Biomedical subjects

Hironori Sato

Publications and source records attributed to Hironori Sato.

18 recordsLinked to original sources

PubMed2006

Cooperative contribution of gag substitutions to nelfinavir-dependent enhancement of precursor cleavage and replication of human immunodeficiency virus type-1.

We previously described a clinical human immunodeficiency virus type-1 (HIV-1) isolate, CL-4, which showed nelfinavir (NFV)-dependent enhancement of replication (Matsuoka-Aizawa, S., Sato, H., Hachiya, A., Tsuchiya, K., Takebe, Y., Gatanaga, H., Kimura, S., Oka, S, 2003. Isolation and molecular characterization of a nelfinavir (NFV)-resistant human immunodeficiency virus type 1 that exhibits NFV-dependent enhancement of replication. J. Virol. 77, 318-327.). To identify the responsible region(s) of HIV-1 proteins for such replication enhancement, we constructed a panel of recombinant HIV-1 clones harboring portions of the Gag and protease of CL-4 and analyzed their replication capabilities and Gag processing patterns. Our data suggested that the substitutions in the matrix and N-terminal half of capsid of CL-4 were indispensable for the NFV-dependent enhancement of replication and that NFV facilitated the cleavage between the matrix and capsid of the Gag precursor harboring these substitutions. The substitutions in C-terminal half of capsid rather decreased the cleavability of Gag precursor and NFV counteracted such negative impact. Efficient replication enhancement with NFV can be observed only in the presence of the substitutions in entire Gag and protease of CL-4.

Amino Acid Sequence↗

PubMed2006

[Skin collagen abnormalities in a Japanese patient with extracranial internal carotid artery dissection followed by extracranial vertebral artery dissection].

A 41-year-old man with hypertension and hyperlipidemia who complained of left hemiparesis after a temporal headache was admitted to our hospital. A cervical MRI with gadolinium enhancement revealed an intramural hematoma is compatible with right extracranial internal carotid artery dissection. Two weeks later, he complained of sudden onset of pain in the right side of his neck. The right extracranial internal carotid artery dissection followed by the right extracranial vertebral artery dissection was diagnosed. Spontaneous cervical artery dissection (SCAD) is one of the causes of stroke in young adults. The pathogenesis of SCAD remains unknown. Minor trauma like an excessive sneeze, migraine, and connective tissue disorders such as fibromuscular dysplasia and Ehlers-Danlos syndrome are well-known as risk factors for SCAD. Pathologically skin collagen abnormalities have been seen in German patients with SCAD without clinical evidence for any specific connective tissue disorder. We examined the ultrastructural morphology of the Japanese patient's dermal connective tissue components by electron microscopy. The patient's collagen fibers contained fibrils with highly variable diameters, and there were other ultrastructural abnormalities, including flower-like fibrils and large-diameter composite fibrils. This is the first report of a case of ultrastructural abnormalities of dermal connective tissue in a Japanese patient with SCAD.

Adult↗

PubMed2006

[Sensory disturbance in the pulp of the fingertips in three patients with cervical myelitis].

We report three patients with cervical myelitis, with sensory disturbance at their fingertips. They exhibited the following clinical features in common: localized sensory disturbance in the pulp of the fingertips, with a positive Lhermitte's sign, but retained deep sensation. T2-weighted MR imaging demonstrated a swelling of the spinal cord at the C2 to C3 level, and a hyperintense lesion in the posterior region of the spinal cord at the same level in all patients. The characteristic symptoms of these three patients might be attributable to the somatotopy in the dorsal column at high cervical levels, because the afferent fibers innervating the fingertips occupy a much wider axial area at the high cervical spinal cord levels than the small surface area actually innervated by them.

Adult↗

PubMed2005

HIV-1 proteases from drug-naive West African patients are differentially less susceptible to protease inhibitors.

BACKGROUND: Now that highly active antiretroviral therapy (HAART) is being initiated on a large scale in West Africa, it remains controversial whether protease inhibitors (PIs), originally designed and tested against human immunodeficiency virus type 1 (HIV-1) subtype B, are equally effective against the non-B subtypes that are prevalent in West African countries. In this study, we investigated whether Ghanaian HIV-1 isolates, as representatives of West African isolates, are susceptible to PIs. METHODS: We first generated an HIV-1 protease cassette vector proviral DNA carrying a luciferase gene, which allows patient-derived HIV-1 proteases to be inserted and to be subjected to both genotypic and phenotypic assays. HIV-1 protease genes derived from 39 treatment-naive Ghanaian patients were used in this experiment as representatives of West African strains. The cloned patient-derived HIV-1 protease genes were first sequenced and then genetically compared. Phenotypic analysis was performed with Ghanaian HIV-1 protease-chimeric viruses in the presence of 6 different PIs. Structural models of HIV-1 protease homodimers were constructed by the molecular modeling software. RESULTS: Genetic analysis of cloned patient-derived HIV-1 protease genes indicated that most of the Ghanaian HIV-1 proteases are placed as subtype CRF02_AG strains, which are phylogenetically distant from subtype B strains, and that Ghanaian HIV-1 proteases do not harbor known major mutations influencing drug resistance but commonly carry 2-3 minor mutations. Phenotypic analysis performed with HIV-1 protease-recombinant viruses in the presence of 6 different PIs revealed that Ghanaian HIV-1 proteases are differentially less susceptible to the PIs. In support of this finding of differential susceptibility, structural analysis showed a significant distortion of nelfinavir, but not of amprenavir, in the Ghanaian protease pocket, suggesting nelfinavir might be less insertable into the Ghanaian protease than into the protease of subtype B. CONCLUSIONS: These findings provide implications for the combination of PIs during the introduction of HAART into West Africa.

Adult↗

PubMed2005

Amino acid 36 in the human immunodeficiency virus type 1 gp41 ectodomain controls fusogenic activity: implications for the molecular mechanism of viral escape from a fusion inhibitor.

We have previously described a human immunodeficiency virus type 1 (HIV-1) proviral clone, pL2, derived from defective viral particles with higher fusogenicity than the prototypic NL4-3 virus. In this study, we attempted to determine the region that confers the enhanced fusion activity by creating envelope recombinants between pL2 and pNL4-3, as well as point mutants based on pNL4-3. The results indicate that amino acid 36 of gp41 is key for the fusogenic activity and infectivity enhancement and that glycine 36 (36G) of gp41 in pL2 is conserved in nearly all HIV-1 isolates except for pNL4-3. The mutation 36G-->D in a primary-isolate-derived Env decreased syncytium-forming activity and infectivity. The assays for cell-cell fusion and viral binding suggested that the enhanced fusion mediated by the 36D-->G mutation is not due to increased binding efficiency but is directly due to actual enhancement of viral fusion activity. Interestingly, this amino acid position is exactly equivalent to that at which the mutation of HIV-1 isolates that have escaped from a fusion inhibitor, enfuvirtide (T-20), has been frequently observed. The correlation between these previous findings and our findings was suggested by structural analysis. Our finding, therefore, has implications for a molecular basis of the viral escape from this drug.

Amino Acids↗

PubMed2005

Human immunodeficiency virus mutagenesis during antiviral therapy: impact of drug-resistant reverse transcriptase and nucleoside and nonnucleoside reverse transcriptase inhibitors on human immunodeficiency virus type 1 mutation frequencies.

The development of antiviral drug resistance is an important problem in the treatment of human immunodeficiency virus type 1 (HIV-1) infection. Potent antiretroviral therapy is currently used for treatment, and typically consists of at least two reverse transcriptase (RT) inhibitors. We have previously reported that both drugs and drug-resistant RT mutants can increase virus mutation frequencies. To further assess the contributions of nucleoside RT inhibitors (NRTIs), nonnucleoside RT inhibitors (NNRTIs), and drug-resistant RTs to HIV mutagenesis, a new high-throughput assay system was developed. This assay system was designed to specifically detect frameshift mutations in the luciferase gene in a single virus replication cycle. New drug-resistant RTs were identified that significantly altered virus mutation frequencies. Consistent with our previous observations of NRTIs, abacavir, stavudine, and zalcitabine increased HIV-1 mutation frequencies, supporting the general hypothesis that the NRTIs currently used in antiviral drug therapy increase virus mutation frequencies. Interestingly, similar observations were made with NNRTIs. This is the first report to show that NNRTIs can influence virus mutation frequencies. NNRTI combinations, NRTI-NNRTI combinations, and combinations of drug and drug-resistant RTs led to significant changes in the virus mutation frequencies compared to virus replication of drug-resistant virus in the absence of drug or wild-type virus in the presence of drug. This indicates that combinations of RT drugs or drugs and drug-resistant virus created during the evolution of drug resistance can act together to increase HIV-1 mutation frequencies, which would have important implications for drug therapy regimens. Finally, the influence of drug-resistant RT mutants from CRF01_AE viruses on HIV-1 mutation frequencies was analyzed and it was found that only a highly drug resistant RT led to altered virus mutation frequencies. The results further suggest that high-level drug-resistant RT can significantly influence virus mutation frequencies. A structural model that explains the mutation frequency data is discussed.

Anti-HIV Agents↗

PubMed2005

[RNA viruses and mutations].

Actively replicating RNA viruses in nature are continually changing their genetic information by spontaneous mutations. These changes often result in alterations in immune-sensitivity, drug-sensitivity, cell-tropism, and host-range, causing uncontrollability of the pathogen and emerging/re-emerging infections. To better understand the virus changes and develop effective methods to control the moving targets, it is essential to obtain information on changes in viral genomes and proteins. Although information on genetic changes is being accumulated very rapidly, assessment of changes in protein structure and function still requires time-consuming works. In this review, we will overview mutation studies of human immunodeficiency virus and other RNA viruses. In addition, we will introduce recent advances in the computational science and its application on mutation studies and drug development.

Animals↗

PubMed2005

[A case of postpartum cerebral angiopathy with intracranial hemorrhage and subarachnoid hemorrhage immediately after delivery].

A 32-year-old woman, gravida 0, para 0, was admitted for delivery at 40 weeks of gestation. She had no history of headache, hypertension, and toxemia. She was delivered of a healthy boy. Although she was given no medication during normal delivery, she suddenly became drowsy and developed left hemiparesis immediately after delivery. Computed tomographic (CT) scan of the brain performed on the admission day revealed a subarachnoid hemorrhage and right putaminal hemorrhage. A 4-vessel cerebral angiogram demonstrated multiple irregular narrowing of the anterior cerebral arteries, middle cerebral arteries, and posterior cerebral arteries. Her conditions seemed to improve without any medication, and the multiple stenoses were no longer observed by angiography in a follow-up examination. On the basis of these observations, she was diagnosed as having postpartum cerebral angiopathy (PCA). Pathogenesis of PCA still remaing unclear to date an ergot alkaloid derivate (ergonovine) and the hydrogenated form of the powerful vasoconstrictor ergot (bromocriptine) have been reported as cause of PCA. We will classify PCA into 3 categories: eclampsia, secondary PCA, and primary PCA. "Primary PCA" is of unknown etiology, "secondary PCA" results from a known etiology such as drugs, and "eclampsia" is a PCA with toxemia of pregnancy. We report here, that PCA may occur even in a normal pregnant woman who was given no medication, and should be considered in the diagnosis of postpartum cerebral vascular diseases in women.

Adult↗

PubMed2005

[A case of aphasia with preserved repetition due to anterior choroidal artery territory infarction].

A 55-year-old right-handed male patient with atrial fibrillation was admitted to our hospital because of a sudden disturbance of consciousness and right hemiparesis. Neurological examinations revealed left conjugate deviation of the eyes, aphasia, right hemianopsia without macula sparing using a Goldmann perimeter, right hemianesthesia, and right hemiparesis. Magnetic resonance imaging showed low intensity areas (left posterior limb of internal capsule, left cerebral peduncle of middle brain, a part of left substantia nigra, left amygdala, ventral posterior lateral nucleus and ventral anterior nucleus of left thalamus, left lateral geniculate body, and left occipital lobe) in T1 weighted image, due to the infarct in the left anterior choroidal artery territory. Aphasia in this case was accompanied with non-fluent speech, good repetition, naming deficits, and perseveration. We suggest that aphasia with anterior choroidal artery syndrome cannot be classified using the conventional system, and emphasize the importance of accurate descriptions of the symptoms characteristic of aphasia with anterior choroidal artery.

Aphasia↗

PubMed2004

Identification of a host gene subset related to disease prognosis of HIV-1 infected individuals.

Although plasma-virus-RNA level and CD4-positive-T-cell count are useful to monitor clinical status of the human immunodeficiency virus (HIV)-infected individuals, clinical course is often varied among patients and sometimes difficult to predict. To identify additional parameters associated with disease progression, we examined by cDNA microarray the expression profiles of 731 immune-response-related genes in the peripheral blood mononuclear cells (PBMCs) from 21 HIV-positive individuals in Uganda. The analysis enabled the patients to be classified into three distinct groups on the basis of the gene expression patterns. Notably, these groups, clusters I, II and III, were highly associated with clinical status of the patients defined by CDC classification, categories A, B, and C, respectively. Statistical analysis identified 40 genes whose expressions were significantly up- or down-regulated in the cluster III patients (p<0.05). Up- and down-regulated genes included ones involved in immature T lymphocytes differentiation, apoptosis signaling, and active HIV replication, suggesting that the levels of active destruction and regeneration of mature T lymphocytes associated with enhanced HIV-1 replication is related to the disease progression. Follow-up study showed that the cluster classification improved prediction of disease prognosis with the CDC classification. These findings provide new clues for studying perturbation of host immunity, pathogenesis, and disease prognosis of HIV-infected individuals.

Adult↗

PubMed2004

Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans.

It has frequently been demonstrated that prior heavy cycling exercise facilitates pulmonary O(2) kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the faster O(2) kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70-75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, the O(2) kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean +/-s.d. of the 'effective' time constant (tau): EX1, 68.6 +/- 15.9, versus EX2, 58.0 +/- 14.4 s. Phase II-tau: EX1, 48.7 +/- 9.0, versus EX2, 41.2 +/- 13.3 s. Empirical index of the slow component (Delta O(2(6-3))): EX1, 78 +/- 44, versus EX2, 57 +/- 36 ml min(-1) (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the 'effective'tau of the femoral artery BF: EX1, 40.8 +/- 16.9, versus EX2, 39.0 +/- 17.1 s (P > 0.05)]. It was concluded that the faster pulmonary O(2) kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.

Adult↗

PubMed2004

[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction].

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.

Aged↗

PubMed2004

[A case of cardiac myxoma presenting with multiple cerebellar hemorrhages and elevation of interleukin-6 in the cerebrospinal fluid].

We report a 25-year old man with cardiac myxoma presenting with multiple cerebellar hemorrhages and elevation of interleukin-6 (IL-6) in the cerebrospinal fluid (CSF). The patient was first admitted to our hospital because of cerebral infarctions at the age of 23. After systemic exploration he was diagnosed as cardiac myxoma. In this patient, the serum level of IL-6 was elevated. The cardiac myxoma was resected and the serum IL-6 level returned to normal. His neurological symptoms improved almost to normal and he was discharged. The patient had been well for two years until he developed headache at the age of 25. Brain MRI revealed multiple cerebellar hemorrhages that overlaid old infarctions. The hemorrhages enlarged in a three months period and his headache became worse, and then he was admitted again. The IL-6 value was normal in serum at that time, but it was elevated in the CSF. The CSF IgG index was also elevated. Cerebral angiograms showed no abnormal vessel in the infratentorium, while multiple fusiform aneurysms were found in both middle cerebral arteries. A transesophageal echocardiography revealed no recurrence of cardiac myxoma. Craniotomy was performed and intracerebellar hematomas were removed. Histopathological examination showed only old and recent bleedings; no metastatic myxoma tissue was found. Although no myxoma tissue was found in biopsy specimen, it seemed reasonable that an elevated level of IL-6 in the CSF was due to metastasized intracranial myxoma, which caused cerebellar embolism, and then invaded the vessel walls and continued to grow. In reviewing the literature we have found no reported case of cardiac myxoma with analysis of IL-6 value in the CSF. We speculate that the level of IL-6 in the CSF might be a good marker for the neurological manifestations of cardiac myxoma.

Adult↗

PubMed2003

Higher levels of IL-18 circulate during primary infection of monkeys with a pathogenic SHIV than with a nonpathogenic SHIV.

We have monitored kinetics of peripheral blood Interleukin (IL)-18 level, viral RNA load, and CD4(+) T cell counts in cynomolgus and rhesus macaques following infections of various simian/human immunodeficiency viruses (SHIVs) causing differential pathogenicity. Infections of cynomolgus and rhesus macaques with pathogenic SHIVs-C2/1 and -89.6PD, respectively, induced high levels of plasma IL-18 (0.1-1 ng/ml) and enhanced apoptosis of peripheral blood T cells during primary viremia, along with a rapid decline of CD4(+) T cells and a high level of set point viral load after primary viremia (six of six cases). In contrast, infections of cynomolgus macaques with nonpathogenic SHIVs-TH09V3 and -MD14 did not cause such IL-18 elevation, showing no decline of CD4(+) T cells and no or low viral set point level following primary viremia (three of three cases). Thus, the elevation of circulating IL-18 level during primary viral infection can be a good indicator of an active pathogenic viral infection. However, the role of increased IL-18 remains to be elucidated and needs further investigation.

Animals↗

PubMed2003

Isolation and molecular characterization of a nelfinavir (NFV)-resistant human immunodeficiency virus type 1 that exhibits NFV-dependent enhancement of replication.

During the use of a phenotypic anti-human immunodeficiency virus type 1 (HIV-1) drug resistance assay in a large set of clinical virus isolates, we found a unique variant (CL-4) that exhibited a high level of nelfinavir (NFV) resistance and rather enhanced replication under subinhibitory concentrations of NFV (0.001 to 0.1 micro M). Comparison of gag-pol sequences of the CL-4 variant and its predecessor virus isolates showed a stepwise accumulation of a total of 19 amino acid substitutions in protease (PR) and Gag p17 during 32-month NFV-containing antiretroviral therapy, while other Gag regions including the cleavage sites of the p55 precursor remained highly conserved. To understand the relationship between the genetic and phenotypic changes in CL-4, we constructed chimeric viruses using pNL4-3, replacing the PR, p24PR, or p17PR gene segment of CL-4 or its predecessor. A series of tissue culture infections with the chimeras in the absence or presence of increasing concentrations of NFV demonstrated that only the p17PR segment of CL-4 could confer the NFV-dependent replication enhancement phenotype on NL4-3. Our data suggest a novel adaptation mechanism of HIV-1 to NFV, in which coevolution of Gag and PR genes generates a variant that replicates more efficiently in the cellular environment in the presence of NFV than without the drug.

Blotting, Western↗

PubMed2002

Relationship between the curvature constant parameter of the power-duration curve and muscle cross-sectional area of the thigh for cycle ergometry in humans.

For high-intensity cycle ergometer exercise, the relationship between power output ( P) and its tolerable duration ( t) has been well characterized by the hyperbolic relationship: ( P- theta;(F)). t=W', where theta;(F) has been termed the "critical power" or "fatigue threshold". The curvature constant (W') reflects a constant amount of work which can be performed above theta;(F), and it may be regarded as a muscle energy store. The relationship of this energy store to muscle mass is not known. Therefore, the purpose of this study was to determine the relationships among W', accumulated peak oxygen deficit (accumulated peak O(2)-deficit), and muscle cross-sectional area (CSA) of the thigh for high-intensity cycle ergometry in humans. A group of 17 healthy male subjects (aged 21-41 years) participated in this study. The theta;(F) and W' of the P- t hyperbolic relationship and the accumulated peak O(2)-deficit was calculated by standard procedures. The CSA of muscle, fat and bone in the right thigh were measured using ultrasonography. The mean (SD) of theta;(F), W', accumulated peak O(2)-deficit, and muscle CSA of the thigh were 200.0 (17.8) W, 12.60 (2.94) kJ, 2.29 (0.41) l, and 185.3 (22.6) cm(2), respectively. The muscle CSA of the thigh was positively correlated with W' ( r=0.59, P<0.01) and with accumulated peak O(2)-deficit ( r=0.54, P<0.05). The relationship between W' and accumulated peak O(2)-deficit also showed a positive correlation ( r=0.63, P<0.005). Our results indicated that W' derived from the P- t hyperbolic curve as anaerobic working capacity is related to the CSA of muscle.

Adult↗

PubMed2002

Cytotoxic T-cell recognition of HIV-1 cross-clade and clade-specific epitopes in HIV-1-infected Thai and Japanese patients.

OBJECTIVE: To identify and characterize cytotoxic T-cell (CTL) epitopes for HIV-1 clade E using eight known HLA-A*1101-restricted HIV-1 clade B epitopes. METHODS: Induction of clade E-specific CTL was examined by stimulating peripheral blood mononuclear cells (PBMC) from clade E-infected Thai individuals with the clade E-specific peptide corresponding to the clade B epitopes. Cross-clade and clade-specific CTL recognition for these epitopes was analysed using CTL clones and bulk CTL specific for these epitopes. To clarify the presentation of these epitopes in HIV-1-infected T cells, CTL recognition for the clade E-specific and cross-clade epitopes was investigated using CD4CXCR4 cells infected with an HIV-1 clade E clone. RESULTS: Three epitopes, which are identical among clades A-E, were recognized as cross-clade CTL epitopes in both individuals. Clade B and E sequences corresponding to three epitopes were recognized as clade-specific epitopes in clade B-infected and clade E-infected individuals, respectively. In contrast, clade E-specific peptides corresponding to two other clade B epitopes failed to elicit clade E-specific CTL. CTL specific for the three cross-clade and three clade E-specific epitopes effectively lysed target cells infected with HIV-1 clade E virus. CONCLUSIONS: These six epitopes are found to be processed naturally in HIV-1 clade E-infected cells. We show here that a strategy utilizing HIV-1 clade B epitopes is very useful for identifying clade E CTL epitopes.

Cross Reactions↗

PubMed2002

Isolation and characterization of replication-competent molecular DNA clones of HIV type 1 CRF01_AE with different coreceptor usages.

We have isolated replication-competent molecular clones of HIV-1 circulating recombinant form CRF01_AE with different coreceptor usages. After lambda phage cloning of unintegrated circular proviral DNAs derived from a CRF01_AE strain (HIV-1NH1), isolated in Japan, the infectious molecular clone, designated p93JP-NH1, was reconstituted. 93JP-NH1 showed an X4 and R5 phenotype in NP2 cell-based coreceptor utilization assays and exerted robust replication in human T cell lines, including MT2, M8166, and PM1 cells, whereas it propagated modestly in peripheral blood mononuclear cells. The CRF01_AE molecular clone with R5 phenotype (p93JP-NH2env) was then constructed by replacing the env gene of p93JP-NH1 with that of a nearly isogenic CRF01_AE R5 strain isolated from an epidemiologically linked case. The phylogeny and recombination break-point analysis confirmed that these clones shared an A/E recombinant structure similar to that of the prototype CRF01_AE strain, CM240. These replication-competent CRF01_AE molecular clones with different coreceptor usages would be useful tools for the study of CRF01_AE, one of the most prevalent strains in Asia.

Base Sequence↗