antibody developed in sentinel horses, sentinel hamsters did not die, mosquitoes yielded no virus, wild rats had no detectable VE virus HI antibody. Unexplained decreases in populations of wild terrestrial mammals possibly limited maintenance of VE virus. However, mosquitoes were plentiful and present in the same species composition found at a focus of enzootic VE virus about 35 km northwest of the epicenter region. (c) In studies at two Guatemalan ranches near the epicenter, where horses died in 1969, VE viruse infected sentinel horses along one of three lakes on one ranch during the wet season of 1972 but not during the dry or wet seasons of 1973; the titers of neutralizing antibodies in these four horses were higher against an enzootic strain of VE virus than against an epizootic strain. During 1970 and 1971, VE virus was isolated from sentinel hamsters exposed at a marsh on the other ranch, but Vero plaque characteristics were those of enzootic VE virus. (d) The only epizootic activity of VE virus discovered in Central America in 1970-1975 occurred in Nicaragua between April and June 1972. Several hundred horses died, and N antibody, like that engendered by epizootic virus, was found in two young, unvaccinated horses. Whether this represented persistence of epizootic VE virus or reintroduction of virus is unknown.

Adolescent↗
PubMed1976

Viremia in young herons and ibis infected with Venezuelan encephalitis virus.

Fifty-seven of 61 nestling, 8- to 30-day-old herons of three species (Black-crowned Night Heron, Great Egret, and Snowy Egret), developed viremia lasting one to three days following subcutaneous inoculation with small doses of endemic or epidemic strains of Venezuelan encephalitis virus from Mexico, Guatemala or Venezuela. Two epidemic strains from Guatemala or Venezuela stimulated levels of viremia similar to those following infection with enzootic strains. Great Egrets, Striated and Boat-billed Herons and Scarlet Ibis older than 30 days of age developed viremias of lower levels and shorter durtions than did young birds. Marked differences in levles of viremia were not observed among Black-crowned Night Herons, Great Egrets, or Snowy Egrets. Over 50% of viremic blood samples from herons 8-30 days of age contained 1000 or more chick embryo cell culture plaque forming units of Venezuelan encephalitis per ml, levels sufficient to infect some vector species mosquitoes.

Aedes↗
PubMed1976

Ecologic studies of Venezuelan encephalitis virus and isolations of Nepuyo and Patois viruses during 1968-1973 at a marsh habitat near the epicenter of the 1969 outbreak in Guatemala.

Ecologic studies of Venezuelan encephalitis (VE) virus at a marsh habitat near the epicenter of the 1969 outbreak in Guatemala revealed that the virus was enzootic there. VE virus was isolated yearly during 1968-1973 from sentinel hamsters exposed during the rainy seasons and from mosquitoes collected during July and August 1970. Hamsters yielded 41 strains of VE virus and virus was detected within 2 km of the edge of the marsh, in its interior, and at its western extreme 18 km from the central study site at La Avellana. One strain of virus came from a hamster that died in the dry season of January 1970. Culex mosquitoes yielded 20 strains of VE virus and Mansonia and Aedes one each. Culex (Melanoconion) and Aedes taeniorhynchus were most prevalent near the marsh. Hemagglutination-inhitibion (HI) and neutralization antibody tests of sera showed that wild terrestrial mammals (opossums and rodents), humans, and dogs, but not wild birds, were frequently infected. Seven of 16 susceptible residents of villages at the edge of the marsh developed antibodies without symptoms during an 18-month period between September 1971 and February 1973. Only 1 of 5 sentinel rabbits, and none of 30 sentinel chickens developed VE HI antibody during August-September 1971, a period when virus activity was readily detected by the use of sentinel hamsters. Five strains of group C arbovirus (one identified as Nepuyo) were recovered from sentinel hamsters during 1968 to 1970, and one strain of Nepuyo virus was isolated from the blood of a person with a febrile illness during 1972. Two strains of Patois group arboviruses were isolated from Culex mosquitoes during 1970.

Adolescent↗