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Biomedical subjects

M Arai

Publications and source records attributed to M Arai.

At least 181 records · Page 10Linked to original sources
PubMed1999

C-Reactive protein in dilated cardiomyopathy.

The prognosis for patients with idiopathic dilated cardiomyopathy (DCM) is poor, although clinical features are variable. Prediction of outcome has been difficult in individual patients based on laboratory data. In some patients with DCM, myocardial damage secondary to viral or immune-mediated myocardial inflammation may persist. To objectively assess inflammation, we measured plasma concentrations of C-reactive protein (CRP) in 188 patients with idiopathic DCM over 5-8 years. All had dyspnea and fatigue at rest; all patients had a left ventricular ejection fraction less than 40% by echocardiography or by contrast or radionuclide ventriculography. We divided these patients into two groups: patients dying within 5 years following admission (n = 49) and the remainder surviving for at least 5 years (n = 139). CRP concentrations in the patients dying early were significantly higher than in the long-term survivors (1. 05 +/- 1.37 vs. 0.49 +/- 1.04 mg/dl, p < 0.05). Sixty-two percent of the patients with CRP>1.0 died within 5 years. In addition to other laboratory tests including electrocardiography and echocardiography, routine CRP measurements proved to be valuable for identifying high-risk patients who require special treatment strategies.

Adult↗
PubMed1999

Developmental expression and regulation of adrenocortical cytochrome P4501B1 in the rat.

A 57-kDa protein whose expression in rat adrenocortical microsomes is increased after weaning has been identified as cytochrome P4501B1 (CYP1B1). Levels of CYP1B1 protein were moderately expressed in late gestation fetuses and on postnatal day 1 (pdl), but were nearly undetectable on pd6 and pd1O. CYP1B1 expression initially increased in the late preweaning period (pd17-19) and again immediately postweaning (pd21-24). The temporal coincidence of CYP1B1 expression and weaning was not due to transition from suckling to solid food, as neonates that were prematurely weaned showed no increase in adrenal CYP1B1 compared with normally weaned littermates. The pattern of CYP1B1 expression paralleled changes in microsomal metabolism of 7,12-dimethylbenz[a]anthracene (DMBA), a marker of CYP1B1 activity. Twice daily injections of ACTH to rat pups (pd3-10) failed to significantly increase the expression of CYP1B1 in pd 10 adrenals, although the injections weakly stimulated steroidogenesis. Adrenocortical cells from pd17 neonates and adult cells, when cultured for 3 days, responded similarly to ACTH induction, although neonates showed more than 4-fold less basal activity. It is concluded that rat adrenal CYP1B1 may be developmentally suppressed, and its expression is independent of diet or the presence of a dam. This suppression is retained in cell culture, but is not due to deficient ACTH signaling. These results may explain the reported resistance of neonatal rat adrenals to the toxic effects of polycyclic aromatic hydrocarbons, which are metabolized by CYP1B1 into mutagenic by-products.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

A novel activating mutation in calcium-sensing receptor gene associated with a family of autosomal dominant hypocalcemia.

Autosomal dominant hypocalcemia (ADH), caused by activating mutations of the calcium-sensing receptor (CaSR), is characterized by hypocalcemia with an inappropriately low concentration of PTH. Among 11 missense mutations of CaSR reported to date in patients with ADH or sporadic hypocalcemia, functional properties of 8 mutant CaSRs were characterized. Here, we describe a novel mutation of CaSR and its functional property in a family with ADH. The 41-yr-old male proband had asymptomatic hypocalcemia with a history of recurrent nephrolithiasis. His father had asymptomatic hypocalcemia, but his mother was normocalcemic. PCR-single strand conformation polymorphism and sequencing revealed that both the proband and the father had a novel heterozygous mutation in CaSR gene that causes lysine to asparagine substitution at codon 47 (K47N), which is in the extracellular domain of CaSR, like 6 of 11 known activating mutations. Using HEK293 cells transfected with wild-type or K47N CaSR complementary DNA, the intracellular Ca2+ concentration was assessed in response to changes in the extracellular Ca2+ concentration. The EC50 of the mutant CaSR for the extracellular Ca2+ concentration was 2.2 mmol/L and was significantly lower than that of wild-type (3.7 mmol/L). These results confirm that this mutation is responsible for ADH in this family. The fact that several inactivating mutations in familial hypocalciuric hypercalcemia occur in amino acid around K47 suggests the importance of the N-terminal portion of the receptor in extracellular Ca sensing.

Adult↗
PubMed1999

Cellular glutathione peroxidase as a predominant scavenger of hydroperoxyeicosatetraenoic acids in rabbit alveolar macrophages.

The cytosol of rabbit lung alveolar macrophages contains a high amount of peroxidase, which reduces 5-hydroperoxyeicosatetraenoic acid (5-HPETE) to 5-hydroxyeicosatetraenoic acid (5-HETE) in the presence of glutathione. This peroxidase was purified 69-fold to homogeneity with overall recovery of activity of 18.5%. The molecular mass of the enzyme was approximately 80 kDa by gel filtration, and emerged as a single band at 23.1 kDa under reducing condition by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The amino-terminal sequence of the purified peroxidase was completely identical to the sequence deduced from cellular glutathione peroxidase (cGPx) gene of rabbit liver. No other activity that reduces 5-HPETE to 5-HETE was observed during purification. These results suggest that cGPx plays an important role in metabolism of lipid hydroperoxides, especially HPETE, in lung alveolar macrophages.

Amino Acid Sequence↗
PubMed1999

Cloning and sequencing of beta-mannosidase gene from Aspergillus aculeatus no. F-50.

The manB gene, coding for a unique beta-mannosidase (MANB) of Aspergillus aculeatus, was cloned from genomic and cDNA libraries, and sequenced. The gene consists of 2,811 bp encoding a polypeptide of 937 amino acid residues with a molecular mass of 104,214 Da. The A. aculeatus MANB shared amino acid sequence identity with MANB of human (24%), goat (24%), bovine (24%), and Caenorhabditis elegans (22%). When the A. aculeatus MANB was compared with other related enzymes, a Glu residue corresponding to the active site identified by the Escherichia coli beta-galactosidase and the human beta-guclonidase was conserved. This is the first fungal gene that encodes MANB.

Amino Acid Sequence↗
PubMed1999

Analysis of a catalytic acidic pair in the active center of cellulase from Aspergillus aculeatus.

Four acidic amino acid residues, Asp97, Asp101, Glu118, and Glu202, were located in the cleft from the X-ray crystallographic analysis of FI-CMCase, endo-1,4-beta-glucanase (EC: 3.2.1.4) of Aspergillus aculeatus No. F-50. To identify the catalytic residues of the FI-CMCase, these residues were mutated to Glu or Ser from Asp97 and Asp101, and to Asp or Ser from Glu118 and Glu202 by site-directed mutagenesis, and totally 8 single mutant enzymes expressed in Escherichia coli were prepared: D97E, D97S, D101E, D101S, E118D, E118S, E202D, and E202S. Mutant enzymes E118S and E202S were not shown to have any detectable activity. Kinetic parameters of other mutant enzymes were measured after purification. The Km of mutant enzymes were not much different from that of wild type FI-CMCase, while the Vmax of mutant enzymes D97E, D97S, D101E, D101S, E118D, and D202E were much decreased to 1/50, 1/20, 1/4000, 1/2000, 1/800, and 1/1600 of the wild type FI-CMCase, respectively. From these results we concluded that Glu118 and Glu202 were most probable candidates for a catalytic pair of acidic amino acids in FI-CMCase.

Amino Acid Sequence↗
PubMed1999

[Effect of body positions in human optokinetic nystagmus and optokinetic after nystagmus].

We determined whether whole body tilt would shift the axis of optokinetic nystagmus (OKN) and optokinetic-after nystagmus (OKAN) induced by full-field rotation at 35 degrees/sec. Fifteen normal people were positioned upright or tilted 30 degrees, 60 degrees or 90 degrees to both sides. Stripes of 5 degrees were projected on a 10-foot dome around the subject's yaw axis. Each trial lasted 45 sec. The lights were then extinguished, and the subject remained in darkness for 30 sec, while after nystagmus (OKAN) was recorded. Horizontal and vertical eye movements were recorded by video-oculography at 60 Hz. Eye position and velocity data were stored on optic disk cartridge by use of the data acquisition system. A. OKAN: For the subject in the upright position, the OKN velocity vector was aligned with both gravity and the subject's yaw axis with two minor exceptions. When the subject was tilted, a vertical OKN component (VOKN) appeared in a majority of subjects. For all 15 subjects, the mean angle of the OKN velocity vector regravity (Vectorg) was 22.6 +/- 7.2 degrees at 30 degrees tilted position. The Vectorg were 48.5 +/- 10.3 degrees at 60 degrees tilted position, and 76.4 +/- 12.6 degrees at 90 degrees tilted position. This represented shifts of the OKN velocity vector from the body axis of 7.4 degrees, 11.5 degrees and 13.6 degrees, respectively. The horizontal OKN (HOKN) gain remained unchanged in different positions. B. OKAN: The duration of HOKAN and initial slow phase velocity (SPV) of HOKAN decreased as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. The incidence and initial SPV of VOKAN and Re-Body did not change as the body position increased from upright to 30 degrees, 60 degrees and 90 degrees tilted position, respectively. Thus, VOKN was observed during HOKN as subjects were tilted and tended to vector to gravity, but VOKAN was not always observed during horizontal OKAN when subjects were tilted.

Adult↗
PubMed1999

[The efficiency of magnetic resonance angiography (MRA) in the diagnosis and vertigo--prediction of vertebrobasilar insufficiency (VBI) and atherosclerosis].

Major causes of vertigo in patients who attend Otolaryngology clinics are peripheral vestibular disorders (PVD) and vertebrobasilar insufficiency (VBI). The purpose of this study was to see whether MRA findings can distinguish VBI from PVD to evaluate the efficiency of MRA in the diagnosis of vertigo. A total of 185 vertigo patients were examined by MRA with the 3D-Phase Contrast method. Three kinds of abnormalities of vessels, that is, (a) disappearance, (b) meandering, and (c) stoppage were found in MRA imaging. Therefore, we classified the MRA patterns into four types with two subtypes: type I; normal, type II-R; right hypoform of the vertebral artery, II-L; left hypoform of the vertebral artery, III; meandering form of the vertebrobasilar artery, IV-1; stoppage form of the basilar artery, IV-2; hypoform of the bilateral vertebral and basilar arteries. Diagnosis of the MRA patterns in each patient was camed out by a radiologist and neurosurgeon with the cooperation of an otolaryngologist. In 185 vertigo patients, 139 patients were clinically diagnosed as having PVD, 41 patients as having VBI, and 5 patients as having cerebellar and brainstem infarctions. The numbers of patients in MRA patterns I, II-R, II-L, III and IV were 140, 17, 12, 8, and 8 cases, respectively. The total number of VBI patients who demonstrated type III or IV patterns in MRA was significantly higher than that of type I, II-R and II-L (P < 0.005). All of the 8 cases with cerebellar and brainstem infarction belonged to type IV. Cerebral angiography was performed in nine cases with type II-R, II-L, III or IV-1, and the number of patients in each group was 3, 3, 1 and 2 cases, respectively. All of the type II-R and II-L cases revealed hypoform of the vertebral artery. The appearance of type III was restricted to type III's view was only meandering and type IV-1 showed severe stenotic changes in the union area. These data show that MRA findings in the diagnosis of vertigo patients are very effective in distinguishing VBI and cerebellar and brainstem infarction from PVD and that some pattern of MRA may correspond to atherosclerosis of the vertebrobasilar artery. We think MRA examination of vertigo patients is useful not only to assist in the diagnosis of the etiology but also to predict the stage of atherosclerosis in each patient.

Adolescent↗
PubMed1999

[A posterior horn syndrome presumably due to direct trauma to the sacral cord: a rare complication of epidural anesthesia].

I report here a case of a posterior horn syndrome presumably due to sacral cord injury during the procedure of epidural anesthesia. A 43-year-old female underwent hysterectomy for myoma uteri. The operation was initially planned to be performed under epidural anesthesia. When a needle was inserted at the level of Th 12/L 1, she felt severe pain in the medial aspect of the left thigh. After the operation under general anesthesia, intolerable pain continued in the buttocks, the medial aspect of the left thigh, and the posterolateral aspect of the left lower leg. Lumbar MR images demonstrated slight disc hernia but no intra- and extramedullary hematomas. Seven weeks after the operation, she was referred to my clinic for neurologic evaluation. Motor functions were intact. Knee jerks on both sides were hyperactive; other tendon reflexes were normal. Plantar reflexes were indifferent. Thermal and pin-prick sensations were lost in the left S1 dermatome, and moderately impaired in the left S2 dermatome. Light touch and vibration sense showed no remarkable changes. Her sensory disturbance could have been caused by a lesion involving the left posterior horn and lateral spinothalamic tract within the S1 segment of the spinal cord.

Adult↗
PubMed1999

[Medial medullary infarction: report of three patients presented with central vestibular dysfunction without limb and lingual weakness].

The purpose of this article is to draw attention to atypical presentation of medial medullary infarction (MMI). With advanced imaging techniques, small infarctions occurring in the medulla are more easily identified. It is difficult, however, to make a clinical diagnosis of MMI if both hypoglossal nerve palsy and limb weakness are absent, because motor weakness is considered a cardinal manifestation of MMI. We describe here three patients who developed central vestibular dysfunction due to MMI without limb and lingual weakness. Case 1: A 44-year-old, diabetic woman developed vomiting and numbness on her left upper limb. Examination revealed unidirectional horizontal and rotatory nystagmus beating toward the right side. There were no Horner syndrome and hypoglossal nerve palsy. Barré arm and leg signs and limb ataxia were absent. Romberg sign was negative. Hypesthesia was present on her left forearm, hand, and fingers. Thumb-localizing test was normal. Cranial MRI demonstrated an infarction in the right paramedian region of the upper medulla. MR angiography demonstrated irregularity of the basilar and the left vertebral arteries. Case 2: A 69-year-old woman suffered from dizziness and nausea. She showed unidirectional, left-beating horizontal nystagmus. There were no Horner syndrome and hypoglossal nerve palsy, Barré arm and leg signs, and limb ataxia. MRI disclosed an infarction in the left upper medial medulla. Case 3: A 47-year-old man developed vertigo when turning over in bed. He showed left-beating nystagmus without latency, when lying down. Horner syndrome and hypoglossal nerve palsy were absent MRI showed bilateral MMI, with the right lesion being larger than the left. MR angiography demonstrated a stenosis in the distal portion of the left internal carotid artery but not in the vertebral and basilar arteries and their branches. This case represents central positional vertigo. Vestibular syndrome seen in cases 1 and 2 was incomplete and incongruent, suggesting dysfunction of the central vestibular system. There have been only nine cases of MMI with horizontal nystagmus in primary position, including unidirectional horizontorotatory nystagmus. In these cases, horizontal nystagmus beats toward the side of the lesion. In sharp contrast, horizontal nystagmus typically beats away from the lesion side in cases of Wallenberg syndrome, suggesting different underlying mechanism. Unidirectional horizontal and rotatory nystagmus is generally associated with peripheral vestibular dysfunction. There has been no reported case of MMI presenting with vestibular dysfunction preserving motor power. Thus, this "benign" form of MMI might have been misdiagnosed as peripheral vestibular dysfunction before the era of MRI.

Adult↗
PubMed1999

Chemotherapeutic malaria control as a selective primary health care activity in the Solomon Islands.

Malaria control by chemotherapy has been established in rural villages of Guadalcanal, the Solomon Islands, following field trials. As a selective primary health care activity, mobile unit teams visited villages once or twice a year to detect malaria positives and gave chloroquine and primaquine to treat the infection and interrupt the transmission. On site diagnosis was by the use of acridine orange fluorescent staining or the ICTPf commercial diagnostic kit. To avoid possible haemolytic crises, a new single step screening method of G6PD deficiency was introduced. This approach has been accepted well by villagers and proved to be an efficient and feasible control method even in remote rural villages with endemic malaria transmission. Epidemiological modelling of the situation predicts reduction of prevalence in five years.

Adult↗
PubMed1998

Molecular cloning of rat klotho cDNA: markedly decreased expression of klotho by acute inflammatory stress.

We have recently identified a novel gene, termed klotho, that is involved in the suppression of several aging phenotypes. The gene encodes a membrane protein that shares sequence similarity with the beta-glucosidases of bacteria and plants. In this study, we isolated rat klotho cDNA and examined its tissue distribution in rats. The deduced amino acid sequence of rat Klotho protein was 1014 amino acids in length and 94 and 85% homologous to those of mouse and human Klotho proteins, respectively. Northern blot analysis using the rat klotho cDNA probe identified a single transcript of 5.2 kb in size expressed predominantly in the kidney, while RT-PCR detected low levels of expression also in the brain, lung, intestine, and ovaries. During development, klotho expression in the kidney was markedly augmented after birth. Chromosomal localization of rat klotho was mapped to 12q12. Northern blot analysis showed that expression of klotho was markedly decreased by lipopolysaccharide (LPS) in vivo, suggesting that expression of klotho is affected by acute inflammatory stress. The present study leads to a better understanding of the physiologic and pathophysiologic roles of Klotho.

Amino Acid Sequence↗
PubMed1998

Feline bone marrow transplantation: its use in FIV-infected cats.

The use of autologous and allogenic bone marrow transplantations (BMT) in FIV-infected and uninfected cats is a novel therapy for feline hematopoietic diseases and retroviral infections. A total of 13 specific pathogen-free (SPF) cats received either autologous or allogenic BMT and seven of these cats were also infected with FIV before autologous or allogenic BMT. All BMT recipients received total body irradiation of 900 cGy just before BMT. Two FIV-infected and four uninfected cats received autologous uninfected BM cells cryopreserved before BMT. Five infected and two uninfected cats received BM cells from allogenic uninfected donors (RBC-, MHC-, and cross-matched). MHC-matching was based on mixed leucocyte reaction (MLR) and the donor-recipient combination which was compatible by MLR analysis, was used in this study. Recipients were monitored for hematology, immunology, virology, and clinical signs. All FIV-infected and uninfected recipients of autologous BMT had complete engraftment with minimal complications. Uninfected recipients of allogenic BMT had a more severe clinical episode with slower rate of engraftment. None of these BMT groups had mortality. In contrast, only two of the five infected recipients of allogenic BMT survived for a significant period of time (23 and 50 weeks) and rest of the cats succumbed to transfusion reactions. Both infected BMT groups had persistent CD4/CD8 inversion, low CD4+ cell counts, and FIV infection of engrafted peripheral blood mononuclear cells (PBMC). Overall, successful autologous and allogenic BMTs were performed in FIV-free cats. All infected recipients of autologous BMT had compete engraftment and are currently alive, with thelongest survival time being over 1 year. Thus, BMT in combination with antiviral drug therapies may be an alternative therapy against retroviral infection.

Animals↗
PubMed1998

A Gln747-->Pro substitution in the IIb subunit is responsible for a moderate IIbbeta3 deficiency in Glanzmann thrombasthenia.

To clarify a molecular defect responsible for moderate alphaIIb beta3 deficiency, we examined two unrelated patients, MT and MS, suffering from type II and type I Glanzmann thrombasthenia (GT), respectively. Sequence analysis of polymerase chain reaction (PCR) fragments derived from platelet mRNA showed a single A-->C substitution at nucleotide (nt) 2334 leading to a Gln747--> Pro in alphaIIb in both patients. Allele-specific restriction enzyme analysis (ASRA) of genomic DNA demonstrated that patient MT was homozygous for the Gln747-->Pro substitution and patient MS was compound heterozygous for this substitution and for an RNA splice mutation at the consensus sequence of the splice acceptor site of exon 18 (AG-->AA). Furthermore, ASRA showed that, among 17 unrelated Japanese GT patients, this Gln747-->Pro substitution was detected in 4 patients, including MT and MS (homozygous, 2 patients; heterozygous, 2 patients). Cotransfection of Pro747alphaIIb and beta3 constructs into 293 cells resulted in moderate reduction in the amount of alphaIIb beta3 within the transfected cells as well as on the cell surface. However, Pro747alphaIIb beta3 bound the ligand mimetic monoclonal antibody (MoAb) PAC-1 after activation of alphaIIb beta3 by the MoAb PT25-2, suggesting that the mutant alphaIIb beta3 possesses the ligand-binding function. The association between the mutant proalphaIIb and beta3 was not disturbed. Surface labeling and pulse chase study showed that the Gln747-->Pro substitution moderately impaired both intracellular transport of the alphaIIb beta3 heterodimers to the Golgi apparatus and endoproteolytic cleavage of proalphaIIb into heavy and light chains. By contrast, replacement of Gln747 with Ala by mutagenesis did not impair alphaIIbbeta3 expression on the cell surface. These results suggest that the presence of Pro, rather than the absence of Gln, at amino acid residue 747 on alphaIIb is responsible for moderate alphaIIbbeta3 deficiency.

Alleles↗
PubMed1998

Contribution of CD14 to endotoxin-induced liver injury may depend on types of macrophage activation in rats.

Activated Kupffer cells and hepatic macrophages can produce massive liver necrosis through microcirculatory disturbance due to sinusoidal fibrin deposition. This mechanism is involved in the development of liver injury after endotoxin administration in rats pretreated with heat-killed Propionibacterium acnes (P.acnes) or undergoing 70% liver resection. The significance of CD14, a receptor for lipopolysaccharide and its binding protein, was evaluated in both models in relation to the activation mechanisms of Kupffer cells and hepatic macrophages. Northern blot analysis revealed that CD14 mRNA expression was increased in the liver of rats following P.acnes administration. In these rats, hepatic macrophages immediately after isolation showed marked increased of CD14 mRNA expression compared to Kupffer cells from normal rats. In contrast, CD14 mRNA expression was minimal in partially resected liver. Interleukin (IL)-18 and IL-2 mRNA expression in the liver and interferon (IFN)-gamma mRNA expression in the spleen were significantly increased in P.acnes-treated rats compared to normal rats, while these increases were absent in partially hepatectomized rats. Thus, CD14 expressed on hepatic macrophages after activation through a cytokine network of IL-18, IFN-gamma, and IL-2 may contribute to endotoxin-induced liver injury in P.acnes-treated rats. In contrast, in partially hepatectomized rats, this network may not operate during Kupffer cell activation, and the liver injury might develop through endotoxin receptors other than CD14 on the cells.

Animals↗
PubMed1998

Coexpression of GTP cyclohydrolase I and inducible nitric oxide synthase mRNAs in mouse osteoblastic cells activated by proinflammatory cytokines.

Proinflammatory cytokines, a combination of IL-1beta, TNF-alpha, and IFN-gamma, caused mRNA expression of GTP cyclohydrolase I (GTP-CH), the rate-limiting enzyme in tetrahydrobiopterin (BH4) biosynthesis, and of inducible nitric oxide synthase (iNOS) in a well-characterized osteoblastic clone MC3T3-E1 cell line. We found the expression of the GTP-CH gene in osteoblasts for the first time. The expression of GTP-CH and iNOS mRNAs was found to be maximal at 3 and 9 h, respectively. The expression of both genes elicited increases in BH4 and NO levels. Pharmacological studies using 2,4-diamino-6-hydroxypyrimidine, an inhibitor of GTP-CH activity, showed that BH4 is involved in the activity of iNOS, but not in the induction of iNOS mRNA. The results using an inhibitor of nuclear factor (NF)-kappaB and activating protein-1 (AP-1) activation suggested that coinduction of the two genes in response to cytokines occurred via activation of NF-kappaB and AP-1. In MC3T3-E1 cells BH4 and sepiapterin, producing BH4, could protect against apoptosis, i.e. the degradation of nuclear DNA in the cells, induced by NO derived from S-nitroso-N-acetyl-D-L-penicillamine. These results suggest that the induction of BH4 together with NO by proinflammatory cytokines could protect against NO-induced apoptosis in MC3T3-E1 cells.

3T3 Cells↗
PubMed1998

High SDF-1 expression in HIV-1 carriers does not correlate with CD8+ T-cell-mediated suppression of viral replication.

Stromal cell-derived factor 1 (SDF-1) inhibits T-cell tropic (T-tropic) HIV-1 infection in vitro. In this study, we examined the regulatory role of SDF-1 on HIV-1 replication in peripheral blood mononuclear cells (PBMC) of HIV-infected individuals. We found that the amount of SDF-1 mRNA in freshly isolated PBMC of HIV-1 carriers was higher than in healthy donors. Moreover, PBMC from some asymptomatic carriers (ACs) exhibited high levels of SDF-1 mRNA expression. The level of SDF-1 expression in PBMC did not correlate with the magnitude of CD8+ T-cell-mediated suppression of HIV-1 among ACs SDF-1 inhibited HIV-1 replication at the viral entry step, whereas a single-cycle HIV-1 infection system showed that the major part of the CD8+ T-cell-mediated suppression occurs after intracellular penetration of the virus. Our results suggest that SDF-1 acts as a suppressor of virus replication in a CD8+ T-cell-independent mechanism in HIV-infected individuals.

Base Sequence↗