Vijay P Bondre

Publications

• 0.40

  Impact points

  Changing clinico-laboratory profile of encephalitis patients in the eastern Uttar Pradesh region of India.

  Girish Chandra Bhatt, V P Bondre, G N Sapkal, Tanya Sharma, Santosh Kumar, M M Gore, K P Kushwaha, A K Rathi

  Tropical doctor. 04/2012; 42(2):106-8.

  A cross-sectional study was done on 100 consecutive paediatric patients presenting with acute encephalitis syndrome. The clinico-laboratory features of all patients were recorded in a prestructured performa. Cerebrospinal fluid and serum samples were tested for: Japanese encephalitis (JE) virus; Cha... [more] A cross-sectional study was done on 100 consecutive paediatric patients presenting with acute encephalitis syndrome. The clinico-laboratory features of all patients were recorded in a prestructured performa. Cerebrospinal fluid and serum samples were tested for: Japanese encephalitis (JE) virus; Chandipura virus; coxsackie virus; dengue virus; enterovirus 76; and West Nile virus. Twenty-two (22.0%) patients were confirmed JE cases and 17% had parasitic or bacteriological aetiology. The remaining 61 cases (61.0%) in which no viral aetiological agent was found were grouped as non-JE cases. Peripheral vascular failure, splenomegaly and hypotonia were distinguishing clinical features found in the non-JE patients. A high mortality of 26.5% was seen in patients with confirmed or presumptive viral encephalitis (22/83). A fatal outcome was independently associated with peripheral vascular failure and pallor at the time of admission. Early recognition of these signs may help clinicians to manage these cases.

• De novo identification of viral pathogens from cell culture hologenomes.

  Ashok Patowary, Rajendra Kumar Chauhan, Meghna Singh, Shamsudheen Kv, Vinita Periwal, Kushwaha Kp, Gajanand N Sapkal, Vijay P Bondre, Milind M Gore, Sridhar Sivasubbu, Vinod Scaria

  BMC research notes. 01/2012; 5:11.

  ABSTRACT: Fast, specific identification and surveillance of pathogens is the cornerstone of any outbreak response system, especially in the case of emerging infectious diseases and viral epidemics. This process is generally tedious and time-consuming thus making it ineffective in traditional setting... [more] ABSTRACT: Fast, specific identification and surveillance of pathogens is the cornerstone of any outbreak response system, especially in the case of emerging infectious diseases and viral epidemics. This process is generally tedious and time-consuming thus making it ineffective in traditional settings. The added complexity in these situations is the non-availability of pure isolates of pathogens as they are present as mixed genomes or hologenomes. Next-generation sequencing approaches offer an attractive solution in this scenario as it provides adequate depth of sequencing at fast and affordable costs, apart from making it possible to decipher complex interactions between genomes at a scale that was not possible before. The widespread application of next-generation sequencing in this field has been limited by the non-availability of an efficient computational pipeline to systematically analyze data to delineate pathogen genomes from mixed population of genomes or hologenomes. We applied next-generation sequencing on a sample containing mixed population of genomes from an epidemic with appropriate processing and enrichment. The data was analyzed using an extensive computational pipeline involving mapping to reference genome sets and de-novo assembly. In depth analysis of the data generated revealed the presence of sequences corresponding to Japanese encephalitis virus. The genome of the virus was also independently de-novo assembled. The presence of the virus was in addition, verified using standard molecular biology techniques. Our approach can accurately identify causative pathogens from cell culture hologenome samples containing mixed population of genomes and in principle can be applied to patient hologenome samples without any background information. This methodology could be widely applied to identify and isolate pathogen genomes and understand their genomic variability during outbreaks.

• De novo identification of viral pathogens from cell culture hologenomes

  Ashok Patowary, Rajendra K Chauhan, Meghna Singh, Shamsudheen K Vellarikkal, Vinita Periwal, Kushwaha K P, Gajanan N Sapkal, Vijay P Bondre, Milind M Gore, Sridhar Sivasubbu, Vinod Scaria

  BMC Research Notes. 01/2012;

  Background Fast, specific identification and surveillance of pathogens is the cornerstone of any outbreak response system, especially in the case of emerging infectious diseases and viral epidemics. This process is generally tedious and time-consuming thus making it ineffective in traditional settin... [more] Background Fast, specific identification and surveillance of pathogens is the cornerstone of any outbreak response system, especially in the case of emerging infectious diseases and viral epidemics. This process is generally tedious and time-consuming thus making it ineffective in traditional settings. The added complexity in these situations is the non-availability of pure isolates of pathogens as they are present as mixed genomes or hologenomes. Next-generation sequencing approaches offer an attractive solution in this scenario as it provides adequate depth of sequencing at fast and affordable costs, apart from making it possible to decipher complex interactions between genomes at a scale that was not possible before. The widespread application of next-generation sequencing in this field has been limited by the non-availability of an efficient computational pipeline to systematically analyze data to delineate pathogen genomes from mixed population of genomes or hologenomes. Findings We applied next-generation sequencing on a sample containing mixed population of genomes from an epidemic with appropriate processing and enrichment. The data was analyzed using an extensive computational pipeline involving mapping to reference genome sets and de-novo assembly. In depth analysis of the data generated revealed the presence of sequences corresponding to Japanese encephalitis virus. The genome of the virus was also independently de-novo assembled. The presence of the virus was in addition, verified using standard molecular biology techniques. Conclusions Our approach can accurately identify causative pathogens from cell culture hologenome samples containing mixed population of genomes and in principle can be applied to patient hologenome samples without any background information. This methodology could be widely applied to identify and isolate pathogen genomes and understand their genomic variability during outbreaks.
• 2.56

  Impact points

  Neutralization escape variant of West Nile virus associated with altered peripheral pathogenicity and differential cytokine profile.

  G N Sapkal, S Harini, V M Ayachit, P V Fulmali, S A Mahamuni, V P Bondre, M M Gore

  Virus research. 04/2011; 158(1-2):130-9.

  In order to understand the factors influencing pathogenicity of a virus, two neutralization escape (NE) variants were selected from wild type lineage 1 West Nile virus (WNV) 68856 strain pathogenic by intra-peritoneal (i.p.) route using monoclonal antibodies (MAbs) against envelope (E) protein. Both... [more] In order to understand the factors influencing pathogenicity of a virus, two neutralization escape (NE) variants were selected from wild type lineage 1 West Nile virus (WNV) 68856 strain pathogenic by intra-peritoneal (i.p.) route using monoclonal antibodies (MAbs) against envelope (E) protein. Both NE IF1A7 1.1 and NE IVC3F10 1.2 were resistant to neutralization and were neurovirulent by intra-cranial (i.c.) inoculation. Growth kinetics in porcine stable (PS) kidney and baby hamster kidney (BHK) cells was unchanged. In contrast to parent WNV only NE IF1A7 1.1 failed to cause lethal encephalitis on i.p. inoculation and was non pathogenic. NE IF1A7 1.1 variant showed delayed replication kinetics in murine peritoneal exudate cells (PEC) and Neuro 346 cells in vitro. In comparison with parent WNV and NE IVC3F10 1.2 variant, non pathogenic variant exhibited significantly reduced tumour necrosis factor α (TNF-α) induction in infected animals and PEC. Other cytokines like Interleukin (IL)-10, IL-6 and Interferon (IFN)-β remained unchanged. However, IL-1β did not follow the pattern and was higher only in parent WNV-infected PEC. The E gene sequences of these NE variants showed three common amino acid substitutions at residues E50, E89 and E242. A unique E156 (ser→pro) substitution in NE IF1A7 1.1, was absent in NE IVC3F10 1.2 variant suggested probable virulence marker. Our data indicates possible role of WNV E protein in induction of TNF-α and IL-1β and its association with WNV pathogenesis.
• 6.79

  Impact points

  Introduction of Japanese encephalitis virus genotype I, India.

  Pradip V Fulmali, Gajanan N Sapkal, Sulabha Athawale, Milind M Gore, Akhilesh C Mishra, Vijay P Bondre

  Emerging infectious diseases. 02/2011; 17(2):319-21.

  To the Editor: Seasonal outbreaks of fatal acute encephalitis syndrome (AES) occur regularly in several parts of India. Japanese encephalitis virus (JEV) has been the major and consistent cause of these outbreaks in the Gorakhpur region of Uttar Pradesh State, accounting for >>10%-15% of total... [more] To the Editor: Seasonal outbreaks of fatal acute encephalitis syndrome (AES) occur regularly in several parts of India. Japanese encephalitis virus (JEV) has been the major and consistent cause of these outbreaks in the Gorakhpur region of Uttar Pradesh State, accounting for >>10%-15% of total AES cases annually (1-3). In India, vaccinations against Japanese encephalitis (JE) are administered in areas where the disease is hyperendemic, including Gorakhpur, and AES cases are regularly investigated to clarify the effects of vaccination. Currently, >2,000 patients with AES are admitted each year to Baba Raghav Das Medical College, Gorakhpur.
• 3.26

  Impact points

  Genetic characterization of Bagaza virus isolated in India and evidence of anti-Bagaza virus antibodies in sera collected from encephalitis patients.

  Vijay P Bondre, Gajanan N Sapkal, Prasanna N Yergolkar, Pradip V Fulmali, Vasudha Sankararaman, Vijay M Ayachit, Akhilesh C Mishra, Milind M Gore

  The Journal of general virology. 08/2009;

  During 1996 encephalitis outbreak investigations in Kerala state of India, an arbovirus was isolated from Culex tritaenorhynchus mosquito pool. It was characterized as Japanese encephalitis and West Nile virus cross reactive arbovirus by complement fixation test. Plaque reduction neutralization test... [more] During 1996 encephalitis outbreak investigations in Kerala state of India, an arbovirus was isolated from Culex tritaenorhynchus mosquito pool. It was characterized as Japanese encephalitis and West Nile virus cross reactive arbovirus by complement fixation test. Plaque reduction neutralization test was preformed using hyperimmune sera raised against plaque purified arbovirus isolate. It did not show reactivity with Japanese encephalitis virus and was weak reactive with West Nile virus. Complete open reading frame sequence analysis characterized the arbovirus as Bagaza virus with 94.80% nucleotide identity with African Bagaza virus strain DakAr B209. Sera collected from the encephalitic patients during the acute phase of illness showed 15% (8/53) positivity for anti-Bagaza virus neutralizing antibodies. This is the first report on Bagaza virus isolation in India. Presence of anti-Bagaza virus neutralizing antibodies suggests exposure of human population to Bagaza virus.
• 6.79

  Impact points

  Enteroviruses in patients with acute encephalitis, uttar pradesh, India.

  Gajanan N Sapkal, Vijay P Bondre, Pradip V Fulmali, Pooja Patil, V Gopalkrishna, Vipul Dadhania, Vijay M Ayachit, Daya Gangale, K P Kushwaha, A K Rathi, Shobha D Chitambar, Akhilesh Chandra Mishra, Milind M Gore

  Emerging infectious diseases. 03/2009; 15(2):295-8.

  An outbreak of viral encephalitis occurred in northern India in 2006. Attempts to identify an etiologic agent in cerebrospinal fluid by using reverse transcription-PCR showed positivity to enterovirus (EV) in 66 (21.6%) of 306 patients. Sequencing and phylogenetic analyses of PCR products from 59 (8... [more] An outbreak of viral encephalitis occurred in northern India in 2006. Attempts to identify an etiologic agent in cerebrospinal fluid by using reverse transcription-PCR showed positivity to enterovirus (EV) in 66 (21.6%) of 306 patients. Sequencing and phylogenetic analyses of PCR products from 59 (89.3%) of 66 specimens showed similarity with EV-89 and EV-76 sequences.
• 2.80

  Impact points

  Detection and isolation of Japanese encephalitis virus from blood clots collected during the acute phase of infection.

  Gajanan N Sapkal, Nitin S Wairagkar, Vijay M Ayachit, Vijay P Bondre, Milind M Gore

  The American journal of tropical medicine and hygiene. 01/2008; 77(6):1139-45.

  Clinical specimens from an encephalitis outbreak in the Lakhimpur area of Uttar Pradesh, India, were investigated for identification and characterization of the etiologic agent. IgM capture ELISA showed recent Japanese encephalitis virus (JEV) infection. JEV isolation was attempted from white blood ... [more] Clinical specimens from an encephalitis outbreak in the Lakhimpur area of Uttar Pradesh, India, were investigated for identification and characterization of the etiologic agent. IgM capture ELISA showed recent Japanese encephalitis virus (JEV) infection. JEV isolation was attempted from white blood cells (WBCs) separated from blood clots of 12 patients (9 IgM positive and 3 negative) by serial co-culturing with phytohemagglutinin P-stimulated peripheral blood mononuclear leukocytes (PBMCs) obtained from pre-screened JEV sero-negative healthy individuals. JEV was isolated from two IgM-positive blood clots. Isolate 014178 was detected in WBCs and in the first passage of PBMCs by ELISA and reverse transcriptase-polymerase chain reaction. Isolate 014173 was detectable only after a second passage in PBMC co-culture. Sequence analysis of 346 nt of the C-prM region showed homology with JEV strain GP78. This is the first report on isolation of JEV from patient blood clots. Our study shows that the co-cultures of PBMCs separated from patient blood clots provide an additional source for JEV isolation.
• 3.26

  Impact points

  West Nile virus isolates from India: evidence for a distinct genetic lineage.

  Vijay P Bondre, R S Jadi, A C Mishra, P N Yergolkar, V A Arankalle

  The Journal of general virology. 04/2007; 88(Pt 3):875-84.

  The complete genomic sequence of one human isolate of West Nile virus (WNV) and the partial genomic sequences of 14 other strains from India isolated in the period 1955-1982 from different hosts and geographical areas were determined. Phylogenetic analyses based on complete and partial genomic seque... [more] The complete genomic sequence of one human isolate of West Nile virus (WNV) and the partial genomic sequences of 14 other strains from India isolated in the period 1955-1982 from different hosts and geographical areas were determined. Phylogenetic analyses based on complete and partial genomic sequences (921 nt of the C-prM-E region) revealed that WNV could be classified into five distinct groups that differed from each other by 20-25% at the complete genome level and by 20-26% using partial sequences. Of the Indian isolates, 13 formed a distinct genetic lineage, lineage 5, whereas two isolates, one from a human patient (1967) and another from a bat (1968), were related closely to lineage 1 strains. The complete genomic sequence of the Indian isolate, 804994, showed 20-22% genetic divergence from the previously proposed lineage 1 and 2 strains and 24-25% divergence from isolates of the newly proposed lineages 3 (Rabensburg isolate 97-103 of 1997) and 4 (Russian isolate LEIV-Krnd88-190 of 1998). Similarly, the partial genomic sequences of the Indian isolates showed 21-26% divergence from lineage 1 and 2 strains and from the Rabensburg (97-103) and Russian (LEIV-Krnd88-190) isolates. Cross-neutralization using strain-specific polyclonal antibodies against lineage 1 strain Eg-101 and representative Indian strains suggests substantial antigenic variation. This study documents circulation of WNV strains typical to India for 27 years and the introduction of lineage 1 strains during 1967-1968. These results indicate strongly that WNV should be classified into five genetic lineages, with Indian viruses constituting the distinct genetic lineage 5.
• 2.20

  Impact points

  Vibrio cholerae persistence in aquatic environments and colonization of intestinal cells: involvement of a common adhesion mechanism.

  Massimiliano Zampini, Carla Pruzzo, Vijay P Bondre, Renato Tarsi, Mariangela Cosmo, Alessandro Bacciaglia, Arvind Chhabra, Renjana Srivastava, Brahm S Srivastava

  FEMS microbiology letters. 04/2005; 244(2):267-73.

  Forty-one Tnpho A mutants of Vibrio cholerae O1 classical strain CD81 were analyzed for their ability to interact with chitin particles, Tigriopus fulvus copepods and the Intestine 407 cell line compared to the parent strain. Thirteen mutants were less adhesive than CD81; in particular, T21, T33 and... [more] Forty-one Tnpho A mutants of Vibrio cholerae O1 classical strain CD81 were analyzed for their ability to interact with chitin particles, Tigriopus fulvus copepods and the Intestine 407 cell line compared to the parent strain. Thirteen mutants were less adhesive than CD81; in particular, T21, T33 and T87 were less adhesive towards all substrates and insensitive to inhibition by N-acetyl glucosamine (GlcNAc). By SDS-PAGE analysis of sarkosyl-insoluble membrane proteins (siMPs) isolated from mutants and parent, it was found that a 53 kDa siMP is missing in T21, T33 and T87 mutants. It is hypothesized that this protein might have the function to mediate adherence to GlcNAc-containing substrates both in the aquatic environment and in human intestine.
• 0.75

  Impact points

  Isolation of chikungunya virus from Aedes aegypti mosquitoes collected in the town of Yawat, Pune District, Maharashtra State, India.

  D T Mourya, J R Thakare, M D Gokhale, A M Powers, S L Hundekar, P C Jayakumar, V P Bondre, Y S Shouche, V S Padbidri

  Acta virologica. 02/2001; 45(5-6):305-9.

  Chikungunya (CHIK) virus is prevalent throughout Southeast Asia and Africa. It has caused numerous large outbreaks in India. No active or passive surveillance has been carried out since the last epidemic occurring in 1971. During a recent outbreak of Dengue (DEN)-like illness in eastern India, Aedes... [more] Chikungunya (CHIK) virus is prevalent throughout Southeast Asia and Africa. It has caused numerous large outbreaks in India. No active or passive surveillance has been carried out since the last epidemic occurring in 1971. During a recent outbreak of Dengue (DEN)-like illness in eastern India, Aedes aegypti mosquitoes collected from the affected area were positive for CHIK virus. Evidence of dual infection with CHIK and DEN typel virus was also obtained. A widely circulating low-virulent CHIK virus is a possible explanation for the epidemiological pattern of the CHIK virus disease in this region.
• 2.27

  Impact points

  Screening of TnphoA mutants of Vibrio cholerae O139 for identification of antigens involved in colonisation.

  V P Bondre, R Srivastava, V B Sinha, B S Srivastava

  Journal of medical microbiology. 01/1998; 46(12):1007-11.

  A new serogroup of Vibrio cholerae non-O1, designated as O139, has emerged causing cholera-like disease among adults. Laboratory and field studies clearly show that there is no cross-protection between O1 and O139 pathogenic strains. Since colonisation of the intestine is a most important step in th... [more] A new serogroup of Vibrio cholerae non-O1, designated as O139, has emerged causing cholera-like disease among adults. Laboratory and field studies clearly show that there is no cross-protection between O1 and O139 pathogenic strains. Since colonisation of the intestine is a most important step in the pathogenesis of cholera caused by O1 strains and colonising antigens are known to be protective, investigation of the colonising antigens of O139 strain was initiated. By TnphoA mutagenesis, mutants were generated with insertions in the genome encoding membrane spanning or secretory proteins. Screening of the mutants for adherence to rabbit intestinal surface and colonisation in 5-day-old mice resulted in the identification of mutant clones, which were less adhesive than was the wild-type parent strain and which could not efficiently colonise the gut. Such non-colonising strains were attenuated in virulence. Analysis of the proteins by SDS-PAGE revealed that the non-colonising mutants did not express a 40-kDa outer-membrane protein.
• 2.34

  Impact points

  Evaluation of different subcellular fractions of Vibrio cholerae O139 in protection to challenge in experimental cholera.

  V P Bondre, V B Sinha, B S Srivastava

  FEMS immunology and medical microbiology. 12/1997; 19(4):323-9.

  Various cellular fractions of Vibrio cholerae O139 were prepared and evaluated in the rabbit ileal loop model of experimental cholera for identification of the protective antigen(s) relevant for vaccine development. Lipopolysaccharides (LPS) and capsular polysaccharides (CPS) of O139 strains and its... [more] Various cellular fractions of Vibrio cholerae O139 were prepared and evaluated in the rabbit ileal loop model of experimental cholera for identification of the protective antigen(s) relevant for vaccine development. Lipopolysaccharides (LPS) and capsular polysaccharides (CPS) of O139 strains and its cell surface, membrane and cytosolic fractions were assayed for antibacterial immunity, whereas the cholera toxin was examined for antitoxic immunity. The lipopolysaccharides, membrane fraction and cholera toxin induced moderate protection, however there was a significant synergistic effect when cholera toxin was combined with membrane proteins or lipopolysaccharides. The O139 strains strongly resembled O1 strains in the profile of proteins and immunological cross reactivity, yet there was no cross protection. The results warrant further investigation of the pathogenesis of O139 strains and identify the critical somatic antigens relevant to protection.