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B A Pancake

Publications and source records attributed to B A Pancake.

24 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↗
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↗
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↗
PubMedDate not supplied

Prevalence of HTLV-I Tax in a subset of patients with rheumatoid arthritis.

OBJECTIVE: In regions of the world where the human T cell lymphotropic virus type I (HTLV-I) is endemic, it is recognized that infection with this virus is associated with autoimmune diseases such as rheumatoid arthritis (RA). Moreover, mice transgenic for the HTLV-I Tax gene develop a disease akin to RA. The observation that about 8% of healthy American blood donors carry HTLV-I Tax in their lymphocytes (1) prompted studies to determine whether Tax positivity is more prevalent among patients with RA and if so, whether its sequence is homologous with prototypic HTLV-I Tax. This proved to be the case. Of 102 patients with RA tested, one was a carrier of HTLV-I and 25 had the Tax sequences in their mononuclear cells and antibodies to p40 Tax in their sera, while being negative for antibodies to the structural proteins of the virus. METHODS: Blood was collectedfrom 102 RA patients. Lysates of their mononuclear cells were assayed for HTLV-I Tax by PCR/Southern analysis, and in some positive cases Tax sequence analysis was performed. Antibodies to p40 Tax, the gene product of the Tax sequence, were detected by western blot assay using recombinant p40 Tax as antigen. Results Of the 102 patients tested, one proved to be a carrier of the virus, having antibodies and sequences for the viral structural proteins, gag and env in addition to p40 Tax. Twenty-five of the 101 HTLV-I/II seronegative patients carried both HTLV-I Tax sequences in their mononuclear cells and had antibodies to p40 Tax. Sequence analysis confirmed homology with HTLV-I Tax. CONCLUSION: The data show that the prevalence of HTLV-I Tax positivity among patients with RA is -3 times higher than among healthy blood donors. Since Tax is known to be involved in the development of numerous autoimmune diseases, the possibility that it is responsible for the development of RA in a subpopulation of patients with this disease is not remote.

Arthritis, Rheumatoid↗