To determine if ketoacidosis contributes to reduced apolipoprotein A1 (apoA1) expression in insulindeficient diabetic rats, we examined the regulation of apoA1 gene expression in response to changes in ambient pH or ketone body concentrations. Hepatic apoAI mRNA levels were reduced 42% in diabetic rats relative to nondiabetic controls (means ..; 321·8 43·7 vs 438·7 58·8 arbitrary units; P<0·03). Neither endogenous apoA1 mRNA nor transcriptional activity of the rat apoA1 gene promoter (from 474 to 7) were altered by sodium butyrate or isobutyramide (0·3 mM to 10 mM) in Hep G2 or Caco-2 cells. Rat hepatic and intestinal apoA1 mRNA levels, and plasma apoA1 concentration, were not altered 24 h after isobutyramide administration (500 mg/kg by gavage). When the effect of altering ambient pH within a wide range commonly encountered in vivo was studied, acidosis (pH 6·7), relative to alkalosis (pH 7·9), decreased apoAI mRNA levels relative to glyceraldehyde-3-phosphate dehydrogenase mRNA by 47% in Hep G2 cells (P<0·025) and by 24% in Caco-2 cells (P<0·017). Acidosis did not alter cytomegalo virus (CMV)--galactosidase activity, or the activity of the simian virus (SV40) early-region promoter, in either cell line transfected with the respective constructs. The lowering of ambient pH was associated with a graded reduction in apoAI promoter activity. At pH 6·7, apoAI promoter activity was reduced by 75% compared with promoter activity at pH 7·9. These observations indicate that acidosis, but not ketosis, contributes to the reduction in apoA1 expression during diabetic ketoacidosis by down-regulating apoAI promoter activity.

Large cardamom (Amomum subulatum Roxb.) is affected by the serious disease ‘foorkey’, which is of unknown etiology (1). Excessive sprouting and formation of bushy dwarf clumps at the base of mother plants that gradually die, characterize the disease. In surveys in the Sikkim-Darjeeling Hill area during 2002 and 2003, as much as 27% of plants were found to be affected. Electron microscopy of negatively stained, partially purified preparations from field-infected large cardamom plants showed the presence of isometric particles measuring 17 to 20 nm. The causal agent was successfully transmitted by the aphid Micromyzus kalimpongensis Basu, in a persistent manner. Ten randomly selected field samples gave A405 0.1 to 0.23 compared with 0.57 with positive control with enzyme-linked immunosorbent assay using antiserum to an Indian isolate of Banana bunchy top virus (BBTV). A fragment of approximately 850 bp was amplified from the diseased plants using polymerase chain reaction (PCR) with primers 5′-ATGGCGCGATATGTGGTATGC-3′ and 5′-TCAGCAAGAAAACCAACTTTATTC-3′, designed to amplify the putative Rep gene based on the sequences of DNA1 of BBTV. The PCR product was cloned and sequenced (GenBank Accession No. AY 485960) and showed 80 to 82% identity with the corresponding region of DNA1 of BBTV and 47.6 to 48.5% with other recognized nanoviruses. These findings indicate that a nanovirus is associated with ‘foorkey’ disease of large cardamom, which is tentatively named as Cardamom bushy dwarf virus. Reference: (1) P. M. Varma and S. P. Capoor. Indian J. Agric. Sci. 34:56, 1964.

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Large cardamom (Amomum subulatum), an important spice crop grown in eastern sub-Himalayan mountains of India, is affected by a viral disease commonly known as 'chirke', which is characterised by light and dark green streaks on the leaf lamina. Although chirke has been known to affect large cardamom for over 50 years, its distribution in large cardamom growing regions and aetiology have remained unaddressed. In this study for the first time, distribution of chirke in the major large cardamom growing regions in India has been determined. North Sikkim and eastern region of Darjeeling hills were endemic region with average disease incidence of 19.2-35%, whereas, Mirik region of Darjeeling hills were free from the disease. Suckers, the commonly used planting material, were the major source for spread of the disease. The virus was sap transmissible to the popular large cardamom cultivars Golsey, Ramsey, Swaney and Varlangey and vectored by Rhopalosiphum maidis and Myzus persicae in a non-persistent manner. Flexuous virus particles measuring 625-650 × 12.5 nm were observed consistently associated with the diseased samples. Polyclonal antiserum to the purified virus showed serological affinity with a macluravirus, cardamom mosaic virus (CdMV) associated with a similar disease known as katte disease of small cardamom (Elettaria cardamomum) occurring in southern India. The 3 terminal genome sequence (1776 nucleotides) of the virus was determined, which revealed a close sequence identity and phylogenetic relationships with the members of the genus Macluravirus. The deduced amino acid sequence of putative coat protein (CP) gene showed maximum similarity of 65.7% with the CdMV. Phylogenetic analysis based on CP and 3 UTR showed that the virus was closer to Alpinia mosaic virus, CdMV and Chinese yam necrotic mosaic virus subclade. The results suggest that the virus associated with the chirke disease of large cardamom is a new species under the genus Macluravirus in the family Potyviridae for which the name large cardamom chirke virus (LCCV) is proposed.