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Biomedical subjects

Y L Lin

Publications and source records attributed to Y L Lin.

At least 37 records · Page 2Linked to original sources

Salicylates inhibit flavivirus replication independently of blocking nuclear factor kappa B activation.

Flaviviruses comprise a positive-sense RNA genome that replicates exclusively in the cytoplasm of infected cells. Whether flaviviruses require an activated nuclear factor(s) to complete their life cycle and trigger apoptosis in infected cells remains elusive. Flavivirus infections quickly activate nuclear factor kappa B (NF-kappaB), and salicylates have been shown to inhibit NF-kappaB activation. In this study, we investigated whether salicylates suppress flavivirus replication and virus-induced apoptosis in cultured cells. In a dose-dependent inhibition, we found salicylates within a range of 1 to 5 mM not only restricted flavivirus replication but also abrogated flavivirus-triggered apoptosis. However, flavivirus replication was not affected by a specific NF-kappaB peptide inhibitor, SN50, and a proteosome inhibitor, lactacystin. Flaviviruses also replicated and triggered apoptosis in cells stably expressing IkappaBalpha-DeltaN, a dominant-negative mutant that antagonizes NF-kappaB activation, as readily as in wild-type BHK-21 cells, suggesting that NF-kappaB activation is not essential for either flavivirus replication or flavivirus-induced apoptosis. Salicylates still diminished flavivirus replication and blocked apoptosis in the same IkappaBalpha-DeltaN cells. This inhibition of flaviviruses by salicylates could be partially reversed by a specific p38 mitogen-activated protein (MAP) kinase inhibitor, SB203580. Together, these results show that the mechanism by which salicylates suppress flavivirus infection may involve p38 MAP kinase activity but is independent of blocking the NF-kappaB pathway.

Animals↗

Homocyclotirucallane and two dihydrophenanthrenes from Spiranthes sinensis.

A novel homocyclotirucallane, sinetirucallol (1), and two additional new dihydrophenanthrenes, sinensols G (2) and H (3), were isolated from the aerial parts of Spiranthes sinensis (Pers.) Ames. Their structures were determined by various spectral analyses, including MS and two-dimentional nuclear magnetic resonance techniques. The structure of compound 1 was further confirmed by single-crystal X-ray analysis. The absolute configuration of 1 was determined by modified Mosher's method.

Acetylation↗

Calcium channel blockade in vascular smooth muscle cells: major hypotensive mechanism of S-petasin, a hypotensive sesquiterpene from Petasites formosanus.

In vivo and in vitro studies were carried out to examine the putative hypotensive actions of S-petasin, a sesquiterpene extracted from the medicinal plant Petasites formosanus. Intravenous S-petasin (0.1-1.5 mg/kg) in anesthetized rats produced a dose-dependent hypotensive effect. In isolated aortic ring, isometric contraction elicited by KCl or the L-type Ca2+ channel agonist Bay K 8644 was reduced by S-petasin (0.1-100 microM), an action not affected by the cyclooxygenase inhibitor indomethacin, nitric-oxide synthase inhibitor N(omega)-nitro-L-arginine, guanylyl cyclase inhibitor methylene blue, or removal of vascular endothelium. Pretreatment with S-petasin for 10 min shifted the concentration-response curve for KCl (15-90 mM)-induced contraction to the right and reduced the maximal response. In Ca2+-depleted and high K+-depolarized aortic rings preincubation with S-petasin attenuated the Ca2+-induced contraction in a concentration-dependent manner, suggesting that S-petasin reduced Ca2+ influx into vascular smooth muscle cells (VSMCs). Moreover, in cultured VSMCs, whole-cell patch-clamp recording indicated that S-petasin (1-50 microM) inhibited the L-type voltage-dependent Ca2+ channel (VDCC) activities. Intracellular Ca2+ concentration ([Ca2+[(i)) estimation using the fluorescent probe 1-[2-(5-carboxyoxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2'-amino-5'-methylphenoxy)-ethane-N,N,N,N-tetraacetic acid pentaacetoxymethyl ester indicated that S-petasin (10, 100 microM) suppressed the KCl-stimulated increase in ([Ca2+[(i)). Taken together, the results suggested that a direct Ca2+ antagonism of L-type VDCC in vascular smooth muscle may account, at least in part, for the hypotensive action of S-petasin.

Animals↗

Screening procedure from cattle feces and the prevalence of Escherichia coli O157:H7 in Taiwan dairy cattle.

A procedure has been established for screening Escherichia coli O157:H7 from bovine feces. It consists of four steps: enrichment, selective culture, phenotyping and genotyping. Modified trypticase soy broth (mTSB) containing 20 microg/mL of novobiocin was used for the enrichment step. The selective culture step was done using sorbitol MacConkey agar containing 0.05 microg/mL of cefixime and 2.5 microg/mL of potassium tellurite. The phenotyping steps include: species confirmation as E. coli, serotyping to O157 and H7, and the detection of verocytotoxin (VT) production. Genotyping was made up of confirmation of the presence of the O157 antigen (rfb), the H7 antigen (ficC), the adherence factor (eaeA), hemolysin (hlyA), and VT production (vt I and vt II) by polymerase chain reaction. mTSB gave better enrichment for E. coli O157 than gram-negative (GN) broth. The detection limit for this screening procedure was 0.85 +/- 0.5 cfu/g. Using the screening procedure described above, E. coli O157 was found in four out of 3062 (0.13%) fresh bovine fecal specimens, and in two out of 78 (2.56%) dairy herds in Taiwan. Three out of the four detected strains were vt II producing E. coli O157:H7, while the other was E. coli O157:H7 which lacked VT-producing ability.

Animals↗

Cytotoxic and antioxidant effects of the water extract of the traditional Chinese herb gusuibu (Drynaria fortunei) on rat osteoblasts.

BACKGROUND AND PURPOSE: Gusuibu (Drynaria fortunei) is a traditional Chinese herb that has been claimed to have therapeutic effects on bone healing; however, a clinical mechanism responsible for this effect has not been identified. This study evaluated the cytotoxic and antioxidant effects of the water extract of gusuibu (WEGSB) on rat osteoblasts. MATERIALS AND METHODS: Osteoblasts were prepared from neonatal Wistar rat calvarias and treated with WEGSB. Cell viability and alkaline phosphatase activity were determined. Intracellular reactive oxygen species were detected using the dye 2',7'-dichlorofluorescin, and mitochondrial membrane potential was detected using the dye 3,3'-dihexyloxacarbocyanine iodide and flow cytometry. RESULTS: WEGSB at 1 and 10 micrograms/mL was not cytotoxic to rat osteoblasts, but WEGSB at 100 micrograms/mL reduced cell viability and alkaline phosphatase activity in a time-dependent manner. Although WEGSB and hydrogen peroxide did not affect the mitochondrial membrane potential of rat osteoblasts, combined treatment with WEGSB (100 micrograms/mL) and hydrogen peroxide lowered the membrane potential of mitochondria and resulted in cell death. The basal level of intracellular reactive oxygen species in rat osteoblasts was significantly suppressed by WEGSB at 10 to 100 micrograms/mL. WEGSB (10 micrograms/mL) specifically inhibited hydrogen peroxide-induced oxidative stress without an effect on nitric oxide-induced stress. Hydrogen peroxide caused concentration-dependent death of rat osteoblasts, but WEGSB significantly protected cells from hydrogen peroxide-induced death. CONCLUSION: This study has shown that WEGSB at 10 micrograms/mL is not cytotoxic to rat osteoblasts in vitro, and also that the extract at 10 micrograms/microL has an antioxidant effect on these cells. The antioxidant activity of WEGSB can protect rat osteoblasts from hydrogen peroxide-induced death and may promote bone recovery under similar pathologic conditions.

Alkaline Phosphatase↗

Correlation of total and specific serum immunoglobulin E levels with the severity of chronic sinusitis in children.

Chronic sinusitis is frequently associated with allergy and asthma. Previous studies have shown that serum immunoglobulin E (IgE) levels correlate with allergy and asthma in adults. Because the role of allergic inflammation in the severity of chronic sinusitis remains controversial in children, we set out to determine whether a correlation exists between serum levels of total and specific IgE and the severity of chronic sinusitis in children. Forty-four children with chronic sinusitis were enrolled in the study. Computed tomographic scans were reviewed and scored for the severity of sinusitis. All children were mite-sensitive. Serum samples were assayed for total IgE and specific IgE antibodies to mite allergen using a fluoroimmunoassay. Fourteen subjects had extensive sinus disease. There was no significant difference in the average of total and specific IgE between the subjects with extensive and limited disease (p = 0.562 and 0.755, respectively). Thirty-four subjects were diagnosed with asthma. The subjects with extensive sinus disease had a higher prevalence of moderate to severe asthma than the subjects with limited disease (p = 0.006), but there was no significant difference in the average of total and specific IgE between the subjects with different severities of asthma. (p = 0.833 and 0.425, respectively). The data suggests that levels of total or specific IgE do not correlate with severity of chronic sinusitis in children. Nonetheless, the severity of chronic sinusitis and asthma correlate well with each other irrespective of total and specific IgE.

Adolescent↗

High-level expression of recombinant dengue viral NS-1 protein and its potential use as a diagnostic antigen.

The prevalence of NS1 Ab response in patients with dengue viral infection and the potential of using recombinant NS1 protein as a diagnostic antigen for dengue viral infection were investigated. In this study, the full-length and C-terminal half of NS1 proteins (rNS1, rNS1-C) were highly expressed (10-30 mg/l) and further purified and refolded. The good antigenicity of the full-length rNS1 protein was confirmed by interaction with 19 dengue NS1-specific monoclonal antibodies (MAbs) in ELISA; however, the antigenicity of rNS1-C was relatively lower. The full-length rNS1 antigen also differentiated reliably between sera from dengue virus-infected patients and sera from normal controls. When rNS1 was used as an antigen to detect human anti-NS1 IgM and IgG Ab, the anti-NS1 Ab response was found in 15 of 17 patients (88%) with primary dengue infection and all 16 patients (100%) with secondary dengue infection. These results indicated that using the full-length rNS1 whose antigenicity is restored as ELISA antigen, a high anti-NS1 antibody prevalence could be detected in patients with either primary or secondary dengue infection. This finding suggested that the anti-NS1 antibody appeared not only in secondary and severe dengue virus infection and might not correlate the pathogenesis of dengue hemorrhagic fever. The study also verified that our purified rNS1 protein showed similar immunological properties as native dengue viral proteins. Genetic engineering production of recombinant NS1 antigen could provide a safe and valuable resource for dengue virus serodiagnosis.

Animals↗

Effects of retinoic acid on pre-implantation embryo development in mice.

BACKGROUND: In a previous study we had investigated the effect of in utero retinoic acid (RA) exposure on early post-implantation development at the blastocyst stage before implantation and immediately after implantation to understand the possible roles of RA in embryogenesis. The results showed that excess RA affected early post-implantation embryogenesis adversely. We designed the present study to investigate the effect of in utero RA exposure on pre-implantation embryos. METHODS: In the prospective animal study, pregnant female mice received early pre-implantation peanut oil with 50 mg/kg t-RA or 100 mg/kg t-RA by oral gavage on the morning of day 1 and 2 or late pre-implantation exposure on the night of day 2 and morning of day 3 of gestation. Mice were sacrificed late in day 3. The number and morphology embryos were recorded. RESULTS: All mice given oral RA were sacrificed on the same day. The mean number of embryos per mouse and the percentage of different embryo stages in the t-RA treated mice administered at early pre-implantation embryo or late pre-implantation embryo stage were not significantly different from the controls. The mean number of embryos per 50 mg/kg mouse and the percentage of expanded blastocysts or early blastocysts/morulas did not differ from controls. In addition, the percentage of expanded blastocysts or early blastocysts/morulas was also not significantly different from the control group in 100 mg/kg late pre-implantation mice. CONCLUSION: Mouse embryo development may not experience dose related adverse effects from non-physiological RA exposure during pre-implantation.

Animals↗

Essential role for caspase-8 in transcription-independent apoptosis triggered by p53.

p53's dual regulation of arrest versus apoptosis may underlie tumor-selective effects of anti-cancer therapy. p53's apoptotic effect has been suggested to involve both transcription-dependent and -independent mechanisms. It is shown here that caspase-8 is activated early in cells undergoing p53-mediated apoptosis and in S100 cell-free extracts that recapitulate transcription-independent apoptosis. Depletion or inactivation of caspase-8 either in cells or cell-free extracts completely prevents this transcription-independent apoptosis and significantly attenuates overall death induced by wild-type p53. Importantly, caspase-8 activation appears to be independent of FADD, and caspase-8 is found in a novel 600-kDa complex following p53 activation. These findings highlight the roles of both transcription-dependent and -independent apoptosis by p53 and identify an essential role for caspase-8 in the transcription-independent pathway.

Adaptor Proteins, Signal Transducing↗

The neuroprotective effects of phytoestrogens on amyloid beta protein-induced toxicity are mediated by abrogating the activation of caspase cascade in rat cortical neurons.

Amyloid beta protein (Abeta) elicits a toxic effect on neurons in vitro and in vivo. In present study we attempt to elucidate the mechanism by which Abeta confers its neurotoxicity. The neuroprotective effects of phytoestrogens on Abeta-mediated toxicity were also investigated. Cortical neurons treated with 5 microm Abeta-(25-35) for 40 h decreased the cell viability by 45.5 +/- 4.6% concomitant with the appearance of apoptotic morphology. 50 microm kaempferol and apigenin decreased the Abeta-induced cell death by 81.5 +/- 9.4% and 49.2 +/- 9.9%, respectively. Abeta increased the activity of caspase 3 by 10.6-fold and to a lesser extent for caspase 2, 8, and 9. The Abeta-induced activation of caspase 3 and release of cytochrome c showed a biphasic pattern. Apigenin abrogated Abeta-induced cytochrome c release, and the activation of caspase cascade. Kaempferol showed a similar effect but to a less extent. Kaempferol was also capable of eliminating Abeta-induced accumulation of reactive oxygen species. These two events accounted for the remarkable effect of kaempferol on neuroprotection. Quercetin and probucol did not affect the Abeta-mediated neurotoxicity. However, they potentiated the protective effect of apigenin. Therefore, these results demonstrate that Abeta elicited activation of caspase cascades and reactive oxygen species accumulation, thereby causing neuronal death. The blockade of caspase activation conferred the major neuroprotective effect of phytoestrogens. The antioxidative activity of phytoestrogens also modulated their neuroprotective effects on Abeta-mediated toxicity.

Amyloid beta-Peptides↗

Suppressive effect of penta-acetyl geniposide on the development of gamma-glutamyl transpeptidase foci-induced by aflatoxin B(1) in rats.

The suppressive effects of penta-acetyl geniposide, (Ac)(5)-GP, on the hepatotoxic lesions-induced by aflatoxin B(1) (AFB(1)) were investigated in male Wistar rats. Rats were divided into six groups: groups I and II served as normal and solvent control, respectively; group III was given AFB(1) (2 mg/kg body weight) alone; group IV was given (Ac)(5)-GP (2 mg/kg) alone; and groups V and VI received both AFB(1) (2 mg/kg body weight) and (Ac)(5)-GP (1 mg and 2 mg/kg body weight, respectively). Rats received treatments for 8 weeks, then were maintained on basal diet for 32 weeks. At the end of the experiment (week 40), the liver lesions (e.g. fatty change, eosinophilic and bile duct dilation) and preneoplastic changes in rats of groups V and VI were reduced when they were compared with group III. There were no liver lesions and preneoplastic changes in rats treated with (Ac)(5)-GP alone. Although no differences in the total number of gamma-glutamyl transpeptidase (GGT)-positive foci was observed between the groups treated with AFB(1) along with or without (Ac)(5)-GP, the treatment of (Ac)(5)-GP significantly reduced the number of AFB(1)-induced GGT positive foci (with diameter larger than 0.3 mm). These results indicated that the protective effect of (Ac)(5)-GP on early hepatocarcinogenesis-induced by AFB(1) was associated with the inhibition of GGT foci development.

Aflatoxin B1↗

Involvement of oxidative stress, NF-IL-6, and RANTES expression in dengue-2-virus-infected human liver cells.

The liver has been suspected to be one of the major targets of dengue virus infection. Here, we detected increasing secretion of the chemokine RANTES (regulated upon activation, normal T cell expressed and secreted), which functions to recruit the immune cells, in dengue-virus-infected liver cells and patients. Three luciferase reporter genes with various deletions at the 5'-end of the RANTES promoter were constructed to explore the RANTES activation mechanism in human liver cells. The reporter gene was optimally activated by dengue-2 virus when the RANTES promoter contains the region from the transcription starting site (+1) to the nucleotide at the -181 position. NF-IL-6 and an undefined factor forming DNA-protein complexes in the RANTES promoter E and A/B regions in the infected cells were demonstrated by electrophoretic mobility shift assay. Further analysis showed that oxidative stress was an upstream inducer of NF-IL-6 and RANTES signaling in dengue-virus-infected liver cells. This finding was demonstrated by three antioxidants (N-acetyl-l-cysteine, nitro-l-arginine methyl ester, and pyrrolidine dithiocarbamate) used to suppress the activation. In contrast, the DNA binding activity of the undefined factor was not affected by the antioxidant treatment, indicating the existence of an oxidant-independent pathway. We hypothesize that dengue virus infection of the liver cells may trigger both an oxidant-dependent and an oxidant-independent pathway to up-regulate RANTES mRNA expression through activating NF-IL-6 and an undefined factor, respectively. In conclusion, the present study suggests a new direction for the study of liver pathogenesis involving RANTES in host immune responses during dengue virus infection.

Adolescent↗

Light-independent inactivation of dengue-2 virus by carboxyfullerene C3 isomer.

Carboxyfullerene (C60) is known as a photosensitizer for virus inactivation. Its regioisomer with C3 symmetry, named the C3 isomer, could also inactivate the dengue-2 virus without light when the dose of C3 isomer was increased to 40 microM, indicating the possible involvement of a light-independent mechanism. Further analysis showed that the C3 isomer blocked viral replication at the attachment and penetration stages, suggesting that a direct interaction between the C3 isomer and the virion is required for inactivation. The C3 isomer with a bipolar structure showed better lipid interaction and dengue-2 virus suppression than D3, another isomer that contains evenly distributed hydrophilic side chains. Moreover, the C3 isomer selectively inactivated enveloped viruses (viz., dengue-2 virus and Japanese encephalitis virus) instead of nonenveloped viruses (viz., enterovirus 71 and coxsackievirus B3). Collectively, these findings support the hypothesis that C3 isomer suppression of enveloped viruses is effected through its hydrophobic interaction with the viral lipid envelope. Our report, which demonstrates the light-dependent and -independent mechanisms of C60 on viral inactivation, will aid in the development of novel anti-viral agents for use against enveloped viruses.

Animals↗

Inhibition of testosterone secretion by S-petasin in rat testicular interstitial cells.

S-petasin, a kind of sesquiterpene ester, is the anti-inflammatory ann analgesic component of the butterbur (Petasites hybridus). The clinical benefit of S-petasin is the spasmolytic activity, but its side effects on the reproductive endocrinology are not clear yet. The present study was to explore the effects of S-petasin on the secretion of testosterone in vivo and in vitro. We found that single intravenous injection of S-petasin (1 microg/kg) decreased basal plasma testosterone concentration in adult male rats. The enzymatically dispersed rat testicular interstitial cells were incubated with S-petasin (0-4.3 x 10(-5)M) in the presence or absence of human chorionic gonadotropin (hCG, 0.05 IU/ml), forskolin (adenylyl cyclase activator, 10(-5) M), and androstenedione (testosterone biosynthesis precursor, 10(-9) M) at 34 degrees C for 1 h. The concentrations of testosterone in the incubation medium were measured by radioimmunoassay. S-petasin at 4.3 x 10(-7) M was effective to reduce the basal and hCG-stimulated release of testosterone in rat testicular interstitial cells. The stimulatory effects of testosterone secretion induced by forskolin and androstenedione were significantly reduced by S-petasin at 4.3 x 10(-5) M and 4.3 x 10(-6) M, respectively. These results suggest that S-petasin inhibits the production of testosterone in rat testicular interstitial cells in part through diminishing the activities of adenylyl cyclase and 17-ketosteroid reductase.

17-Hydroxysteroid Dehydrogenases↗

Effects of baicalein and wogonin on drug-metabolizing enzymes in C57BL/6J mice.

Effects of baicalein and wogonin, the major flavonoids of Scutellariae radix, on cytochrome P450 (CYP), UDP-glucuronosyl transferase (UGT), and glutathione S-transferase (GST) were studied in C57BL/6J mice. One-week treatment of mice with a liquid diet containing 5 mM baicalein resulted in 29%, 14%, 36%, 28%, and 46% decreases of hepatic benzo(a)pyrene hydroxylation (AHH), benzphetamine N-demethylation (BDM), N-nitrosodimethylamine N-demethylation (NDM), nifedipine oxidation (NFO), and erythromycin N-demethylation (EMDM) activities, respectively. Treatment with a liquid diet containing 5 mM wogonin resulted in 43%, 22%, 21%, 24%, and 35% decreases of hepatic AHH, BDM, NDM, NFO, and EMDM activities, respectively. However, hepatic 7-methoxyresorufin O-demethylation (MROD) activity was increased and decreased by baicalein- and wogonin-treatments, respectively. Similar modulation was observed with caffeine 3-demethylation (CDM) activity. Immunoblot analysis showed that the levels of hepatic CYP2E1 and CYP3A proteins were decreased by both baicalein- and wogonin-treatments. Hepatic CYP1A2 protein level was increased by baicalein but decreased by wogonin. In extrahepatic tissues, renal AHH activity was decreased by wogonin whereas pulmonary AHH, 7-ethoxyresorufin O-deethylation (EROD), and MROD activities were increased by both flavonoids. Both baicalein and wogonin strongly increased CYP1A protein level in mouse lung. Hepatic and renal UGT activities toward p-nitrophenol were suppressed by baicalein- and wogonin-treatments. However, cytosolic GST activity was not affected by flavonoids. These results suggest that ingestion of baicalein or wogonin can modulate drug-metabolizing enzymes and the modulation shows tissue specificity.

Animals↗

Association of protein phosphatase 2A with its substrate vimentin intermediate filaments in 9L rat brain tumor cells.

The importance of protein phosphatases in maintaining the integrity of intermediate filaments is supported by the fact that intermediate filaments would undergo a massive reorganization in cells treated with inhibitors of protein phosphatases 1 and 2A. Herein we used okadaic acid to investigate the differential roles of protein phosphatases 1 and 2A in the maintenance of intermediate filament integrity in 9L rat brain tumor cells. Protein phosphatase 2A activity was substantially inhibited after treatment with 400 nM okadaic acid for 2 h, whereas the activity of protein phosphatase 1 was only slightly affected. Furthermore, protein phosphatase 2A shows selective specificity toward phosphovimentin, which was immunologically precipitated from isotopically labeled and okadaic acid-treated cells. Further biochemical fractionation and microscopic studies revealed that vimentin intermediate filaments were colocalized with protein phosphatase 2A, but not protein phosphatase 1, in control cells. On okadaic acid treatment, vimentin filament disassembled and protein phosphatase 2A redistributed throughout the cytoplasm, suggesting that these two proteins separate from each other, whereas protein phosphatase 2A was inhibited. This working hypothesis was further supported by treatment with a low concentration (40 nM) of okadaic acid, which causes the same phenomenon. Taken together, our results showed that protein phosphatase 2A could be assigned to the intermediate filaments to serve the physiological role in maintaining the proper phosphorylation level of intermediate filaments in normal cells. This finding should pave the way for the elucidation of the regulatory mechanism of intermediate filament organization governed by protein phosphorylation.

Animals↗

Molecular epidemiological studies on foot-and-mouth disease type O Taiwan viruses from the 1997 epidemic.

Sequence diversity was assessed of the complete VP1 gene directly amplified from 49 clinical specimens during an explosive foot-and-mouth disease (FMD) outbreak in Taiwan. Type O Taiwan FMD viruses are genetically highly homogenous, as seen by the minute divergence of 0.2-0.9% revealed in 20 variants. The O/HCP-0314/TW/97 and O/TCP-022/TW/97 viral variants dominated FMD outbreaks and were prevalent in most affected pig-raising areas. Comparison of deduced amino acid sequences around the main neutralizable antigenic sites on the VP1 polypeptide showed no significant antigenic variation. However, the O/CHP-158/TW/97 variant had an alternative critical residue at position 43 in antigenic site 3, which may be due to selective pressure in the field. Two vaccine production strains (O1/Manisa/Turkey/69 and O1/Campos/Brazil/71) probably provide partial heterologous protection of swine against O Taiwan viruses. The type O Taiwan variants clustered in sublineage A1 of four main lineages in the phylogenetic tree. The O/Hong Kong/9/94 and O/1685/Moscow/Russia/95 viruses in sublineage A2 are closely related to the O Taiwan variants. The causative agent for the 1997 epidemic presumably originated from a single common source of type O FMD viruses prevalent in neighboring areas.

Amino Acid Sequence↗