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Papers by SUBRATA DAS
The Journal of Infectious Diseases, 2001
Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenom... more Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenomenon, known as tick immunity, that is partially mediated by antibody. To determine the salivary gland antigens that elicit antibodies in the host, an I. scapularis salivary gland cDNA expression library was probed with serum from tick-immune rabbits. Sera from sensitized rabbits strongly recognized 47 of 100,000 library clones in an antibody-screening assay. These 47 clones encoded 14 different I. scapularis genes, including a glutathione peroxidase homologue. Expression of these 14 genes in engorged tick salivary glands was confirmed by reverse-transcription polymerase chain reaction. The I. scapularis glutathione peroxidase homologue, named salp25D, was expressed in both unfed and fed nymphal salivary glands. Recombinant Salp25D was able to catalyze the reduction of hydrogen peroxide in the presence of reduced glutathione and glutathione reductase. These results categorize the prominent salivary gland proteins in I. scapularis and demonstrate the presence of a potent antioxidant in tick saliva. Mammals that have been infested by ticks acquire immunity to subsequent bites by the vector, a phenomenon known as tick immunity. Acquired resistance to ticks was first described by Trager in 1939, who showed that guinea pigs on which Dermacentor variabilis (the common dog tick) had fed became resistant to future tick bites [1]. Many authors have extended these findings over the last 50 years [2]. Repeated exposure of rabbits, cattle, dogs, and guinea pigs to ticks has been shown to interfere with vector feeding, molting, and fecundity [1, 3-7]. Even a natural host like Clethrionomys glareolus, the bank vole, develops resistance to Ixodes ricinus with repeated infestations [8]. Tick immunity can interfere with pathogen transmission. Rabbits pre-exposed to uninfected D. andersoni were partially protected when exposed to Francisella tularensis-infected nymphs [9]. Transmission of tick-borne Babesia bovis was impaired in tick-immune cattle [5]. Immunity to I. ricinus in C. glareolus reduced the efficiency of I. ricinus-mediated Borrelia burgdorferi transmission [10]. Similarly, I. scapularis-sensitized guinea pigs do not acquire infection when challenged with B.
The Journal of Infectious Diseases, 2001
Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenom... more Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenomenon, known as tick immunity, that is partially mediated by antibody. To determine the salivary gland antigens that elicit antibodies in the host, an I. scapularis salivary gland cDNA expression library was probed with serum from tick-immune rabbits. Sera from sensitized rabbits strongly recognized 47 of 100,000 library clones in an antibody-screening assay. These 47 clones encoded 14 different I. scapularis genes, including a glutathione peroxidase homologue. Expression of these 14 genes in engorged tick salivary glands was confirmed by reverse-transcription polymerase chain reaction. The I. scapularis glutathione peroxidase homologue, named salp25D, was expressed in both unfed and fed nymphal salivary glands. Recombinant Salp25D was able to catalyze the reduction of hydrogen peroxide in the presence of reduced glutathione and glutathione reductase. These results categorize the prominent salivary gland proteins in I. scapularis and demonstrate the presence of a potent antioxidant in tick saliva. Mammals that have been infested by ticks acquire immunity to subsequent bites by the vector, a phenomenon known as tick immunity. Acquired resistance to ticks was first described by Trager in 1939, who showed that guinea pigs on which Dermacentor variabilis (the common dog tick) had fed became resistant to future tick bites [1]. Many authors have extended these findings over the last 50 years [2]. Repeated exposure of rabbits, cattle, dogs, and guinea pigs to ticks has been shown to interfere with vector feeding, molting, and fecundity [1, 3-7]. Even a natural host like Clethrionomys glareolus, the bank vole, develops resistance to Ixodes ricinus with repeated infestations [8]. Tick immunity can interfere with pathogen transmission. Rabbits pre-exposed to uninfected D. andersoni were partially protected when exposed to Francisella tularensis-infected nymphs [9]. Transmission of tick-borne Babesia bovis was impaired in tick-immune cattle [5]. Immunity to I. ricinus in C. glareolus reduced the efficiency of I. ricinus-mediated Borrelia burgdorferi transmission [10]. Similarly, I. scapularis-sensitized guinea pigs do not acquire infection when challenged with B.
We have identified a 55-kDa antigen encoded by a gene on a 49-kb plasmid of Borrelia burgdorferi.... more We have identified a 55-kDa antigen encoded by a gene on a 49-kb plasmid of Borrelia burgdorferi. The screening of a B. burgdorferi DNA expression library (N40 strain) with rabbit anti-B. burgdorferi serum and then with serum from a patient with Lyme disease arthritis revealed a clone that synthesized an antigen that was reactive with both sera. DNA sequence analysis identified an operon with two genes, s1 and s2 (1,254 and 780 nucleotides), that expressed antigens with the predicted molecular masses of 55 and 29 kDa, respectively. Pulsed-field gel electrophoresis showed that the s1-s2 operon was located on the 49-kb plasmid. Recombinant S1 was synthesized as a glutathione S-transferase fusion protein in Escherichia coli. Antibodies to recombinant S1 bound to a 55-kDa protein in lysates of B. burgdorferi, indicating that cultured spirochetes synthesized S1. Thirty-one of 100 Lyme disease patients had immunoglobulin G (IgG) and/or IgM antibodies to S1. IgG antibodies to S1 were detected by enzyme-linked immunosorbent assay and immunoblots in the sera of 21 (21%) of 100 patients with Lyme disease; 11 (27.5%) of the S1-positive samples were from patients (40) with early-stage Lyme disease, and 10 (16.7%) were from patients (60) with late-stage Lyme disease. Fifteen (38.5%) of 40 serum samples from patients with early-stage Lyme disease had IgM antibodies to S1. These data suggest that the S1 antigen encoded by a gene on the 49-kb plasmid is recognized serologically by a subset of patients with early-or late-stage Lyme disease. Lyme disease, caused by the spirochete Borrelia burgdorferi, is characterized by an initial cutaneous infection which can disseminate to involve multiple organ systems, including the heart, nervous system, and joints (34). B. burgdorferi is transmitted to humans by the bite of Ixodes ticks (34). The spirochete initially resides in the skin and must gain access to the bloodstream to cause infection resulting in carditis, arthritis, or neurologic symptoms. B. burgdorferi antigens may play important roles in immunity and the pathogenesis of infection. The genome of B. burgdorferi consists of a linear chromosome (10) and a series of linear and circular plasmids (18). In B. burgdorferi, the genes encoding several known surface-exposed lipoproteins have been cloned. The genes for the major outer surface proteins (Osps) A and B are located on a 49-kb linear plasmid (2, 3). The ospC gene (17) is found on a 27-kb circular plasmid (28) and demonstrated to be actively transcribed in selected B. burgdorferi strains (22). The ospD gene is located on a 38-kb linear plasmid and preferentially expressed by low-passage, virulent B. burgdorferi organisms (24). An operon encoding the ospE and ospF genes is on a 42-kb plasmid (21), a 27-kDa antigen (P27) is encoded by a gene on a 55-kb linear plasmid (27), and the gene for the IpLA7 (P22) is encoded on the chromosome (20, 35). OspA, OspB, OspC, and OspF play roles in protective immunity to B. burgdorferi infection. Active immunization with
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](Acta Crystallographica Section E Structure Reports Online, 2009
The title compound, C 19 H 21 ClN 6 O 4 , is a 1:2 adduct of pchlorobenzaldehyde and uracil. It c... more The title compound, C 19 H 21 ClN 6 O 4 , is a 1:2 adduct of pchlorobenzaldehyde and uracil. It crystallizes with two molecules in the asymmetric unit. The two uracil units in the same molecule are connected by a pair of strong N-HÁ Á ÁO hydrogen bonds. The packing is stabilized by N-HÁ Á ÁO, C-HÁ Á ÁO and C-HÁ Á ÁN interactions. Related literature For the biological activity and medicinal applications of heterocyclic compounds, especially pyrimidine derivatives, see: Zheng et al. (2007); Jain et al. (2006). The title compound was synthesized from 6-amino-1,3-dimethylpyrimidine-2,4(1H, 3H)-dione, which is an important building block, see:
The Journal of Infectious Diseases, 2001
Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenom... more Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenomenon, known as tick immunity, that is partially mediated by antibody. To determine the salivary gland antigens that elicit antibodies in the host, an I. scapularis salivary gland cDNA expression library was probed with serum from tick-immune rabbits. Sera from sensitized rabbits strongly recognized 47 of 100,000 library clones in an antibody-screening assay. These 47 clones encoded 14 different I. scapularis genes, including a glutathione peroxidase homologue. Expression of these 14 genes in engorged tick salivary glands was confirmed by reverse-transcription polymerase chain reaction. The I. scapularis glutathione peroxidase homologue, named salp25D, was expressed in both unfed and fed nymphal salivary glands. Recombinant Salp25D was able to catalyze the reduction of hydrogen peroxide in the presence of reduced glutathione and glutathione reductase. These results categorize the prominent salivary gland proteins in I. scapularis and demonstrate the presence of a potent antioxidant in tick saliva. Mammals that have been infested by ticks acquire immunity to subsequent bites by the vector, a phenomenon known as tick immunity. Acquired resistance to ticks was first described by Trager in 1939, who showed that guinea pigs on which Dermacentor variabilis (the common dog tick) had fed became resistant to future tick bites [1]. Many authors have extended these findings over the last 50 years [2]. Repeated exposure of rabbits, cattle, dogs, and guinea pigs to ticks has been shown to interfere with vector feeding, molting, and fecundity [1, 3-7]. Even a natural host like Clethrionomys glareolus, the bank vole, develops resistance to Ixodes ricinus with repeated infestations [8]. Tick immunity can interfere with pathogen transmission. Rabbits pre-exposed to uninfected D. andersoni were partially protected when exposed to Francisella tularensis-infected nymphs [9]. Transmission of tick-borne Babesia bovis was impaired in tick-immune cattle [5]. Immunity to I. ricinus in C. glareolus reduced the efficiency of I. ricinus-mediated Borrelia burgdorferi transmission [10]. Similarly, I. scapularis-sensitized guinea pigs do not acquire infection when challenged with B.
The Journal of Infectious Diseases, 2001
Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenom... more Rabbits or guinea pigs infested with Ixodes scapularis acquire resistance to tick bites, a phenomenon, known as tick immunity, that is partially mediated by antibody. To determine the salivary gland antigens that elicit antibodies in the host, an I. scapularis salivary gland cDNA expression library was probed with serum from tick-immune rabbits. Sera from sensitized rabbits strongly recognized 47 of 100,000 library clones in an antibody-screening assay. These 47 clones encoded 14 different I. scapularis genes, including a glutathione peroxidase homologue. Expression of these 14 genes in engorged tick salivary glands was confirmed by reverse-transcription polymerase chain reaction. The I. scapularis glutathione peroxidase homologue, named salp25D, was expressed in both unfed and fed nymphal salivary glands. Recombinant Salp25D was able to catalyze the reduction of hydrogen peroxide in the presence of reduced glutathione and glutathione reductase. These results categorize the prominent salivary gland proteins in I. scapularis and demonstrate the presence of a potent antioxidant in tick saliva. Mammals that have been infested by ticks acquire immunity to subsequent bites by the vector, a phenomenon known as tick immunity. Acquired resistance to ticks was first described by Trager in 1939, who showed that guinea pigs on which Dermacentor variabilis (the common dog tick) had fed became resistant to future tick bites [1]. Many authors have extended these findings over the last 50 years [2]. Repeated exposure of rabbits, cattle, dogs, and guinea pigs to ticks has been shown to interfere with vector feeding, molting, and fecundity [1, 3-7]. Even a natural host like Clethrionomys glareolus, the bank vole, develops resistance to Ixodes ricinus with repeated infestations [8]. Tick immunity can interfere with pathogen transmission. Rabbits pre-exposed to uninfected D. andersoni were partially protected when exposed to Francisella tularensis-infected nymphs [9]. Transmission of tick-borne Babesia bovis was impaired in tick-immune cattle [5]. Immunity to I. ricinus in C. glareolus reduced the efficiency of I. ricinus-mediated Borrelia burgdorferi transmission [10]. Similarly, I. scapularis-sensitized guinea pigs do not acquire infection when challenged with B.
We have identified a 55-kDa antigen encoded by a gene on a 49-kb plasmid of Borrelia burgdorferi.... more We have identified a 55-kDa antigen encoded by a gene on a 49-kb plasmid of Borrelia burgdorferi. The screening of a B. burgdorferi DNA expression library (N40 strain) with rabbit anti-B. burgdorferi serum and then with serum from a patient with Lyme disease arthritis revealed a clone that synthesized an antigen that was reactive with both sera. DNA sequence analysis identified an operon with two genes, s1 and s2 (1,254 and 780 nucleotides), that expressed antigens with the predicted molecular masses of 55 and 29 kDa, respectively. Pulsed-field gel electrophoresis showed that the s1-s2 operon was located on the 49-kb plasmid. Recombinant S1 was synthesized as a glutathione S-transferase fusion protein in Escherichia coli. Antibodies to recombinant S1 bound to a 55-kDa protein in lysates of B. burgdorferi, indicating that cultured spirochetes synthesized S1. Thirty-one of 100 Lyme disease patients had immunoglobulin G (IgG) and/or IgM antibodies to S1. IgG antibodies to S1 were detected by enzyme-linked immunosorbent assay and immunoblots in the sera of 21 (21%) of 100 patients with Lyme disease; 11 (27.5%) of the S1-positive samples were from patients (40) with early-stage Lyme disease, and 10 (16.7%) were from patients (60) with late-stage Lyme disease. Fifteen (38.5%) of 40 serum samples from patients with early-stage Lyme disease had IgM antibodies to S1. These data suggest that the S1 antigen encoded by a gene on the 49-kb plasmid is recognized serologically by a subset of patients with early-or late-stage Lyme disease. Lyme disease, caused by the spirochete Borrelia burgdorferi, is characterized by an initial cutaneous infection which can disseminate to involve multiple organ systems, including the heart, nervous system, and joints (34). B. burgdorferi is transmitted to humans by the bite of Ixodes ticks (34). The spirochete initially resides in the skin and must gain access to the bloodstream to cause infection resulting in carditis, arthritis, or neurologic symptoms. B. burgdorferi antigens may play important roles in immunity and the pathogenesis of infection. The genome of B. burgdorferi consists of a linear chromosome (10) and a series of linear and circular plasmids (18). In B. burgdorferi, the genes encoding several known surface-exposed lipoproteins have been cloned. The genes for the major outer surface proteins (Osps) A and B are located on a 49-kb linear plasmid (2, 3). The ospC gene (17) is found on a 27-kb circular plasmid (28) and demonstrated to be actively transcribed in selected B. burgdorferi strains (22). The ospD gene is located on a 38-kb linear plasmid and preferentially expressed by low-passage, virulent B. burgdorferi organisms (24). An operon encoding the ospE and ospF genes is on a 42-kb plasmid (21), a 27-kDa antigen (P27) is encoded by a gene on a 55-kb linear plasmid (27), and the gene for the IpLA7 (P22) is encoded on the chromosome (20, 35). OspA, OspB, OspC, and OspF play roles in protective immunity to B. burgdorferi infection. Active immunization with
Acta Crystallographica Section E Structure Reports Online, 2009
The title compound, C 19 H 21 ClN 6 O 4 , is a 1:2 adduct of pchlorobenzaldehyde and uracil. It c... more The title compound, C 19 H 21 ClN 6 O 4 , is a 1:2 adduct of pchlorobenzaldehyde and uracil. It crystallizes with two molecules in the asymmetric unit. The two uracil units in the same molecule are connected by a pair of strong N-HÁ Á ÁO hydrogen bonds. The packing is stabilized by N-HÁ Á ÁO, C-HÁ Á ÁO and C-HÁ Á ÁN interactions. Related literature For the biological activity and medicinal applications of heterocyclic compounds, especially pyrimidine derivatives, see: Zheng et al. (2007); Jain et al. (2006). The title compound was synthesized from 6-amino-1,3-dimethylpyrimidine-2,4(1H, 3H)-dione, which is an important building block, see: