Pumpkin yellow vein mosaic disease is caused by two distinct begomoviruses: complete viral sequences and comparative transmission by an indigenous Bemisia tabaci and the introduced B-biotype

Pumpkin yellow vein mosaic disease (PYVMD) causes significant damage to pumpkin production throughout India. A begomovirus causing PYVMD in South India was characterized recently but the nature of virus causing the disease in North India was not known. Samples of PYVMD were obtained from North India and two putative begomoviruses were PCR-amplified and sequenced. Comparison of complete DNA-A sequences indicated that PYVMD in North and South India were caused by two distinct begomoviruses and shared only approximately 88% DNA-A nucleotide identity. The South Indian isolate was most closely related to Squash leaf curl China virus between 91 and 96% identities, and the two North Indian isolates to Tomato leaf curl New Delhi virus between 94 and 96% identities. The South Indian isolate was previously shown to be transmitted by the indigenous biotype of Bemisia tabaci, however, the situation has since changed with the introduction of the B-biotype to South India in 1999. Comparative transmission experiments between the indigenous biotype v/s the introduced B-biotype for the time required for virus acquisition (30 min v/s 15 min), inoculation (15 min v/s 10 min) and incubation (30 min v/s 4 h) have indicated that the B-biotype transmits the virus quickly and more efficiently than the indigenous biotype. An epidemic of PYVMD was recorded for the first time in South India in 2004 with disease incidences of up to 100% and significant yield losses. This may be due to a combination of several factors including the large numbers of B-biotype populations, the ability of the B-biotype to transmit the virus efficiently and the cultivation of susceptible varieties. These possibilities and the threat to pumpkin cultivation associated with the spread of the B-biotype in India are discussed

Inflammatory response of disc cells against Propionibacterium acnes depends on the presence of lumbar Modic changes

PurposeIntervertebral disc with Propionibacterium acnes (P. acnes) is suggested to be an etiology of Modic type I changes in the adjacent bone marrow. However it is unknown if disc cells can respond to P. acnes and if bone marrow cells respond to bacterial and disc metabolites draining from infected discs.MethodsHuman disc cells (n = 10) were co-cultured with 10- and 100-fold excess of P. acnes over disc cells for 3 h and 24 h. Lipopolysaccharide was used as positive control. Expression of IL1, IL6, IL8, and CCL2 by disc cells was quantified by quantitative PCR. Lipase activity was measured in culture supernatants (n = 6). Human vertebral bone marrow mononuclear cells (BMNCs) (n = 2) were cultured in conditioned media from disc cell/P. acnes co-cultures and expression of IL1, IL6, IL8, and CCL2 was measured after 24 h.ResultsAll disc cells responded to lipopolysaccharide but only 6/10 responded to P. acnes with increased cytokine expression. Cytokine increase was time- but not P. acnes concentration-dependent. Disc cell responsiveness was associated with the presence of lumbar Modic changes in the donor. Lipase activity was increased independent of disc cell responsiveness. BMNCs responded with inflammatory activity only when cultured in supernatants from responsive disc cell lines.ConclusionDisc cell responsiveness to P. acnes associates with the presence of lumbar Modic changes. Furthermore, bone marrow cells had an inflammatory response to the cocktail of disc cytokines and P. acnes metabolites. These data indicate that low virulent P. acnes infection of the disc is a potential exacerbating factor to Modic changes