Salient Findings on Host Range, Resistance Screening, and Molecular Studies on Sterility Mosaic Disease of Pigeonpea Induced by Pigeonpea sterility mosaic viruses (PPSMV-I and PPSMV-II).

Two distinct emaraviruses, Pigeonpea sterility mosaic virus-I (PPSMV-I) and Pigeonpea sterility mosaic virus-II (PPSMV-II) were found to be associated with sterility mosaic disease (SMD) of pigeonpea [Cajanus cajan (L.) Millsp.]. The host range of both these viruses and their vector are narrow, confined to Nicotiana benthamiana identified through mechanical transmission, and to Phaseolus vulgaris cvs. Top Crop, Kintoki, and Bountiful (F: Fabaceae) through mite transmission. A weed host Chrozophora rottleri (F: Euphorbiaceae) was also infected and tested positive for both the viruses in RT-PCR. Among the wild Cajanus species tested, Cajanus platycarpus accessions 15661, 15668, and 15671, and Cajanus scarabaeoides accessions 15683, 15686, and 15922 were infected by both the viruses and mite vector suggesting possible sources of SMD inoculum. Though accession 15666 of C. platycarpus, 15696 of C. scarabaeoides, and 15639 of Cajanus lanceolatus were infected by both the viruses, no mite infestation was observed on them. Phylogenetic analysis of nucleotide sequences of RNA-1 and RNA-2 of PPSMV-I and PPSMV-II isolates in southern India revealed significant divergence especially PPSMV-II, which is closely related to the Fig mosaic virus (FMV) than PPSMV-I. In multilocation testing of pigeonpea genotypes for their broad-based resistance to SMD for two consecutive years, genotypes ICPL-16086 and ICPL-16087 showed resistance reaction (<10% incidence) in all three locations studied. Overall, the present study gives a clear idea about the host range of PPSMV-I and PPSMV-II, their molecular relationship, and sources of resistance. This information is critical for the development of reliable diagnostic tools and improved disease management strategies.

The association between exposure to aflatoxin, mutation in TP53, infection with hepatitis B virus, and occurrence of liver disease in a selected population in Hyderabad, India.

Aflatoxin B1 is a carcinogen produced by Aspergillus flavus and a few related fungi that are often present in many food substances. It interacts synergistically with Hepatitis B or C virus (HBV, HBC) infection, thereby increasing the risk of hepatocellular carcinoma (HCC). The G to T transversion at the third position of codon 249 (AGG) of the TP53 gene, substituting arginine to serine, is the most common aflatoxin-induced mutation linked to HCC. This study examined mutations in TP53 by PCR-RFLP analysis and by measurement of an aflatoxin-albumin adduct as a biomarker for human exposure of aflatoxin B1 by indirect-competitive ELISA, in samples collected from healthy controls as well as patients with hepatitis in Hyderabad, Andhra Pradesh, India. A total of 238 blood samples were analyzed the presence of the G to T mutation. Eighteen of these samples were from HBV-positive subjects, 112 of these were from subjects who had HBV-induced liver cirrhosis, and 108 samples were taken from subjects without HBV infection or liver cirrhosis (control group). The G to T mutation was detected in 10 samples, 8 of which were from subjects positive to both HBV and aflatoxin-albumin adduct in blood (p=0.07); whilst two were from individuals who were HBV-negative, but positive for the aflatoxin-albumin adduct (p=0.14). The aflatoxin-albumin adduct was detected in 37 of 238 samples, 29 samples were from HBV-positive subjects and eight were from individuals who were positive for both HBV and the TP53 mutation (p=0.07). The concentration of aflatoxin-albumin adduct ranged from 2.5 to 667pg/mg albumin. Despite low incidence of the G to T mutation, its detection in subjects positive to aflatoxin-adducts is indicative of a strong association between the mutation and aflatoxin exposure in India.

Comparison of soil fungal community structure in different peanut rotation sequences using ribosomal intergenic spacer analysis in relation to aflatoxin-producing fungi.

The present study focuses on determining soil fungal community structure in different peanut-cropping sequences by using a high-resolution DNA fingerprinting technique: ribosomal intergenic spacer analysis (RISA). This study was initiated to determine fungal community profiles in four peanut-cropping sequences (continuous peanut, 4 years of continuous bahiagrass followed by peanut, peanut-corn-cotton, and peanut-cotton rotations), with a special focus to evaluate whether the profiles under investigation may have also indicated microbial differences that could affect Aspergillus flavus populations. Results indicated 75% similarities among fungal communities from the same cropping sequences as well as with similar times of sampling. Polymerase chain reaction (PCR)-based detection of A. flavus directly from these soils was carried out using A. flavus-specific primers (FLA1 and FLA2) and also through quantitative estimation on A. flavus and A. parasiticus agar medium. Population levels of A. flavus in soil samples ranged from zero to 1.2 × 10(3) CFU g(-1) of soil (based on culturable methods); however, the fungus was not detected with A. flavus-specific primers. The minimum threshold limit at which these aflatoxin-producing fungi could be detected from the total soil genomic DNA was determined through artificial inoculation of samples with 10-fold increases in concentrations. The results indicated that a minimum population density of 2.6 × 10(6) CFU g(-1) of soil is required for PCR detection in our conditions. These results are useful in further determining the relative population levels of these fungi in peanut soils with other soil fungi. This is a new approach to understanding soil fungal communities and how they might change over time and under different rotation systems.