Edward Klucking Interview

Edward (Ed) Klucking taught in the biology and geology departments at Central Washington University from 1960 into the 1990s.https://digitalcommons.cwu.edu/cwura_interviews/1124/thumbnail.jp

Resistance to Infection by Subgroups B, D, and E Avian Sarcoma and Leukosis Viruses Is Explained by a Premature Stop Codon within a Resistance Allele of the tvb Receptor Gene

Here we present the first molecular characterization of the defect associated with an avian sarcoma and leukosis virus (ASLV) receptor resistance allele, tvb(r). We show that resistance to infection by subgroups B, D, and E ASLV is explained by the presence of a single base pair mutation that distinguishes this allele from tvb(s1), an allele which encodes a receptor for all three viral subgroups. This mutation generates an in-frame stop codon that is predicted to lead to the production of a severely truncated protein

Avian Sarcoma and Leukosis Virus Cytopathic Effect in the Absence of TVB Death Domain Signaling

The cytopathic effect (CPE) seen with some subgroups of avian sarcoma and leukosis virus (ASLV) is associated with viral Env activation of the death-promoting activity of TVB (a tumor necrosis factor receptor-related receptor that is most closely related to mammalian TNF-related apoptosis-inducing ligand [TRAIL] receptors) and with viral superinfection leading to unintegrated viral DNA (UVD) accumulation, which is presumed to activate a cellular DNA damage response. In this study, we employed cells that express signaling-deficient ASLV receptors to demonstrate that an ASLV CPE can be uncoupled from the death-promoting functions of the TVB receptor. However, these cell-killing events were associated with much higher levels of viral superinfection and DNA accumulation than those seen when the virus used signaling-competent TVB receptors. These findings suggest that a putative cellular DNA damage response that is activated by UVD accumulation might act in concert with the death-signaling pathways activated by Env-TVB interactions to trigger cell death. Such a model is consistent with the well-established synergy that exists between TRAIL-signaling pathways and DNA damage responses which is currently being exploited in cancer therapy regimens

Immune Responses Elicited by Recombinant Vaccinia-Human Immunodeficiency Virus (HIV) Envelope and HIV Envelope Protein: Analysis of the Durability of Responses and Effect of Repeated Boosting

Previous studies indicate that immunization with recombinant (r) vaccinia-human immunodeficiency virus type 1 (HIV-1) gp160 and boosting with baculovirus-derived HIV-1 rgp160 results in stronger cellular and antibody responses than those following either vaccine alone. The durability of immunity over 1 year was evaluated in 12 recipients. Both cellular and binding antibody responses remained detectable but diminished, and neutralizing antibodies were absent. To boost immunity, rgpI60 was given again 1 year after the initial boost. Reboosting elicited strong HIV-specific lymphoproliferative responses. Binding antibody levels also rose dramatically, and the magnitude of the peak responses was significantly greater following the 2-year than following the 1-year boost. However, neutralizing antibody titers were low (1:10–1:20) and detected in only 4 of 12 persons. Moreover, persistent CD8+ cytolytic responses were not induced. Thus, although repeated rgp 160 boosting after vaccinia-envelope priming can augment selected immune components, an altered regimen may be necessary to achieve protective long-term immunity to HIV-1

Laminar heat transfer in constructal Microchannel networks with loops

10.1115/1.2229228Journal of Electronic Packaging, Transactions of the ASME1283273-280JEPA