Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 9 de 9
Filter
1.
Diagnostics (Basel) ; 12(2)2022 Feb 01.
Article in English | MEDLINE | ID: mdl-35204453

ABSTRACT

The aetiology of non-malaria vector-borne diseases in malaria-endemic, forested, rural, and tribal-dominated areas of Dhalai, Tripura, in north-east India, was studied for the first time in the samples collected from malaria Rapid Diagnostic Kit negative febrile patients by door-to-door visits in the villages and primary health centres. Two hundred and sixty serum samples were tested for the Dengue NS1 antigen and the IgM antibodies of Dengue, Chikungunya, Scrub Typhus (ST), and Japanese Encephalitis (JE) during April 2019-March 2020. Fifteen Dengue, six JE, twelve Chikungunya, nine ST and three Leptospirosis, and mixed infections of three JE + Chikungunya, four Dengue + Chikungunya, three Dengue + JE + Chikungunya, one Dengue + Chikungunya + ST, and one Dengue + ST were found positive by IgM ELISA tests, and four for the Dengue NS1 antigen, all without any travel history. True prevalence values estimated for infections detected by Dengue IgM were 0.134 (95% CI: 0.08-0.2), Chikungunya were 0.084 (95% CI: 0.05-0.13), Scrub were 0.043 (95% CI: 0.01-0.09), and Japanese Encephalitis were 0.045 (95% CI: 0.02-0.09). Dengue and Chikungunya were associated significantly more with a younger age. There was a lack of a defined set of symptoms for any of the Dengue, Chikungunya, JE or ST infections, as indicated by the k-modes cluster analysis. Interestingly, most of these symptoms have an overlapping set with malaria; thereby, it becomes imperative that malaria and these non-malaria vector-borne disease diagnoses are made in a coordinated manner. Findings from this study call for advances in routine diagnostic procedures and the development of a protocol that can accommodate, currently, in practicing the rapid diagnosis of malaria and other vector-borne diseases, which is doable even in the resource-poor settings of rural hospitals and during community fever surveillance.

3.
3 Biotech ; 8(10): 408, 2018 Oct.
Article in English | MEDLINE | ID: mdl-30237955

ABSTRACT

Since its emergence in 2009, Influenza A/H1N1pdm09 virus has evolved continuously. Marked genetic variations have occurred in the HA1 domain of the hemagglutinin gene causing the emergence of new variants. The present study genetically characterized the hemagglutinin (HA) gene of Influenza A/H1N1pdm09 strains from Assam circulating in 2016 that caused a mild outbreak without any reported mortality. Sequence analysis of the HA gene of 20 positive Assam/H1N1pdm09 strains revealed 3 mutations (K180Q, S202T, S220T) at the antigenic sites along with several other reported mutations which are in close proximity to the antigenic sites and therefore might affect the viral antigenicity. Phylogenetically, the Assam/H1N1pdm09 strains clustered into genogroup 6B. These genetic variations highlight the importance of continuous surveillance and characterization of Influenza A/H1N1pdm09 virus activity to track the genetic makeup and diversification that may affect the behavior of the virus.

4.
Indian J Med Microbiol ; 36(1): 37-42, 2018.
Article in English | MEDLINE | ID: mdl-29735824

ABSTRACT

BACKGROUND AND OBJECTIVES: Dengue is one of the most prevalent arboviral diseases in the world with 390 million dengue infections per year. In this study, we report the molecular characterisation of dengue outbreak in Pasighat, Arunachal Pradesh, Northeast India during 2015. SUBJECTS AND METHODS: : A total of 613 dengue-suspected cases were screened for dengue virus by dengue NS1 Ag and anti-dengue IgM antibody depending on the duration of sample collection and onset of symptom. Further, molecular characterisation was done by amplifying the C-PrM region by real-time polymerase chain reaction followed by phylogenetic analysis. RESULTS: Molecular characterisation revealed that the dengue outbreak was predominantly due to dengue virus serotype-1 (DENV-1) (90.9%) while DENV-2 was detected in 7.5% of samples. Co-infection of DENV-1 and DENV-2 was detected in one case. Phylogenetic analysis of the DENV-1 strains with the prototype revealed that the DENV-1 strains were grouped within genotype III. Similarly, DENV-2 strains were clustered within genotype IV. The study revealed a change in the predominant serotype in recent years with DENV-3 in 2012 to DENV-1, 2, 3 and 4 in 2014 to DENV-1 in 2015 in the study region. A unique L24M mutation was observed in the DENV-1 strains of Arunachal Pradesh which was absent in all the circulating strains in India except one strain from the state of Kerala in South India. Marked variation within the DENV-2 strains was observed at A102V and I163V in one strain similar to earlier circulating isolates in India. CONCLUSIONS: The present study reveals a shift in the serotype dominance in the study region. As serotype shifts and secondary infection with a heterologous DENV serotype are frequently associated with disease severity, there is an urgent need for sustained monitoring of the circulating serotypes and enhanced surveillance operations, especially in the monsoon and post-monsoon periods to prevent large-scale, severe dengue outbreaks in this region.


Subject(s)
Antibodies, Viral/immunology , Dengue Virus/classification , Dengue Virus/isolation & purification , Dengue/epidemiology , Viral Nonstructural Proteins/immunology , Dengue/virology , Dengue Virus/genetics , Disease Outbreaks , Genotype , Glycoproteins/immunology , Humans , Immunoglobulin M/immunology , India/epidemiology , Molecular Epidemiology/methods , Phylogeny , Serogroup , Serotyping
5.
Tumour Biol ; 39(5): 1010428317698384, 2017 May.
Article in English | MEDLINE | ID: mdl-28459370

ABSTRACT

The high incidence of esophageal cancer in Northeast India and the unique ethnic background and dietary habits provide a great opportunity to study the molecular genetics behind esophageal squamous cell carcinoma in this part of the region. We hypothesized that in addition to currently known environmental risk factors for esophageal cancer, genetic and epigenetic factors are also involved in esophageal carcinogenesis in Northeast India. Therefore, in this study, we explored the possible association between the two important G1 cell cycle regulatory genes p16 and p53 and environmental risk factors and risk of esophageal carcinogenesis. A total of 100 newly diagnosed esophageal cancer cases along with equal number of age-, sex-, and ethnicity-matched controls were included in this study. Methylation-specific polymerase chain reaction was used to determine the p16 promoter methylation status. Single-nucleotide polymorphism at codon 72 of p53 gene was assessed by the polymerase chain reaction-restriction fragment length polymorphism method. Aberrant methylation of p16 gene was seen in 81% of esophageal cancer cases. Hypermethylation of p16 gene was not found in healthy controls. p53 Pro/Pro genotype was found to be a risk genotype in Northeast India compared with Arg/Pro and Arg/Arg. p53 variant/polymorphism was significantly associated with esophageal cancer risk in the study population under all three genetic models, namely, dominant model (Arg/Pro + Pro/Pro vs Arg/Arg odds ratio = 2.25, confidence interval = 1.19-4.26; p = 0.012), recessive model (Arg/Arg + Arg/Pro vs Pro/Pro odds ratio = 2.35, confidence interval = 1.24-4.44; p = 0.008), and homozygous model (Pro/Pro vs Arg/Arg odds ratio = 3.33, confidence interval = 1.54-7.20; p = 0.002). However, p53 variant/polymorphism was not statistically associated with esophageal cancer risk under the heterozygous model (Pro/Pro vs Arg/Pro). In the case-only analysis based on p16 methylation, the p53 variant/polymorphism (Pro/Pro or Arg/Pro) showed significant association for esophageal cancer risk (odds ratio = 3.33, confidence interval = 1.54-7.20; p = 0.002). Gene-gene and gene-environment interaction using the case-only approach revealed a strong association between p16 methylation, p53 single-nucleotide polymorphism, and environmental factors and esophageal cancer risk. Cases with p16 methylation and p53 variant/polymorphism (Pro/Pro or Arg/Pro) along with both betel quid and tobacco chewing habit (odds ratio = 8.29, confidence interval = 1.14-60.23; p = 0.037) conferred eightfold increased risk toward esophageal cancer development. This study reveals a synergistic interaction between epigenetic, genetic, and environmental factors and risk of esophageal cancer in this high-incidence region of Northeast India. The inactivation of either p16 or p53 in a majority of esophageal cancer cases in this study suggests the possible crosstalk between the important cell cycle genes.


Subject(s)
Cyclin-Dependent Kinase Inhibitor p16/genetics , Esophageal Neoplasms/genetics , Genetic Predisposition to Disease , Tumor Suppressor Protein p53/genetics , Adult , Aged , Cyclin-Dependent Kinase Inhibitor p16/antagonists & inhibitors , DNA Methylation/genetics , Esophageal Neoplasms/pathology , Female , Gene Expression Regulation, Neoplastic , Gene Silencing , Gene-Environment Interaction , Genotype , Humans , India , Male , Middle Aged , Polymorphism, Single Nucleotide , Promoter Regions, Genetic , Risk Factors
6.
Tumour Biol ; 36(3): 1627-42, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25361631

ABSTRACT

Esophageal cancer is one of the most common cancers in North East India. The molecular mechanisms of esophageal cancer susceptibility in North East India have not been fully understood. There is a need for identification of biomarkers to identify people at risk of esophageal cancer. p16 is an essential G1 cell cycle regulatory gene whose loss of function is associated with carcinogenesis. Therefore, we conducted this study to determine the prevalence of p16 gene methylation in patients with esophageal cancer to assess the feasibility of using gene methylation as a biomarker. A total of 100 newly diagnosed esophageal cancer cases along with equal number of age, sex, and ethnicity-matched controls were included in this study. Methylation-specific PCR was used to determine the p16 methylation status. Aberrant promoter methylation of the p16 gene was detected in 81 of 100 (81%) esophageal cancer cases. Hypermethylation of p16 gene was found to be influenced by lifestyle factors. Betel quid and tobacco chewing habit synergistically with p16 methylation elevated the risk for esophageal cancer development (adjusted odds ratio (OR) = 6.88, 95% confidence interval (CI) = 1.64-28.81, p = 0.003 for betel quid chewing and adjusted OR = 7.02, 95% CI = 1.87-26.38, p = 0.001 for tobacco chewing). Further, intake of green leafy vegetables and fruits lowered the risk of esophageal cancer (adjusted OR = 0.16, 95 % CI = 0.04-0.58, p = 0.05 for green leafy vegetables and adjusted OR = 0.15, 95% CI = 0.04-0.64, p = 0.01 for fruits). Thus, p16 hypermethylation may aid as a biomarker in identifying habitués at greater risk for esophageal cancer susceptibility in high incidence region of North East India.


Subject(s)
Biomarkers, Tumor/genetics , DNA Methylation , Esophageal Neoplasms/diagnosis , Esophageal Neoplasms/genetics , Genes, p16 , Adult , Aged , Asian People/genetics , Case-Control Studies , Cyclin-Dependent Kinase Inhibitor p16/genetics , Esophageal Neoplasms/epidemiology , Female , Genetic Predisposition to Disease , Humans , Incidence , India/epidemiology , Male , Middle Aged , Promoter Regions, Genetic
7.
Asian Pac J Cancer Prev ; 15(22): 9955-60, 2014.
Article in English | MEDLINE | ID: mdl-25520135

ABSTRACT

BACKGROUND: Promoter hypermethylation is a common event in human cancer. O6-methylguanine-DNA methyltransferase (MGMT) is a gene involved in DNA repair, which is methylated in a variety of cancers. We aimed to explore the methylation status of MGMT gene among the North Eastern population where esophageal cancer incidence and exposure to carcinogens like nitrosamines is high. MATERIALS AND METHODS: A total of 100 newly diagnosed esophageal cancer cases along with equal number of age, sex and ethnicity matched controls were included in this study. Methylation specific PCR was used to determine the MGMT methylation status in serum samples. RESULTS: Aberrant promoter methylation of the MGMT gene was detected in 70% of esophageal cancer cases. Hypermethylation of MGMT gene was found to be influenced by environmental factors like betel quid and tobacco which contain potent carcinogens like nitrosamines. Tobacco chewing and tobacco smoking habit synergistically with MGMT methylation elevated the risk for esophageal cancer development [adjusted OR=5.02, 95% CI=1.35-18.74; p=0.010 for tobacco chewing and Adjusted OR=3.00, 95% CI=1.22-7.36; p=0.014 for tobacco smoking]. CONCLUSIONS: Results suggest that the DNA hypermethylation of MGMT is an important mechanism for MGMT gene silencing resulting in esophageal cancer development and is influenced by the environmental factors. Thus MGMT hypermethylation can be used as a biomarker for esophageal cancer in high incidence region of North East India.


Subject(s)
Biomarkers, Tumor/genetics , Carcinoma, Squamous Cell/genetics , DNA Methylation , DNA Modification Methylases/genetics , DNA Repair Enzymes/genetics , Esophageal Neoplasms/genetics , Promoter Regions, Genetic/genetics , Tumor Suppressor Proteins/genetics , Adult , Aged , Biomarkers, Tumor/blood , Carcinoma, Squamous Cell/blood , Carcinoma, Squamous Cell/pathology , Case-Control Studies , DNA Modification Methylases/blood , DNA Repair Enzymes/blood , Esophageal Neoplasms/blood , Esophageal Neoplasms/pathology , Female , Follow-Up Studies , Humans , India , Male , Middle Aged , Neoplasm Staging , Prognosis , Risk Factors , Tumor Suppressor Proteins/blood
8.
Asian Pac J Cancer Prev ; 15(24): 10653-8, 2014.
Article in English | MEDLINE | ID: mdl-25605155

ABSTRACT

BACKGROUND: A very high incidence of lung cancer is observed in Mizoram and Manipur, North East India. We conducted a population based case control study to establish associations of p53 codon 72 polymorphisms and interactions with environmental factors for this high incidence. MATERIAL AND METHODS: A total of 272 lung cancer cases and 544 controls matched for age (±5 years), sex and ethnicity were collected and p53 codon 72 polymorphism genotypes were analyzed using a polymerase chain based restriction fragment length polymorphism assay. We used conditional multiple logistic regression analysis to calculate adjusted odds ratios and 95% confidence intervals after adjusting for confounding factors. RESULTS: p53 Pro/Pro genotype was significantly associated with increased risk of lung cancer in the study population (adjusted OR=2.14, CI=1.35-3.38, p=0.001). Interactions of the p53 Pro/Pro genotype with exposure to wood smoke (adjusted OR=3.60, CI=1.85-6.98, p<0.001) and cooking oil fumes (adjusted OR=3.27, CI=1.55-6.87, p=0.002), betel quid chewing (adjusted OR=3.85, CI=1.96- 7.55, p<0.001), tobacco smoking (adjusted OR=4.42, CI=2.27-8.63, p<0.001) and alcohol consumption (adjusted OR=3.31, CI=1.10-10.03, p=0.034) were significant regarding the increased risk of lung cancer in the study population. CONCLUSIONS: The present study provided preliminary evidence that a p53 codon 72 polymorphism may effect lung cancer risk in the study population, interacting synergistically with environmental factors.


Subject(s)
Codon/genetics , Environment , Lung Neoplasms/etiology , Polymorphism, Genetic/genetics , Tumor Suppressor Protein p53/genetics , Alcohol Drinking/adverse effects , Areca/adverse effects , Case-Control Studies , Female , Follow-Up Studies , Genetic Predisposition to Disease , Genotype , Humans , Incidence , India/epidemiology , Lung Neoplasms/epidemiology , Male , Neoplasm Staging , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Prognosis , Risk Factors , Smoking/adverse effects
9.
Asian Pac J Cancer Prev ; 15(24): 10691-5, 2014.
Article in English | MEDLINE | ID: mdl-25605160

ABSTRACT

BACKGROUND: Association of angiotensin converting enzyme (ACE) gene polymorphisms with lung cancer susceptibility remains uncertain and varies with ethnicity. Northeast India represents a geographically, culturally, and ethnically isolated population. The area reports an especially high rate of tobacco usage in a variety of ways of consumption, compared with the rest of the Indian population. MATERIALS AND METHODS: We conducted a population based case control study in two major high risk region for lung cancer from Northeast India. A total of 151 consecutive lung cancer cases diagnosed histopathologically and equal numbers of controls were recruited with record of relevant sociodemographic information. Blood samples were collected and processed to identify ACE gene polymorphism. RESULTS: Significantly higher (40.4 % vs 29.1%, OR=1.97, CI=1.04-3.72; p=0.037) prevalence of the ACE II genotype was observed among lung cancer cases. Smoking was significantly associated with increased risk of lung cancer (OR=1.70, CI=1.02-2.81; p=0.041). An enhanced risk was also observed for interaction of ACE II genotype with tobacco smoking (OR=4.09, CI=1.51-11.05; p=0.005) and chewing (OR=3.68, CI=1.22-11.13; p=0.021). CONCLUSIONS: The present study indicates significant association s of the ACE II genotype with lung cancer in high risk Northeast India.


Subject(s)
Areca/adverse effects , Carcinoma, Non-Small-Cell Lung/etiology , Lung Neoplasms/etiology , Peptidyl-Dipeptidase A/genetics , Polymorphism, Genetic/genetics , Small Cell Lung Carcinoma/etiology , Smoking/adverse effects , Adult , Aged , Aged, 80 and over , Carcinoma, Non-Small-Cell Lung/enzymology , Carcinoma, Non-Small-Cell Lung/epidemiology , Case-Control Studies , Female , Follow-Up Studies , Genetic Predisposition to Disease , Humans , India/epidemiology , Lung Neoplasms/enzymology , Lung Neoplasms/epidemiology , Male , Middle Aged , Neoplasm Staging , Prognosis , Risk Factors , Small Cell Lung Carcinoma/enzymology , Small Cell Lung Carcinoma/epidemiology
SELECTION OF CITATIONS
SEARCH DETAIL
...