Problems of confidentiality in genetic counselling.
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Confidentiality↗
Biomedical subjects
M S Smith
Publications and source records attributed to M S Smith.
Identification of the mRNA for the novel alpha 1D-adrenoceptor and two other alpha 1-adrenoceptors in vascular smooth muscle.
In situ hybridization histochemistry, radioligand binding, and in vitro contractile studies were used to characterize the vascular distribution of the recently discovered alpha 1D-adrenoceptor. In situ hybridization with an antisense probe localized the mRNA for the alpha 1D-adrenoceptor to the medial layer of the rat aorta renal and mesenteric resistance arteries. If the tissues were first treated with RNase or a sense probe was used, no specific hybridization signal was detected. The extent to which this receptor was expressed as protein was assessed with radioligand binding studies. A series of ligands used to characterize alpha 1-adrenoceptors interacted with two sites labeled by [3H]prazosin in homogenates from the aorta and mesenteric vascular bed. The high affinity site had the characteristics of an alpha 1A-adrenoceptor. However, the low affinity site had ligand binding characteristics distinct from those of the alpha 1D-adrenoceptor or any other known alpha 1-adrenoceptor subtype. mRNA for the alpha 1B- and alpha 1C-adrenoceptors was also detected in the aorta, renal arteries, and mesenteric resistance arteries. Chloroethylclonidine (CEC) (1 and 10 microM) had differential effects on phenylephrine-induced contractions of vascular smooth muscle. CEC completely inhibited the response in the aorta and caused a partial inhibition in the mesenteric resistance artery. The same concentrations of CEC had little effect on phenylephrine responses in the renal artery. The data suggest the following. 1) mRNA for the novel alpha 1D-adrenoceptor is localized in vascular smooth muscle. 2) Definitive identification of expression of this receptor was not possible; this may be related to coexpression of other subtypes of alpha 1-adrenoceptors. 3) mRNA for the alpha 1C-adrenoceptor was detected in rat peripheral vasculature. 4) The alpha 1A-adrenoceptor is also localized in the vasculature. 5) Three and possibly four alpha 1-adrenoceptors participate in vascular smooth muscle regulation.
Adrenergic alpha-1 Receptor Antagonists↗
Long-term persistence of AZT-resistance mutations in the plasma HIV-1 of patients removed from AZT therapy.
Zidovudine (3'-azido-2',3'-dideoxythymidine) resistant isolates of human immunodeficiency virus type I (HIV-1) were previously demonstrated in zidovudine-treated AIDS patients. The genetic linkage of multiple mutations characteristic of zidovudine-resistance as well as dideoxyinosine-resistance were demonstrated by examining clones of viral reverse transcriptase after polymerase chain reaction (PCR) amplification of plasma culture DNA. The zidovudine-resistance mutations persisted in seven timepoints from four patients for 5 to 22 months despite cessation of zidovudine therapy (and while patients underwent ddI therapy). One patient's plasma virus isolate at 14 months possessed a genotype doubly resistant to ZDV and ddI. Virus recovered from four timepoints showed Intermediate to high levels of zidovudine-resistance. As these genotypes were mainly derived from plasma culture, the zidovudine resistant virus appears to persist and replicate well in vivo after cessation of zidovudine therapy.
Acquired Immunodeficiency Syndrome↗
Cortical refractoriness to N-methyl-D,L-aspartic acid (NMA) stimulation in the lactating rat: recovery after pup removal and blockade of progesterone receptors.
We have previously reported that lactating rats, unlike cycling rats, are refractory to N-methyl-D,L-aspartic acid (NMA), but not kainate, in terms of behavioral responses and activation of cFos expression in the neocortex and hippocampus. To study the factors involved in the suppression of cortical activation in lactating rats in response to NMA, we examined the effects of removing either the suckling stimulus and/or progesterone. The degree of cFos expression was used as a marker for cortical activation. Whereas control suckled animals exhibited little or no cFos activation in the piriform cortex in response to NMA, cycling rats showed a high degree of activation. Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA. Total recovery was observed only in animals who had their pups removed for 24 h and the effects of progesterone were blocked. In general, similar results were obtained in the hippocampus except that the total recovery of hippocampal activation took longer than the cortex. Thus, the deficits in cortical activation depend on the presence of both the suckling stimulus and progesterone. However, progesterone alone cannot induce these cortical deficits since pregnant rats showed no deficits in cortical activation in response to NMA when compared to cycling rats. Therefore, the suckling stimulus is required for the inhibition of NMDA-receptor mediated activation of the cortex and hippocampus. The effects of progesterone appear to act synergistically with the effects of suckling.
Animals↗
c-Fos and related immediate early gene products as markers of activity in neuroendocrine systems.
Expression of c-Fos, or other immediate early gene products, by individual neurons can be used as a marker of cell activation, making staining of these proteins an extremely useful technique for functional anatomical mapping of neuroendocrine systems. Because these proteins are located in the nucleus, identification of the phenotype of the activated neuron using substances located within the cytoplasm can be accomplished with standard double-labeling immunocytochemical techniques. Although it is clear that neurons have the capacity to express a number of immediate early gene products, what remains to be established is whether there is a different pattern of expression following various stimuli. In our studies, we focus primarily on expression of one immediate early gene product, the c-Fos protein. We also include some experiments using expression of other members of the Fos family and Jun proteins as markers for neuronal activation. Our studies describe uses of c-Fos expression in both parvocellular and magnocellular hypothalamic systems to address the following issues: (a) identification of neuroendocrine cells activated by specific treatments and conditions, (b) ascertainment of functional differences in subpopulations activated by specific stimuli, (c) evaluation of neuronal activity in complex areas containing multiple neuroendocrine systems, (d) identification of other brain areas activated in conjunction with neuroendocrine systems following specific stimuli, (e) analysis of connectivity of activated neuroendocrine systems with other parts of the brain, and (f) identification of stimuli that decrease neuronal activity. The neuroendocrine systems studied include those that secrete arginine vasopressin (AVP), oxytocin (OT), corticotropin-releasing hormone (CRH), luteinizing hormone-releasing hormone (LHRH), and dopamine (DA). The use of c-Fos expression has permitted functional neuroanatomical mapping of these systems in response to specific stimuli such as cholecystokinin (CCK), hyperosmolality, and volume depletion, or during various physiological states such as the proestrous ovulatory luteinizing hormone (LH) surge and lactation. Although the use of c-Fos as a marker of neuronal activation will continue to be an extremely powerful technique, future studies will also be directed at relating immediate early gene expression to changes in neuroendocrine gene expression. To this end, we have shown that both c-Fos and c-Jun are expressed in neuroendocrine neurons in response to a number of stimuli, setting the stage for potential regulatory drive to genes containing AP-1 binding sites.
Animals↗
Zidovudine-resistant human immunodeficiency virus type 1 genomes detected in plasma distinct from viral genomes in peripheral blood mononuclear cells.
The emergence of zidovudine (3'-azido-2',3'-deoxythymidine)-resistant strains of human immunodeficiency virus type 1 (HIV-1) from AIDS patients treated with zidovudine has been linked to six amino acid substitutions localized within the viral polymerase gene. Here, in 2 patients, three resistance mutations were detected by polymerase chain reaction amplification of HIV-1 polymerase (reverse transcriptase) sequences from cultures of patient plasma only and not from the same patients' uncultured leukocytes. The differences in distribution of the mutant genotypes from the two sources were highly significant. Both plasma- and peripheral blood mononuclear cell (PBMC)-derived virus (and/or RNA genomes) should be studied in additional subjects to confirm the hypothesis raised by these data that zidovudine-resistant virus may be more frequent in plasma than in uncultured PBMC.
Acquired Immunodeficiency Syndrome↗
Neural tube defects in the parietal region of human embryos: failure to close or closure-reopening?
This is a follow-up study to earlier investigations on neural tube defects (NTD) in the Kyoto collection of human embryos. It includes an extensive examination of abnormal embryos which have been photographed and serially sectioned following routine histological preparation. Two new types of NTD are described in the parietal region (the roof of the third ventricle) which had previously been overlooked. These anomalies were found most commonly in embryos at the developmental period. Carnegie stage [CS] 16-23 (embryonic days 38-52). Hypotheses are advanced regarding the genesis of NTD and whether encephaloceles and NTD are part of a spectrum of malformation. This study also reinforces evidence that the occurrence of NTD is significantly higher in the embryonic period than at birth. Animal studies, using the guinea-pig are discussed with regard to the investigation of hypotheses put forward to explain the genesis of NTD.
Cerebral Ventricles↗
Evaluation of synergy between carbovir and 3'-azido-2',3'-deoxythymidine for inhibition of human immunodeficiency virus type 1.
3'-Azido-2',3'-deoxythymidine and carbovir [racemic and (-) enantiomer] were evaluated individually and in combination for antiviral activity against human immunodeficiency virus type 1 replication and cytotoxicity in vitro. The combination of these drugs synergistically inhibited human immunodeficiency virus type 1 replication in C3 and Jurkat cells and in human peripheral blood mononuclear cells, although the same combination also produced synergistic cytotoxicity in human peripheral blood mononuclear cells.
Antiviral Agents↗
Analysis of human immunodeficiency virus type 1 nef gene sequences present in vivo.
The nef genes of the human immunodeficiency viruses type 1 and 2 (HIV-1 and HIV-2) and the related simian immunodeficiency viruses (SIVs) encode a protein (Nef) whose role in virus replication and cytopathicity remains uncertain. As an attempt to elucidate the function of nef, we characterized the nucleotide and corresponding protein sequences of naturally occurring nef genes obtained from several HIV-1-infected individuals. A consensus Nef sequence was derived and used to identify several features that were highly conserved among the Nef sequences. These features included a nearly invariant myristylation signal, regions of sequence polymorphism and variable duplication, a region with an acidic charge, a (Pxx)4 repeat sequence, and a potential protein kinase C phosphorylation site. Clustering of premature stop codons at position 124 was noted in 6 of the 54 Nef sequences. Further analysis revealed four stretches of residues that were highly conserved not only among the patient-derived HIV-1 Nef sequences, but also among the Nef sequences of HIV-2 and the SIVs, suggesting that Nef proteins expressed by these retroviruses are functionally equivalent. The "Nef-defining" sequences were used to evaluate the sequence alignments of known proteins reported to share sequence similarity with Nef sequences and to conduct additional computer-based searches for similar protein sequences. A gene encoding the consensus Nef sequence was also generated. This gene encodes a full-length Nef protein that should be a valuable tool in further studies of Nef function.
Acquired Immunodeficiency Syndrome↗
Altered luteinizing hormone and prolactin responses to excitatory amino acids during lactation.
We have used excitatory amino acids as tools to elucidate changes in hypothalamic function associated with lactation, focusing on the regulation of luteinizing hormone (LH) and prolactin secretion. In these studies, we have compared the responsiveness to NMA (N-methyl-D,L-aspartate), an agonist for the N-methyl-D-aspartate (NMDA) receptor, with that of kainate, an agonist for another type of glutamate receptor, the kainate receptor. To address the issue of the permeability of the blood-brain barrier to either NMA or kainate, systemic and central administration of the drugs were compared. Four injections of either drug were administered at 10-min intervals to cycling or lactating rats suckling 8 pups. All of these treatment significantly stimulated LH secretion in cycling rats. However, neither systemic injections of NMA (40 mg/kg) or kainate (2.5-3.5 mg/kg), nor third-ventricular administration of NMA (2 micrograms/2 microliters) or kainate (0.2-0.3 micrograms/2 microliters) stimulated LH secretion during lactation. In contrast, LH responses to NMA were observed in lactating animals suckling 2 pups. These data demonstrate that the intensity of the suckling stimulus determines the degree of gonadotropin-releasing hormone (GnRH) neuronal inhibition during lactation. Recovery of the LH response to NMA in animals suckling 8 pups was not observed after treatment with RU 486 to block the effects of progesterone. Thus, the elevated levels of progesterone during lactation do not appear to play a role in inhibiting GnRH neuronal responsiveness. Removal of the 8-pup suckling stimulus for 24 h also did not restore the LH response to NMA. However, treatment with RU 486 and removal of the suckling stimulus for 24 h did restore LH responses to NMA, suggesting that progesterone may play a role in prolonging the recovery of GnRH neuronal responsiveness. The prolactin responses to NMA and kainate changed with the reproductive state of the animal and the site of administration. Central injections of either drug stimulated prolactin release in both cycling and lactating animals. In contrast, whereas systemic administration of NMA stimulated prolactin secretion in cycling animals, kainate had no effect. In the lactating animals, systemic administration of either drug inhibited prolactin secretion. Thus, the difference in the prolactin responses to systemic administration of the drugs may not only be due to a difference in the distribution of kainate and NMDA receptors but also to the steady state level of activity of the prolactin-releasing and -inhibiting factors which is determined by the reproductive state of the animal.(ABSTRACT TRUNCATED AT 400 WORDS)
Amino Acids↗
Regulation of galanin gene expression in gonadotropin-releasing hormone neurons during the estrous cycle of the rat.
Galanin is colocalized with GnRH in neurons of the hypothalamus and basal forebrain of female rats, and this neuropeptide may play a role in the generation of the midcycle surge of gonadotropin secretion. We tested the hypothesis that galanin gene expression in GnRH cells increases during proestrus. To accomplish this, we killed groups of adult female rats at 1200 and 1800 h on the day of proestrus as well as at 1800 h on the day of estrus and used double labeling in situ hybridization and image analysis to estimate and compare the levels of galanin mRNA in cells coexpressing GnRH mRNA. GnRH mRNA was detected with an antisense cRNA probe labeled with the hapten digoxigenin, while the galanin cRNA probe was labeled with 35S and detected by autoradiography. There was no significant difference in the total number of GnRH cells identified in each animal in any of the different groups in any experiment. The relative number of silver grains over these cells, reflecting galanin mRNA content in GnRH neurons (identified by their purple color), was counted with a computerized image analysis system. In an initial experiment, we observed a 2-fold (P < 0.03) higher galanin mRNA signal level in the animals killed at 1800 h than in those killed at 1200 h on the day of proestrus. Animals killed at 1800 h on the day of estrus had galanin mRNA signal levels that were not statistically different from those in the proestrous 1800 h group, indicating that the increase in galanin mRNA at proestrus is maintained for at least 24 h. Galanin mRNA levels in GnRH neurons returned to basal levels equivalent to those in the proestrous 1200 h group by 1000 h on diestrous day 1. In conjunction with the studies of galanin gene expression in GnRH neurons, we compared the relative cellular contents of GnRH mRNA among the same groups. Here, we used single labeling isotopic in situ hybridization for GnRH mRNA and computerized image analysis to count the resulting silver grains. We could detect no difference in GnRH mRNA signal levels (proestrus, 1200 h vs. proestrus, 1800 h vs. estrus, 1800 h). In a final experiment, we investigated the possible role of estrogen in the induction of galanin mRNA expression at proestrus by comparing relative galanin mRNA contents in GnRH neurons among groups of ovariectomized, intact (diestrous day 1), and ovariectomized 17 beta-estradiol-replaced female rats.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Regulation of gonadotropin-releasing hormone (GnRH) and galanin gene expression in GnRH neurons during lactation in the rat.
Galanin is colocalized with GnRH, and its expression in these neurons is enhanced at proestrus, a time of activation of GnRH neurons. We tested the hypothesis that the expression of both the GnRH and galanin mRNAs in GnRH neurons decrease during lactation in the rat, a reproductive state characterized by reduced gonadotropin secretion. For double label in situ hybridization, GnRH mRNA was detected with an antisense cRNA probe labeled with the hapten digoxigenin, whereas galanin mRNA was detected with a cRNA probe labeled with 35S. The number of silver grains deposited over a digoxigenin-labeled cell body provided an index of galanin mRNA levels in GnRH cells. We observed a 60% reduction in signal (grains per cell) for galanin mRNA in GnRH neurons of lactating animals compared with those of diestrus animals (P < 0.004), with no difference in the number of GnRH neurons between groups. To compare cellular GnRH mRNA content between groups, we used single label in situ hybridization and image analysis. Signal levels (grains per cell) for GnRH mRNA were not different between diestrus and lactating animals in either an initial (diestrus, 121.4 +/- 5.9; lactation, 117.3 +/- 8.0; P > 0.7) or in a subsequent trial (diestrus, 184.0 +/- 10.4; lactation, 197.5 +/- 13.0; P > 0.7). To confirm and extend these findings, we used a RNAse protection assay to measure and compare the content of GnRH mRNA in hypothalamic fragments between diestrus and lactating animals. The concentration of GnRH mRNA (picograms of mRNA per 25 micrograms total RNA) was not different between the two groups (diestrus, 1.21 +/- 0.25; lactation, 1.25 +/- 0.13; P > 0.7). A determination of the total GnRH peptide content by RIA in a separate set of hypothalamic dissections revealed no difference between groups in the level of GnRH content (nanograms) per hypothalamus (diestrus, 6.0 +/- 0.6; lactation, 5.7 +/- 0.4; P > 0.4). We conclude that galanin mRNA expression in GnRH neurons of the rat is diminished during lactation, whereas GnRH expression continues unabated. This decrease in galanin gene expression associated with lactation may lead to decreased synthesis and secretion of galanin, which, in turn, could diminish the pulsatile secretion of GnRH or reduce its activity at the pituitary.
Animals↗
Lactation alters neuropeptide-Y and proopiomelanocortin gene expression in the arcuate nucleus of the rat.
To identify possible factors associated with lactation that may be involved in the suppression of GnRH neuronal function, we have examined whether lactation induces changes in arcuate nucleus neuronal function, focusing on changes in neuropeptide-Y (NPY) and POMC neuronal activity. Animals were studied during diestrous day 1 of the estrous cycle or during day 10 postpartum. Lactating animals had their litters adjusted to eight pups on day 2 postpartum. Brain tissue was removed to measure NPY peptide content in the median eminence (ME) or the ME-arcuate nucleus (ME-ARC) and to quantify NPY or POMC mRNA by in situ hybridization, using 35S-labeled antisense riboprobes. The NPY peptide content was significantly increased in the ME (1.8-fold) and ME-ARC (1.5-fold) during lactation compared to those on diestrus. The NPY mRNA content throughout the ARC did not differ between diestrous and lactating animals. However, if specific subdivisions of the ARC were examined, a significant increase (1.8-fold) in NPY mRNA in the ARC-C region of the ARC (at the plane of the dorsal medial hypothalamic nucleus) was observed during lactation. Dorsal to the ARC in this same plane, there was also an induction of NPY expression in cells lateral to the dorsal medial hypothalamic nucleus. The increases in NPY mRNA in the ARC-C region of the arcuate nucleus persisted for at least 24 h after removal of the suckling stimulus. The other subdivisions of the ARC did not show any differences in NPY mRNA between diestrus and lactation. The POMC mRNA content was decreased by 20-30% during lactation compared with that on diestrus. The effects of lactation to decrease POMC mRNA content were not specific to any subdivision of the ARC, but were observed throughout the entire ARC. Given that lactation is an estrogen-deficient state, the increase in NPY neuronal activity, as indicated by increased gene expression in the caudal portion of the ARC and increased content in the ME, could play an inhibitory role in the regulation of GnRH secretion. However, the decrease in POMC neuronal activity, as suggested by the decrease in gene expression throughout the ARC, would not appear to be involved in the suppression of GnRH neuronal activity. These changes in ARC neuronal function could be related to hormonal changes or metabolic signals regulating food intake during lactation.
Animals↗
Suppressed tyrosine hydroxylase gene expression in the tuberoinfundibular dopaminergic system during lactation.
Suckling-induced PRL secretion is regulated in part by a reduction in tuberoinfundibular dopamine (TIDA) neuronal activity. We have examined the effects of suckling on TIDA activity in the arcuate nucleus by measuring changes in gene expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. TH gene expression was assessed by performing in situ hybridization, using a 35S-labeled antisense riboprobe for quantitating TH mRNA and analyzing grain density with the aid of an Optimas Bioscan image analysis system. Lactating rats suckled by eight pups were studied on postpartum day 10, and diestrous day 1 rats were used as controls. The results showed that lactation suppressed TH mRNA content throughout the arcuate nucleus to about 10% of diestrous levels. The dramatic reduction in TH mRNA during lactation was specific to the arcuate nucleus, as TH mRNA levels in the zona incerta were similar during lactation and diestrus. The suckling stimulus was the primary signal responsible for the suppression of TH mRNA in the arcuate nucleus, as removal of the pups for 6 h restored TH mRNA content to diestrous levels. By 24 h after pup removal, TH mRNA had reached almost twice diestrous levels. In view of the dramatic reduction in TH mRNA levels during lactation, we examined whether TH protein in the arcuate nucleus was similarly diminished. TH protein was detected by immunocytochemistry using a monoclonal antibody to TH. Qualitatively, TH staining was heavier in cell bodies, nerve fibers, and median eminence during diestrus. There was a small, but significant, decrease in TH-positive cell numbers during lactation (14% reduction) compared to those on diestrus. These data provide clear evidence that TH expression is suppressed during lactation, as evidenced by the decrease in TH mRNA and TH protein. The reduction in TH expression most likely contributes to the decrease in dopaminergic tone during lactation.
Animals↗
Changes in pituitary gonadotropin-releasing hormone receptor messenger ribonucleic acid content during lactation and after pup removal.
Lactation is associated with a reduction in pituitary GnRH receptor content (GnRH-R) when compared with diestrus of the estrous cycle. These studies examined whether the changes in GnRH-R during lactation involved alterations in GnRH-R gene expression. GnRH-R messenger RNA (mRNA) levels were assessed by in situ hybridization, using a 35S-labeled antisense riboprobe coding for the transmembrane region of the mouse GnRH-R gene. The area occupied by grains in 20-microns sections of the pituitary was assessed with an image analysis program. The specificity of the probe for GnRH-R mRNA was demonstrated by the presence of only background grains over the pituitary when a sense riboprobe to GnRH-R mRNA was used. Also, there was an absence of clusters of grains over the posterior pituitary, an area devoid of gonadotropes. In lactating rats suckling eight pups on day 10 postpartum, GnRH-R mRNA levels in the anterior pituitary were suppressed by 60% when compared with the levels observed during diestrus. Removal of the eight-pup suckling stimulus for 24 h reestablished the diestrous pattern of GnRH-R mRNA expression. These results demonstrate that the suckling stimulus results in a significant suppression of GnRH-R mRNA levels that is reversed by removal of the stimulus. These changes in GnRH-R mRNA most likely contribute to the changes in GnRH-R content observed in response to the suckling stimulus.
Animals↗
Effects of N-methyl-D-aspartate receptor activation on cFos expression in luteinizing hormone-releasing hormone neurons in female rats.
N-Methyl-D,L-aspartic acid (NMA), an agonist of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors, stimulates the secretion of LH by increasing the release of LHRH. During proestrus, LHRH neurons express cFos in association with the LH surge. To determine the involvement of NMDA receptors in the activation of LHRH neurons on proestrus, we treated animals with an NMDA receptor blocker, MK-801. Treatment with MK-801 (0.3 mg/kg, sc) at 1130 h blocked both the LH and PRL surges and cFos expression in LHRH neurons. These data suggest that NMDA receptors are involved in the regulation of LHRH neuronal activation during the LH surge. We then determined whether NMA treatment could restore LH secretion and cFos expression in LHRH neurons in animals whose endogenous proestrous LH surges were blocked with pentobarbital. In the pentobarbital-blocked rats, NMA failed to induce cFos expression in LHRH neurons and increase LH secretion, but it did result in an increase in PRL secretion. To determine if NMA treatment alone could induce cFos expression in LHRH neurons, diestrous rats were treated with NMA by either systemic (40 mg/kg BW; four injections, 10 min apart) or third ventricular (2 micrograms in 2 microliters; four injections, 10 min apart) injections. NMA administration (regardless of the route of administration) caused an increase in LH secretion and significant cFos expression in many regions of the brain, including sites where the LHRH perikarya are concentrated. However, neither systemic nor intraventricular administration of NMA induced cFos expression in LHRH neurons. Thus, even though NMA results in increased activity of LHRH neurons, as evidenced by increased LH secretion, NMDA receptor activation alone appears to be insufficient to induce cFos expression in the LHRH neurons.
Animals↗
Rabies and bats in a rabies-endemic area of southern Africa: application of two commercial test kits for antigen and antibody detection.
In southern Africa, isolates of rabies-related viruses (i.e. Duvenhage virus and Lagos bat virus) have been made from insectivorous and frugivorous bats. As no recent formal bat virus survey has been reported in southern Africa, a survey of bats in rabies-endemic areas was undertaken. Five hundred and forty-seven bats (13 species) were collected from 21 localities in the Orange Free State, Lesotho and the northern Cape Province. None of the 190 bat sera tested using the "Trousse Platelia Rage" ELISA kit (Diagnostic Pasteur), had antibodies to rabies virus glycoprotein G. Rabies virus nucleocapsid antigen was also sought for in the brains of 530 bats (13 species) by means of the "Rapid rabies enzyme immunodiagnosis" (RREID) test (Diagnostics Pasteur). No positive results were obtained. These results show that bats are unlikely to play an important role as hosts of rabies in these parts of Africa, although a low rate of infection cannot be excluded.
Africa, Southern↗