William C. Wallen
National Institutes of Health
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Featured researches published by William C. Wallen.
Neurology | 1985
J. L. Woyciechowska; J. Dambrozia; P. Leinikki; C. Shekarchi; William C. Wallen; John L. Sever; H. McFarland; D. McFarlin
Viral antibodies to measles, rubella, corona, vaccinia, and mumps viruses in serum and CSF (and to Epstein-Barr virus in serum only) were studied in 24 twin pairs, both discordant and concordant for clinical MS. In pairs, CSF antibody titers for rubella in MS monozygotic and dizygotic twins and for vaccinia in dizygotic twins were higher than for unaffected twins. Increased CSF titers among MS twins existed for measles, rubella, and vaccinia when pairing was ignored. Among MS twins, serum rubella and measles and CSF measles antibody titers, and CSF:serum ratios for measles virus, were higher in those who were DW, positive.
Neurology | 1981
William C. Wallen; Sidney A. Houff; Matti Iivanainen; Vincent P. Calabrese; George H. De Vries
Patients with multiple sclerosis and matched controls were tested for lymphocyte stimulation response and induction of suppressor cell activity in response to concanavalin A (Con A) and antigens from axolemma or myelin. Of 17 stable patients, 6 failed to have a suppressor cell response activated by one of these brain cell antigens. Among the patients who lacked these suppressor responses, five had lymphocyte stimulation responses to the same antigens. All matched controls except for one had suppressor cell responses to these antigens, and none responded with a positive cellular immune reaction. We found no difference in lymphoproliferative responses to Con A in patients and controls. The level of suppressor cell activity induced by Con A in the stable MS patients varied but did not differ significantly from that of controls.
Gynecologic Oncology | 1980
Ashir Kumar; Mostafa S. Selim; David L. Madden; William C. Wallen; Hector H. Vasquez; George A. Nankervis
Abstract The humoral and cellular immune responses were studied in 35 patients with cervical carcinoma (Ca Cx) and 32 healthy controls. Complement fixing (CF) and indirect hemagglutinating antibody (IHA) titers for herpes simplex type 1 (HSV-1), herpes simplex type 2 (HSV-2), and cytomegalovirus (CMV), and fluorescent antibody (FA) titers for viral capsid antigen for Epstein-Barr virus (EBV) were determined. Cellular immune response was measured by the technique of [ 3 H]thymidine uptake by stimulated lymphocytes. Phytohemagglutinin (PHA), HSV-1, HSV-2, and CMV antigens were used as stimulants. CF titers (≥ 1:4) to HSV-1, HSV-2, and CMV were present in 34 ( P P P P P P P P
Archive | 1979
David L. Madden; William C. Wallen; JohnL. Sever
In the past few years a number of studies have been conducted on possible altered immune responses to viruses in patients with multiple sclerosis (MS). Several groups, including our own, have found slightly increased measles antibody levels in MS patients (1, 2). Recently, altered cellular immune responses to measles have been reported (5). Other studies have suggested the association of measles and an unidentified agent with MS (3, 4, 5, 6, 7, 8).
Comparative Immunology Microbiology and Infectious Diseases | 1979
Paul H. Levine; William C. Wallen; Patrick K Lai; Thomas R. Jerrells; David A. Fuccillo
Abstract Nonhuman primates have become increasingly important to studies on the pathogenesis of Epstein-Barr virus (EBV)-associated diseases in man. The observation that EBV causes a spectrum of illnesses in cotton-topped marmosets (subclinical infection, self-limited lymphoproliferative disease and lymphoma) similar to the spectrum of EBV-associated diseases in humans permits the study of host factors determining the outcome of EBV infection. Although such studies could subsequently lead to control of EBV-associated diseases in man, the scarcity of cotton-topped marmosets has led to the evaluation of other nonhuman primates as possible model systems. In this paper we describe our studies on marmosets, owl monkeys, rhesus and chimpanzees, particularly noting the comparability of the cell-mediated immunity (CMI) response of these animals and their relationship to CMI in humans.
Archive | 1979
JohnL. Sever; David L. Madden; William C. Wallen
Studies of the cellular immune responses of patients with multiple sclerosis (MS) have received increasing attention in recent years. Nimerous investigations have involved studies of general immunocompetence of patients during various phases of the disease while others have tested specific cell-mediated immune reactions with viral or other antigens. We will present reports on these studies in three parts: l) Introduction and History; 2) Current Studies; and 3) Studies on Regulatory Cells.
Archive | 1979
William C. Wallen; JohnL. Sever; David L. Madden
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Although the etiology of MS remains undefined, many have suggested that immune mechanisms play a central role in the pathogenesis of the disease. Two hypotheses for the pathogenesis of MS have recently received widespread interest: l) the disease is the result of a chronic viral infection which is not controlled due to a faulty immune response; and 2) the disease is an autoimmune response resulting from an inherent immunological defect. These hypotheses may not be mutually exclusive in that chronic viral infection may result in altered immune function and autoimmunity.
Annals of Neurology | 1983
Anita B. Chu; John L. Sever; David L. Madden; Marti Iivanainen; Marta Leon; William C. Wallen; Benjamin Rix Brooks; Young Jack Lee; Sidney A. Houff
Teratology | 1986
W. T. London; A. J. Martinez; S. A. Houff; William C. Wallen; B. L. Curfman; R. G. Traub; JohnL. Sever
JAMA Neurology | 1981
Matti Iivanainen; William C. Wallen; Marta Leon; Jormak Keski-Oja; Vincent P. Calabrese; Mary A. Krasny; Edward A. Waybright; John B. Selhorst; John W. Harbison; David L. Madden; John L. Sever