Vein Disease

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John Stanley - One of the best experts on this subject based on the ideXlab platform.

  • The DNA β satellite component associated with ageratum yellow Vein Disease encodes an essential pathogenicity protein (βC1)
    Virology, 2004
    Co-Authors: Keith Saunders, Alexandra Norman, Sebastien Gucciardo, John Stanley
    Abstract:

    Ageratum yellow Vein Disease (AYVD) is caused by the geminivirus ageratum yellow Vein virus (AYVV) and an associated DNA beta satellite. We have mapped a DNA beta transcript to a highly conserved open reading frame (betaC1 ORF). The most abundant transcript 5'-terminus is located 8 bases upstream of the betaC1 ORF putative initiation codon while the transcript terminates at multiple sites downstream from the putative termination codon. Disruption of betaC1 protein expression by the introduction of an internal nonsense codon prevented infection of the AYVV-satellite complex in ageratum and altered the phenotype in Nicotiana benthamiana to that produced by AYVV alone although the mutant was maintained in systemically infected tissues. Modification of the putative initiation codon to a nonsense codon produced an intermediate phenotype in N. benthamiana and a mild yellow Vein phenotype in ageratum, suggesting that betaC1 protein expression could be initiated from an alternative site. N. benthamiana plants containing a dimeric DNA beta transgene produced severe developmental abnormalities, Vein-greening, and cell proliferation in the vascular bundles. Expression of betaC1 protein from a potato virus X (PVX) vector also induced abnormal plant growth. Our results demonstrate that the satellite encodes at least one protein that plays a major role in symptom development and is essential for Disease progression in ageratum, the natural host of the AYVD complex.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease
    Journal of General Virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA β satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA β for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease.
    The Journal of general virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA beta satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA beta for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • pathogenicity of a natural recombinant associated with ageratum yellow Vein Disease implications for geminivirus evolution and Disease aetiology
    Virology, 2001
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Abstract Yellow Vein Disease of Ageratum conyzoides is caused by a viral DNA complex consisting of the genomic component (DNA A) of the monopartite begomovirus Ageratum yellow Vein virus (AYVV, family: Geminiviridae ) and a small satellite-like DNA β component. AYVV DNA A is unable to induce symptoms in this host alone but can systemically infect A. conyzoides in which it accumulates to low levels. Here, we demonstrate that the yellow Vein phenotype can also be produced by co-inoculating A. conyzoides with AYVV DNA A and recDNA-Aβ17, a naturally occurring recombinant of approximately the same size as DNA β that contains sequences from both DNA A and DNA β. Symptoms induced by DNA A and recDNA-Aβ17 in A. conyzoides and Nicotiana glutinosa are qualitatively similar to those associated with DNA A and DNA β although milder. Recombination between DNA A and DNA β to produce a chimera resembling recDNA-Aβ17 was observed after whitefly transmission of the Disease in A. conyzoides. Hence, such recombination events are likely to occur frequently, implying that recombinants will normally be associated with this type of Disease complex in the field. Possible implications of these findings for the evolution of begomoviruses and the aetiology of their Diseases are discussed.

  • a unique virus complex causes ageratum yellow Vein Disease
    Proceedings of the National Academy of Sciences of the United States of America, 2000
    Co-Authors: Keith Saunders, Ian D. Bedford, Rob W. Briddon, Peter G. Markham, Sekman Wong, John Stanley
    Abstract:

    Ageratum conyzoides L., a weed species widely distributed throughout southeast Asia, frequently exhibits striking yellow Vein symptoms associated with infection by Ageratum yellow Vein virus (AYVV), a member of the Geminiviridae (genus Begomovirus). Most begomoviruses have bipartite genomes (DNAs A and B), but only a DNA A has been identified for AYVV. We demonstrate that yellow Vein Disease of A. conyzoides results from co-infection by AYVV DNA A (2,741 nt) and a circular DNA that is approximately half its size (1,347 nt) that we designate DNA β. Apart from the sequence TAATATTAC, common to all geminiviruses and containing the initiation site of rolling circle replication, DNA β shows negligible sequence homology either to AYVV DNA A or to DNA B associated with bipartite begomoviruses. DNA β depends on DNA A for replication and is encapsidated by DNA A-encoded coat protein and so has characteristics of a DNA satellite. However, systemic infection of A. conyzoides by DNA A alone is sporadic and asymptomatic, and DNA A accumulation is reduced to 5% or less of its accumulation in the presence of DNA β. Therefore, DNA A and DNA β together form a previously unrecognized Disease-inducing complex. Our data also demonstrate that the nanovirus-like DNA 1 component associated with infected A. conyzoides plays no essential role in the Disease and represents a satellite-like DNA. Furthermore, the satellite DNA previously found associated with tomato leaf curl virus is probably a defective DNA β homologue.

Keith Saunders - One of the best experts on this subject based on the ideXlab platform.

  • The DNA β satellite component associated with ageratum yellow Vein Disease encodes an essential pathogenicity protein (βC1)
    Virology, 2004
    Co-Authors: Keith Saunders, Alexandra Norman, Sebastien Gucciardo, John Stanley
    Abstract:

    Ageratum yellow Vein Disease (AYVD) is caused by the geminivirus ageratum yellow Vein virus (AYVV) and an associated DNA beta satellite. We have mapped a DNA beta transcript to a highly conserved open reading frame (betaC1 ORF). The most abundant transcript 5'-terminus is located 8 bases upstream of the betaC1 ORF putative initiation codon while the transcript terminates at multiple sites downstream from the putative termination codon. Disruption of betaC1 protein expression by the introduction of an internal nonsense codon prevented infection of the AYVV-satellite complex in ageratum and altered the phenotype in Nicotiana benthamiana to that produced by AYVV alone although the mutant was maintained in systemically infected tissues. Modification of the putative initiation codon to a nonsense codon produced an intermediate phenotype in N. benthamiana and a mild yellow Vein phenotype in ageratum, suggesting that betaC1 protein expression could be initiated from an alternative site. N. benthamiana plants containing a dimeric DNA beta transgene produced severe developmental abnormalities, Vein-greening, and cell proliferation in the vascular bundles. Expression of betaC1 protein from a potato virus X (PVX) vector also induced abnormal plant growth. Our results demonstrate that the satellite encodes at least one protein that plays a major role in symptom development and is essential for Disease progression in ageratum, the natural host of the AYVD complex.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease
    Journal of General Virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA β satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA β for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease.
    The Journal of general virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA beta satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA beta for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • pathogenicity of a natural recombinant associated with ageratum yellow Vein Disease implications for geminivirus evolution and Disease aetiology
    Virology, 2001
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Abstract Yellow Vein Disease of Ageratum conyzoides is caused by a viral DNA complex consisting of the genomic component (DNA A) of the monopartite begomovirus Ageratum yellow Vein virus (AYVV, family: Geminiviridae ) and a small satellite-like DNA β component. AYVV DNA A is unable to induce symptoms in this host alone but can systemically infect A. conyzoides in which it accumulates to low levels. Here, we demonstrate that the yellow Vein phenotype can also be produced by co-inoculating A. conyzoides with AYVV DNA A and recDNA-Aβ17, a naturally occurring recombinant of approximately the same size as DNA β that contains sequences from both DNA A and DNA β. Symptoms induced by DNA A and recDNA-Aβ17 in A. conyzoides and Nicotiana glutinosa are qualitatively similar to those associated with DNA A and DNA β although milder. Recombination between DNA A and DNA β to produce a chimera resembling recDNA-Aβ17 was observed after whitefly transmission of the Disease in A. conyzoides. Hence, such recombination events are likely to occur frequently, implying that recombinants will normally be associated with this type of Disease complex in the field. Possible implications of these findings for the evolution of begomoviruses and the aetiology of their Diseases are discussed.

  • a unique virus complex causes ageratum yellow Vein Disease
    Proceedings of the National Academy of Sciences of the United States of America, 2000
    Co-Authors: Keith Saunders, Ian D. Bedford, Rob W. Briddon, Peter G. Markham, Sekman Wong, John Stanley
    Abstract:

    Ageratum conyzoides L., a weed species widely distributed throughout southeast Asia, frequently exhibits striking yellow Vein symptoms associated with infection by Ageratum yellow Vein virus (AYVV), a member of the Geminiviridae (genus Begomovirus). Most begomoviruses have bipartite genomes (DNAs A and B), but only a DNA A has been identified for AYVV. We demonstrate that yellow Vein Disease of A. conyzoides results from co-infection by AYVV DNA A (2,741 nt) and a circular DNA that is approximately half its size (1,347 nt) that we designate DNA β. Apart from the sequence TAATATTAC, common to all geminiviruses and containing the initiation site of rolling circle replication, DNA β shows negligible sequence homology either to AYVV DNA A or to DNA B associated with bipartite begomoviruses. DNA β depends on DNA A for replication and is encapsidated by DNA A-encoded coat protein and so has characteristics of a DNA satellite. However, systemic infection of A. conyzoides by DNA A alone is sporadic and asymptomatic, and DNA A accumulation is reduced to 5% or less of its accumulation in the presence of DNA β. Therefore, DNA A and DNA β together form a previously unrecognized Disease-inducing complex. Our data also demonstrate that the nanovirus-like DNA 1 component associated with infected A. conyzoides plays no essential role in the Disease and represents a satellite-like DNA. Furthermore, the satellite DNA previously found associated with tomato leaf curl virus is probably a defective DNA β homologue.

Jean-michel Lett - One of the best experts on this subject based on the ideXlab platform.

Padma Ramachandran - One of the best experts on this subject based on the ideXlab platform.

  • Development of viroid free nucleus material for rootstock of citrus: an approach for management of yellow corky Vein Disease
    Indian phytopathology, 2008
    Co-Authors: Anirban Roy, Padma Ramachandran
    Abstract:

    Yellow corky Vein Disease of citrus has been shown to be associated with two viroids,citrus exocortis viroid (CEVd) and hop stunt viroid (HSVd). The Disease causes heavy yield reduction: Viroid-free nucleus material for rootstocks (rough lemon and trifoliate orange) have been developed after’ standardization of micropropagation protocol. Present study constitutes the first record of development of viroid-free rootstock plant for citrus through micropropagation. Growth pattern of two species are slightly different; initial shooting is higher in trifoliate orange, but callusing and rooting are much faster in rough lemon. Viroid free micropropagated plants were indexed by NASH test using radiolabelled cDNA probes to two groups of viroid viz. citrus exocortis viroid and hop stunt viroid.

  • occurrence of a hop stunt viroid hsvd variant in yellow corky Vein Disease of citrus in india
    Current Science, 2003
    Co-Authors: Padma Ramachandran
    Abstract:

    A viroid was isolated and purified from total nucleic acid extract of Kagzi lime (Citrus aurantifolia) leaves affected by yellow corky Vein Disease. It was cloned in pGEMT-easy vector system and sequenced. In silico analysis showed that it consisted of 295 nucleotides. In BLAST analysis the sequence aligned with different Hop stunt viroid (HSVd) variants showing nearly 100% sequence identity with six citrus cachexia isolates of HSVd. The viroid was tentatively named as yellow corky Vein variant of Hop stunt viroid (HSVd-ycv). This constitutes the first report of molecular evidence for occurrence of a Hop stunt viroid variant from citrus in India.

  • Diagnostics for Citrus exocortis and Hop stunt viroids associated with yellow corky Vein Disease in citrus
    Indian phytopathology, 2003
    Co-Authors: Padma Ramachandran, Anirban Roy, S. Mathur, J. Agarwal, Y. S. Ahlawat
    Abstract:

    The techniques of return polyacrylamide gel electrophoresis (R-PAGE), reverse transcriptase polymerase chain reaction (RT- PCR) and nucleic acid spot hybridization (NASH) were evaluated with special reference to yellow corky Vein Disease infecting Kagzi lime plants. The technology for quick and reliable detection of two different groups of viroids viz. Citrus exocortis viroid (CEVd) and Hop stunt viroid (HSVd) infecting citrus has been standardized for the first time in the country. The tools developed will help to identify viroid-free rootstock for use in the budwod certification programme.

  • occurrence of a hop stunt viroid hsvd variant in yellow corky Vein Disease of citrus in india
    Current Science, 2003
    Co-Authors: Padma Ramachandran
    Abstract:

    A viroid was isolated and purified from total nucleic acid extract of Kagzi lime (Citrus aurantifolia) leaves affected by yellow corky Vein Disease. It was cloned in pGEMT-easy vector system and sequenced. In silico analysis showed that it consisted of 295 nucleotides. In BLAST analysis the sequence aligned with different Hop stunt viroid (HSVd) variants showing nearly 100% sequence identity with six citrus cachexia isolates of HSVd. The viroid was tentatively named as yellow corky Vein variant of Hop stunt viroid (HSVd-ycv). This constitutes the first report of molecular evidence for occurrence of a Hop stunt viroid variant from citrus in India.

Ian D. Bedford - One of the best experts on this subject based on the ideXlab platform.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease
    Journal of General Virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA β satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA β for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • Adaptation from whitefly to leafhopper transmission of an autonomously replicating nanovirus-like DNA component associated with ageratum yellow Vein Disease.
    The Journal of general virology, 2002
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Ageratum yellow Vein Disease is caused by the whitefly-transmitted monopartite begomovirus Ageratum yellow Vein virus and a DNA beta satellite component. Naturally occurring symptomatic plants also contain an autonomously replicating nanovirus-like DNA 1 component that relies on the begomovirus and DNA beta for systemic spread and whitefly transmission but is not required for maintenance of the Disease. Here, we show that systemic movement of DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf virus. BCTV also mediates the systemic movement of DNA 1 in sugar beet, and the nanovirus-like component is transmitted between plants by the BCTV leafhopper vector Circulifer tenellus. We also describe a second nanovirus-like component, referred to as DNA 2, that has only 47% nucleotide sequence identity with DNA 1. The diversity and adaptation of nanovirus components are discussed.

  • pathogenicity of a natural recombinant associated with ageratum yellow Vein Disease implications for geminivirus evolution and Disease aetiology
    Virology, 2001
    Co-Authors: Keith Saunders, Ian D. Bedford, John Stanley
    Abstract:

    Abstract Yellow Vein Disease of Ageratum conyzoides is caused by a viral DNA complex consisting of the genomic component (DNA A) of the monopartite begomovirus Ageratum yellow Vein virus (AYVV, family: Geminiviridae ) and a small satellite-like DNA β component. AYVV DNA A is unable to induce symptoms in this host alone but can systemically infect A. conyzoides in which it accumulates to low levels. Here, we demonstrate that the yellow Vein phenotype can also be produced by co-inoculating A. conyzoides with AYVV DNA A and recDNA-Aβ17, a naturally occurring recombinant of approximately the same size as DNA β that contains sequences from both DNA A and DNA β. Symptoms induced by DNA A and recDNA-Aβ17 in A. conyzoides and Nicotiana glutinosa are qualitatively similar to those associated with DNA A and DNA β although milder. Recombination between DNA A and DNA β to produce a chimera resembling recDNA-Aβ17 was observed after whitefly transmission of the Disease in A. conyzoides. Hence, such recombination events are likely to occur frequently, implying that recombinants will normally be associated with this type of Disease complex in the field. Possible implications of these findings for the evolution of begomoviruses and the aetiology of their Diseases are discussed.

  • a unique virus complex causes ageratum yellow Vein Disease
    Proceedings of the National Academy of Sciences of the United States of America, 2000
    Co-Authors: Keith Saunders, Ian D. Bedford, Rob W. Briddon, Peter G. Markham, Sekman Wong, John Stanley
    Abstract:

    Ageratum conyzoides L., a weed species widely distributed throughout southeast Asia, frequently exhibits striking yellow Vein symptoms associated with infection by Ageratum yellow Vein virus (AYVV), a member of the Geminiviridae (genus Begomovirus). Most begomoviruses have bipartite genomes (DNAs A and B), but only a DNA A has been identified for AYVV. We demonstrate that yellow Vein Disease of A. conyzoides results from co-infection by AYVV DNA A (2,741 nt) and a circular DNA that is approximately half its size (1,347 nt) that we designate DNA β. Apart from the sequence TAATATTAC, common to all geminiviruses and containing the initiation site of rolling circle replication, DNA β shows negligible sequence homology either to AYVV DNA A or to DNA B associated with bipartite begomoviruses. DNA β depends on DNA A for replication and is encapsidated by DNA A-encoded coat protein and so has characteristics of a DNA satellite. However, systemic infection of A. conyzoides by DNA A alone is sporadic and asymptomatic, and DNA A accumulation is reduced to 5% or less of its accumulation in the presence of DNA β. Therefore, DNA A and DNA β together form a previously unrecognized Disease-inducing complex. Our data also demonstrate that the nanovirus-like DNA 1 component associated with infected A. conyzoides plays no essential role in the Disease and represents a satellite-like DNA. Furthermore, the satellite DNA previously found associated with tomato leaf curl virus is probably a defective DNA β homologue.

  • A unique virus complex causes Ageratum yellow Vein Disease.
    Proceedings of the National Academy of Sciences of the United States of America, 2000
    Co-Authors: Keith Saunders, Ian D. Bedford, Rob W. Briddon, Peter G. Markham, Sekman Wong, John Stanley
    Abstract:

    Ageratum conyzoides L., a weed species widely distributed throughout southeast Asia, frequently exhibits striking yellow Vein symptoms associated with infection by Ageratum yellow Vein virus (AYVV), a member of the Geminiviridae (genus Begomovirus). Most begomoviruses have bipartite genomes (DNAs A and B), but only a DNA A has been identified for AYVV. We demonstrate that yellow Vein Disease of A. conyzoides results from co-infection by AYVV DNA A (2,741 nt) and a circular DNA that is approximately half its size (1,347 nt) that we designate DNA beta. Apart from the sequence TAATATTAC, common to all geminiviruses and containing the initiation site of rolling circle replication, DNA beta shows negligible sequence homology either to AYVV DNA A or to DNA B associated with bipartite begomoviruses. DNA beta depends on DNA A for replication and is encapsidated by DNA A-encoded coat protein and so has characteristics of a DNA satellite. However, systemic infection of A. conyzoides by DNA A alone is sporadic and asymptomatic, and DNA A accumulation is reduced to 5% or less of its accumulation in the presence of DNA beta. Therefore, DNA A and DNA beta together form a previously unrecognized Disease-inducing complex. Our data also demonstrate that the nanovirus-like DNA 1 component associated with infected A. conyzoides plays no essential role in the Disease and represents a satellite-like DNA. Furthermore, the satellite DNA previously found associated with tomato leaf curl virus is probably a defective DNA beta homologue.