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S E Straus

Publications and source records attributed to S E Straus.

At least 163 records · Page 9Linked to original sources
PubMed1992

A novel lymphoproliferative/autoimmune syndrome resembling murine lpr/gld disease.

In mice, the two distinct autosomal recessive genes lpr and gld can induce a syndrome characterized by autoantibody formation and the progressive accumulation of an unusual CD4-CD8- T cell population in peripheral lymphoid tissue. This phenotype does not precisely mirror any human disease. In this report we describe two patients with a progressive lymphoproliferative disorder associated with autoimmunity. The peripheral blood and lymph nodes of these patients contained large numbers of an unusual CD4-CD8- T cell population. These CD4-CD8- T cells express surface markers characteristic of mature peripheral blood T cells (CD3, CD2, CD5), express the alpha/beta form of the T cell receptor, and do not express surface markers characteristic of immature thymocytes (CD1) or NK cells (CD16, CD56). Functionally, these cells exhibited deficient proliferation and lymphokine production upon stimulation with mitogenic antibodies to CD3 or CD2. Both proliferation and lymphokine production could be augmented by co-stimulation with an antibody directed at the CD28 determinant. The clinical and immunological features of this syndrome resemble the lymphoproliferative/autoimmune disease seen in lpr and gld mice.

Animals↗
PubMed1992

Latency in vitro of varicella-zoster virus in cells derived from human fetal dorsal root ganglia.

A potential in vitro model of varicella-zoster virus (VZV) latency was developed. Dissociated human dorsal root ganglion cultures were infected with VZV and maintained for 1 wk in the presence of bromovinyl arabinosyl uracil, a potent inhibitor of VZV. Seven to 21 d after removing the inhibitor (> or = 14 d after infection), the cells were trypsinized, passed to monolayers of human embryonic lung fibroblasts, and observed for VZV reactivation as indicated by typical cytopathic effects and the appearance of VZV antigens. VZV reactivated from 56% of the cultures containing both neurons and satellite cells but not from cultures specifically enriched for either neurons, satellite cells, or ganglion-derived fibroblasts. The failure to isolate VZV from cell suspensions that were sonicated before cocultivation with fibroblasts indicated that infectious VZV was not present before reactivation. Moreover, immunohistochemical and immunoprecipitation studies revealed no VZV-specific antigens in any cultures before the reactivation stimulus. VZV antigens were detected after trypsinization and cocultivation. These findings suggest that cultures containing both neurons and satellite cells provide a model system for VZV persistence that possesses many properties of a latent infection.

Cells, Cultured↗
PubMed1992

Attention and short-term memory in chronic fatigue syndrome patients: an event-related potential analysis.

We recorded event-related brain potentials (ERPs) from 13 patients with chronic fatigue syndrome (CFS) and 13 matched normal controls. To assess attentional and memory deficits in CFS patients, we used a short-term memory task in which events occurred in different spatial locations and the patients made a rapid-response (RT) when a letter in a relevant location matched a letter in the prememorized set (Attention paradigm). Time-on-task effects on the ERP and behavioral measures were assessed over the 2 1/4-hour duration of this task. Both groups also performed a visual Oddball paradigm, with an RT, before and after the Attention paradigm. The patients' RTs were much more variable and, in nine of 13 cases, slower than the mean RT of the controls in both paradigms. The patients' memory performance was not significantly different from that of the controls and there were no group differences in the overall amplitude, latency, or scalp distribution of the N1, P2, N2, or P300 components of the ERP in either paradigm. The ERP and performance data from both paradigms suggest that perceptual, attentional, and short-term memory processes were unaffected in CFS patients and that the differences were limited to response-related processes.

Adult↗
PubMed1992

TORCH infections. Diagnosis in the molecular age.

TORCH agents cause a varied spectrum of disease. Advances in ultrasound, invasive perinatal procedures and molecular diagnostics have allowed in utero evaluation. Infected fetuses, especially those which are sonographically abnormal, may be treated in utero depending upon the pathogen and attendant pathophysiology. Subclinical perinatal infections may lead to later childhood deficits. Such infected fetuses may benefit from early diagnosis and prompt initiation of rehabilitative measures.

Abbreviations as Topic↗
PubMed1991

Prevention of ultraviolet-light-induced herpes labialis by sunscreen.

Sunlight exposure is reported by some patients to precede onset of recurrent herpes labialis. Ultraviolet (UV) B light is known to be a stimulus for the reactivation of herpes simplex virus (HSV) infections. We assessed the effect of a sunblocking agent on UV-light-induced reactivation of recurrent herpes labialis in a double-blind, placebo-controlled crossover trial. 38 patients were exposed on two separate occasions to four minimum erythema doses of UV light at an area of previous labial herpes recurrence. A solution containing sunscreen was applied to the lips before one exposure and a matched placebo before the other. After placebo and UV exposure, herpes labialis developed in 27 (71%) of the 38 patients, with a mean time to recurrence of 2.9 (SEM 0.2) days. In contrast, when sunscreen was applied before UV exposure, no lesions developed, but 1 of the 35 patients shed virus at the exposure site. We conclude that UV light is a potent stimulus for inducing reactivation of herpes labialis, and that application of sunscreen may be effective in the prevention of sunlight-induced recurrent infection.

Adolescent↗
PubMed1991

Chronic fatigue syndrome: lack of association with hepatitis C virus infection.

Chronic fatigue syndrome (CFS) is a debilitating heterogeneous disorder lacking consistent, objective physical or laboratory abnormalities. Among the hypothetical etiologies for CFS are chronic viral infections. The present controlled seroprevalence study found that, among typical CFS patients, evidence of hepatitis C virus (HCV) infection is uncommon. Only one of 36 patients and none of 14 controls were anti-HCV positive. The positive patient had persistent aminotransferase elevations and prior posttransfusion hepatitis. Thus HCV infection is not a common feature of CFS and should not be routinely sought.

Adult↗
PubMed1991

In utero diagnosis of congenital varicella zoster virus infection by chorionic villus sampling and polymerase chain reaction.

Varicella zoster virus infection acquired in pregnancy is reported to cause fetal damage in 5% to 10% of cases. We used polymerase chain reaction to attempt molecular diagnosis of fetoplacental varicella zoster virus infection in two patients. Tissue obtained by chorionic villus sampling in the second trimester was analyzed by polymerase chain reaction with a varicella zoster virus-specific primer, ORF-63, and was found to be positive in both patients. Viral cultures were negative. One patient elected pregnancy termination at 23 weeks. Southern blot hybridization of neonatal brain tissue for varicella zoster virus was negative. The second patient carried the pregnancy to term and was delivered of a normal infant. Varicella zoster virus immunoglobulin M and viral cultures were negative. The presence of viral deoxyribonucleic acid sequences in placental tissue does not correlate with fetal disease.

Adolescent↗
PubMed1991

Characterization of herpes simplex virus type 2 latency-associated transcription in human sacral ganglia and in cell culture.

The ability of herpes simplex virus type 2 (HSV-2) to establish latency in and reactivate from sacral dorsal root sensory ganglia is the basis for recurrent genital herpes. The expression of HSV-2 genes in latently infected human sacral ganglia was investigated by in situ hybridization. Hybridizations with a probe from the long repeat region of HSV-2 revealed strong nuclear signals overlying neurons in sacral ganglia from five of nine individuals. The RNA detected overlaps with the transcript for infected cell protein O but in the opposite, or "anti-sense," orientation. These observations mimic those made previously with HSV-1 in human trigeminal ganglia and confirm the recent findings during latency in HSV-2-infected mice and guinea pigs. Northern hybridization of RNA from infected Vero cells showed that an HSV-2 latency-associated transcript was similar in size to the larger (1.85 kb) latency transcript of HSV-1. Thus, HSV-1 and HSV-2 latency in human sensory ganglia are similar, if not identical, in terms of their cellular localization and pattern of transcription.

Adult↗
PubMed1991

The nucleotide sequence, 5' end, promoter domain, and kinetics of expression of the gene encoding the herpes simplex virus type 2 latency-associated transcript.

The sequence of the herpes simplex virus type 2 (HSV-2) latency-associated transcript (LAT) region resembles that of HSV-1 only where the LATs overlap ICP0 and in the putative promoter region. Otherwise, the LAT 5' ends, kinetics of expression, and promoter elements are mostly conserved between HSV-1 and HSV-2. The remaining differences between the LATs could contribute to each virus's distinctive pattern of reactivation.

Amino Acid Sequence↗
PubMed1991

Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome.

Chronic fatigue syndrome is characterized by persistent or relapsing debilitating fatigue for at least 6 months in the absence of a medical diagnosis that would explain the clinical presentation. Because primary glucocorticoid deficiency states and affective disorders putatively associated with a deficiency of the arousal-producing neuropeptide CRH can be associated with similar symptoms, we report here a study of the functional integrity of the various components of the hypothalamic-pituitary-adrenal axis in patients meeting research case criteria for chronic fatigue syndrome. Thirty patients and 72 normal volunteers were studied. Basal activity of the hypothalamic-pituitary-adrenal axis was estimated by determinations of 24-h urinary free cortisol-excretion, evening basal plasma total and free cortisol concentrations, and the cortisol binding globulin-binding capacity. The adrenal cortex was evaluated indirectly by cortisol responses during ovine CRH (oCRH) stimulation testing and directly by cortisol responses to graded submaximal doses of ACTH. Plasma ACTH and cortisol responses to oCRH were employed as a direct measure of the functional integrity of the pituitary corticotroph cell. Central CRH secretion was assessed by measuring its level in cerebrospinal fluid. Compared to normal subjects, patients demonstrated significantly reduced basal evening glucocorticoid levels (89.0 +/- 8.7 vs. 148.4 +/- 20.3 nmol/L; P less than 0.01) and low 24-h urinary free cortisol excretion (122.7 +/- 8.9 vs. 203.1 +/- 10.7 nmol/24 h; P less than 0.0002), but elevated basal evening ACTH concentrations. There was increased adrenocortical sensitivity to ACTH, but a reduced maximal response [F(3.26, 65.16) = 5.50; P = 0.0015). Patients showed attenuated net integrated ACTH responses to oCRH (128.0 +/- 26.4 vs. 225.4 +/- 34.5 pmol/L.min, P less than 0.04). Cerebrospinal fluid CRH levels in patients were no different from control values (8.4 +/- 0.6 vs. 7.7 +/- 0.5 pmol/L; P = NS). Although we cannot definitively account for the etiology of the mild glucocorticoid deficiency seen in chronic fatigue syndrome patients, the enhanced adrenocortical sensitivity to exogenous ACTH and blunted ACTH responses to oCRH are incompatible with a primary adrenal insufficiency. A pituitary source is also unlikely, since basal evening plasma ACTH concentrations were elevated. Hence, the data are most compatible with a mild central adrenal insufficiency secondary to either a deficiency of CRH or some other central stimulus to the pituitary-adrenal axis. Whether a mild glucocorticoid deficiency or a putative deficiency of an arousal-producing neuropeptide such as CRH is related to the clinical symptomatology of the chronic fatigue syndrome remains to be determined.

Adrenal Cortex↗
PubMed1990

Antibodies to Epstein-Barr virus in iridocorneal endothelial syndrome.

Antibody titers to Epstein-Barr virus were determined in 13 patients with iridocorneal endothelial syndrome and in 13 healthy race-, age-, and sex-matched controls. Both the geometric mean titer of IgG antibodies to the Epstein-Barr virus capsid antigen and the proportion with high titers of IgG antibodies to the Epstein-Barr virus capsid antigen (greater than or equal to 1:640) were significantly higher in 12 seropositive patients with iridocorneal endothelial syndrome than in 12 seropositive controls (1/761:1/202, P = .001; 83.3%:8.3%, P less than .001). Ten of 12 seropositive patients with iridocorneal endothelial syndrome and five of 12 seropositive controls had antibodies to Epstein-Barr virus-induced early antigens (greater than or equal to 1:10) (Fisher's Exact Test, P less than .05), while four seropositive patients with iridocorneal endothelial syndrome and one seropositive control had low to undetectable levels of antibodies to Epstein-Barr virus-associated nuclear antigen (less than or equal to 1:5) (P greater than .1). Antibody levels to cytomegalovirus or measles virus were not different between patients with iridocorneal endothelial syndrome and controls. Additional studies showed no evidence of humoral immune disorder or collagen vascular disease in the patients with iridocorneal endothelial syndrome. The serologic profiles suggest that the patients with iridocorneal endothelial syndrome examined had a cellular immune abnormality sufficient to permit reactivation of latent Epstein-Barr virus infection and imply, but do not establish, a role for Epstein-Barr virus infection in the pathogenesis of some cases of the iridocorneal endothelial syndrome.

Adult↗
PubMed1990

Varicella-zoster virus infection of human astrocytes, Schwann cells, and neurons.

Human fetal cell cultures enriched for astrocytes, Schwann cells, or dorsal root ganglia neurons were infected with cell-free varicella-zoster virus (VZV), and the course of these infections was compared with that in fetal fibroblasts. Virus replication was detected in each neural cell type as early as 10-16 hr postinfection. Permissiveness of each cell type was confirmed by electron microscopy. However, the kinetics of virus spread varied between the neural cell types. Moreover, the accumulation, progression, and localization of VZV putative immediate early (IE), early (E), and late proteins was neural cell-type specific. VZV replication was slower in Schwann cells and neurons than in astrocytes. In Schwann cells and neurons VZV E proteins could be detected before IE proteins, a reversal of the order of accumulation noted with astrocytes and fibroblasts. There was also relatively more VZV IE protein in the perinuclear cytoplasm of Schwann cells and neurons, suggesting a delay in the transport of this antigen to its nuclear site. The permissiveness of non-neuronal cell types suggests that they could play a role in the pathogenesis of herpes zoster.

Antigens, Viral↗
PubMed1990

Acute infectious mononucleosis. CD30 (Ki-1) antigen expression and histologic correlations.

Lymph nodes from patients with acute infectious mononucleosis (AIM) typically show marked paracortical expansion and a prominent immunoblastic proliferation that can occur in nodules and sheets, as well as within sinuses. The marked immunoblastic proliferation, coupled with Reed-Sternberg-like cells and a polymorphous inflammatory cell background, may simulate either non-Hodgkin's lymphoma or Hodgkin's disease. A recently described entity, Ki-1-positive lymphoma, or large cell anaplastic lymphoma, shares some clinicopathologic and phenotypic features with AIM and must be considered in the differential diagnosis. The present case describes a 20-year-old male who had signs and symptoms consistent with AIM, which he was later proven serologically to have, but whose cervical lymph node showed features suspicious for large cell anaplastic lymphoma. In addition, the Ki-1 (CD30) antigen was expressed by some of the atypical immunoblasts, further raising this possibility.

Acute Disease↗