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Dive into the research topics where Kathleen A. Hay is active.

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Featured researches published by Kathleen A. Hay.


Antimicrobial Agents and Chemotherapy | 2001

Inhibition of Herpes Simplex Virus Reactivation by Dipyridamole

Richard B. Tenser; Andrew Gaydos; Kathleen A. Hay

ABSTRACT Herpes simplex virus (HSV) reactivation from latency was investigated. Reactivation of thymidine kinase-negative HSV, which is defective for reactivation, was greatly enhanced by thymidine (TdR). The reactivation-enhancing effect of TdR was blocked by dipyridamole (DPM), a known nucleoside transport inhibitor. DPM also inhibited wild-type HSV reactivation, suggesting potential antiviral use.


Multiple Sclerosis Journal | 2000

Leukotropic herpesviruses in multiple sclerosis

Kathleen A. Hay; Richard B. Tenser

Detection frequency of human herpesvirus 6 (HHV-6) and Epstein Barr virus (EBV) DNA in multiple sclerosis (MS) patient and controls was investigated. DNA of peripheral blood mononuclear leukocytes (PBL) was isolated and amplified by polymerase chain reaction techniques. EBV DNA was detected in all patients and controls. HHV-6 DNA was detected in 7% of MS patient and in 14% of controls. Result are compared with other investigations of HHV-6 DNA in PBL, serum, CSF and brain of patient with MS. Result of the present study and other investigations do not show an association between HHV-6 in PBL and MS.


Journal of Neuroimmunology | 1995

The role of herpes simplex thymidine kinase expression in neurovirulence and latency in newborn vs. adult mice

Kathleen A. Hay; Andrew Gaydos; Richard B. Tenser

Infection by standard thymidine kinase-positive (TK+) and TK- mutant herpes simplex virus (HSV) was performed in order to evaluate the role of HSV TK expression in neurovirulence and in HSV latency. In newborn mice, mortality and trigeminal ganglion (TG) HSV titer correlated (both were high) for TK+ and TK- HSV. In adult mice after TK- HSV infection they also correlated (both were low). After TK+ infection of adult mice, correlation was not present; mortality was low while HSV titer was moderately high. During the period of HSV latent infection (> 28 days after HSV infection), the number of neurons expressing HSV latency-associated transcript (LAT) was much greater for TK- HSV newborn-inoculated mice (average of 943/ganglion) than adult-inoculated mice (average of 138/ganglion). In addition, total amount of TG LAT was greater in the former than the latter. Reactivation from latency was restricted, however, for both groups. This result supported the important role of HSV TK expression in HSV reactivation, even when the number of LAT-positive neurons was greatly increased. The following conclusions were drawn from the study of TK- HSV in newborn mice: (i) HSV TK expression was of limited importance for neurovirulence and in vivo HSV TG infection (but was of importance in adult mice); (ii) increased in vivo HSV TG infection correlated with increased number of LAT-positive neurons, so that HSV replication and establishment of latency were not completely separable; and (iii) even with greatly increased numbers of latently infected neurons, HSV TK expression was important for reactivation from latency. Results in newborn mice suggested that the role of HSV TK expression in reactivation from latency and in neurovirulence were separable. To further investigate HSV replication in newborn and adult mice, ganglia were infected with HSV in vitro and either maintained in vitro or transplanted beneath the renal capsule of adult recipients. In both of these studies, HSV titers in ganglia were much higher in newborn than adult ganglia. This suggested that in addition to the well-know role of the immune system in HSV neurovirulence in newborn mice, it is likely that HSV replication per se in neural tissue is greater in newborn than adult mice. This may be related to the high level of HSV neurovirulence in newborn mice.


Virology | 1988

Herpes simplex virus latent infection: reactivation and elimination of latency after neurectomy

Richard B. Tenser; Wade A. Edris; Kathleen A. Hay

Section of the sciatic nerve during the period of herpes simplex virus (HSV) latent infection was performed to evaluate residual latency in mouse dorsal root ganglion. In control mice without sciatic neurectomy, latency was present in 90-100%, while in those which underwent a neurectomy procedure, latent infection was surprisingly decreased to 28-50%. To investigate the hypothesis that the decrease of latency resulted from HSV reactivation and replication (with subsequent neuron destruction), groups of mice were treated with acyclovir to inhibit HSV reactivation, after having undergone a neurectomy procedure. Acyclovir treatment largely prevented the neurectomy-related elimination of latency and supported the hypothesized mechanism.


Intervirology | 1980

Expression of type-common envelope antigens by herpes simplex virus type 2-transformed hamster cells.

Phalguni Gupta; Robert N. Lausch; Kathleen A. Hay; Fred Rapp

At least ten polypeptides were detected on the surface of the herpes simplex virus type 1 (HSV-1) virion. Two of these polypeptides, having molecular weights of 30,000 and 33,000, were identified in two herpes simplex virus type 2-transformed cell lines (333-8-9 and 333-2-29) by immunoprecipitation and SDS-PAGE. The same two virion polypeptides previously were shown to be present in an HSV-1-transformed cell line (14-012-8-1, T-10). These observations suggest that genetic information coding for these polypeptides is in close proximity to that portion of the virus genome involved in transformation.


Journal of NeuroVirology | 1998

Herpes simplex virus latency after direct ganglion virus inoculation

Kathleen A. Hay; Wade A. Edris; Andrew Gaydos; Richard B. Tenser

Herpes simplex virus (HSV) latent infection of ganglion neurons follows axoplasmic transport of HSV, probably in the form of nucleocapsid from peripheral sites of infection (e.g. footpad). This raises the possibility that latency is dependent on this particular means of presenting HSV to ganglion neurons. To investigate this, we directly infected ganglia of mice with HSV and evaluated latency. Initially, ganglia were surgically exposed in intact mice, infected with HSV and after 4 weeks evaluated for HSV latency-associated transcript (LAT) expression. LAT expression suggested latency. To more fully evaluate latency after direct ganglion inoculation, a transplant model was developed. In this model, ganglia were removed from mice, inoculated with HSV, transplanted into syngeneic recipients and evaluated for latency after several weeks. Latency was evident in transplanted ganglia by (1) the presence of LAT in neurons; (2) the lack of HSV ICP4 RNA or viral antigen, and (3) the isolation of HSV from explants of transplants but not from direct homogenates. The transplant model was then used to evaluate the effect of inhibition of HSV replication on latency. Antivirals which inhibited HSV replication markedly decreased the number of LAT-positive neurons in transplants, suggesting a role for HSV replication mechanisms and latency. It is thought that direct ganglion inoculation and ganglion transplant methods will permit unique investigations of mechanisms of latency.


Journal of Medical Virology | 1996

Inhibition of herpes simplex virus reactivation by dipyridamole in a mouse model

Kathleen A. Hay; Andrew Gaydos; Richard B. Tenser

Herpes simplex virus (HSV) thymidine kinase (TK) has been demonstrated to be important for reactivation from latency. Specifically, HSV latency‐associated transcripts (LAT) are expressed during latent infection established by TK‐negative (TK‐) HSV mutants, but reactivation is minimal. TK‐ HSV, however, readily reactivated in the presence of exogenous thymidine (TdR) in explant medium [Tenser et al. (1996): Journal of Virology 70:1271–1276]. In the present report this was further studied by evaluating the effect of dipyridamole (DPM) on HSV reactivation. DPM is known to interfere with nucleoside transport. Inhibition of TdR‐enhanced reactivation of TK HSV and inhibition of reactivation of wild‐type TK+ HSV were evaluated in an experimental mouse model of latency. Without DPM, TK HSV reactivation was increased from 0% to 88% with TdR in explant medium, demonstrating TdR‐enhanced reactivation of TK‐ HSV (as seen previously). TdR‐enhanced reactivation of TK HSV was decreased when DPM (25 or 50 μM) was also present, to 30%‐60% and to 0%, respectively. Secondly, DPM also decreased reactivation of wild‐type TK+ HSV. The reactivation frequency of latently infected dorsal root ganglia was 90% in standard medium (no added TdR), and this was decreased by DPM to 9% and 0%, respectively. Reactivation of trigeminal ganglia in standard medium was 100%, and this decreased to 59% and 23%, respectively. The possibility of a direct toxic effect of DPM on ganglion neurons to explain the results was unlikely. DPM had a modest antiviral effect on HSV replication in cell culture, and its efficacy in blocking reactivation may be related to this activity, probably by inhibition of nucleoside transport.


Journal of Virology | 1989

Latency-associated transcript but not reactivatable virus is present in sensory ganglion neurons after inoculation of thymidine kinase-negative mutants of herpes simplex virus type 1.

Richard B. Tenser; Kathleen A. Hay; Wade A. Edris


Virology | 1993

Neuronal control of herpes simplex virus latency

Richard B. Tenser; Wade A. Edris; Kathleen A. Hay


JAMA Neurology | 1993

Immunoglobulin G Immunosuppression of Multiple Sclerosis: Suppression of All Three Major Lymphocyte Subsets

Richard B. Tenser; Kathleen A. Hay; Judith A. Aberg

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Richard B. Tenser

Pennsylvania State University

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Wade A. Edris

Pennsylvania State University

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Andrew Gaydos

Pennsylvania State University

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Fred Rapp

Pennsylvania State University

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Robert N. Lausch

University of South Alabama

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Constance J. Jones

Pennsylvania State University

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Judith A. Aberg

Pennsylvania State University

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Phalguni Gupta

Pennsylvania State University

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