Defective RNA virus

Defective Virus

Defective interfering viruses are a special class of defective viruses that arise by recombination and rearrangement of viral genomes during replication.

From: Viruses and Human Disease (Second Edition), 2008

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Defective-Interfering Viruses*

L. Roux, in Encyclopedia of Virology (Third Edition), 2008

Assay for DI Particles

DI particles can be detected by physical separation on velocity or density gradients when applicable (see the section titled 'Structure'). The presence of subgenomic nucleic acids in viral stocks or in infected cells (distinct from viral messengers) can also be diagnostic. The ability to decrease the infectivity of a viral stock or to protect infected cells from the lytic infectious virus (see the section titled, 'Biological effects') are used in various biological assays to estimate quantitatively and qualitatively the DI particle composition of a viral stock. These assays, although appropriate to characterize DI particle preparations, are generally not sensitive enough to exclude, when negative, the presence of DI particles in a viral preparation. The test that still remains the most dependable to assess presence or absence of DI particles consists of multiple independent serial undiluted passages. It is based on the observation that a viral stock contaminated with an undetectable amount of DI particles will, on subsequent independent serial passages, promote in each series amplification of the same contaminating DI particles. A DI particle-free stock, on the other hand, will yield in each series different DI particles or different sets of DI particles.

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Subviral Agents

JAMES H. STRAUSS, ELLEN G. STRAUSS, in Viruses and Human Disease (Second Edition), 2008

DEFECTIVE INTERFERING VIRUSES

Defective interfering viruses are a special class of defective viruses that arise by recombination and rearrangement of viral genomes during replication. DIs are defective because they have lost essential functions required for replication. Thus, they require the simultaneous infection of a cell by a helper virus, which is normally the parental wild-type virus from which the DI arose. They interfere with the replication of the parental virus by competition for resources within the cell. These resources include the machinery that replicates the viral nucleic acid, which is in part encoded by the helper virus, and the proteins that encapsidate the viral genome to form virions.

DIs of many RNA viruses have been the best studied. Because DI RNAs must retain all cis-acting sequences required for the replication of the RNA and its encapsidation into progeny particles, sequencing of such DI RNAs can provide clues as to the identity of these sequences. Identification of cis-acting sequences is important for the construction of virus vectors used to express a particular gene of interest, whether in a laboratory experiment or for gene therapy.

The most highly evolved DI RNAs are often not translated and consist of deleted and rearranged versions of the parental genome. In the case of alphaviruses, whose genome is about 12kb (Chapter 3), DI RNAs have been described that are about 2kb in length. However, they have a sequence complexity of only 600 nucleotides, because sequences are repeated one or more times. The sequences of two such DI RNAs of Semliki Forest virus (SFV) are illustrated schematically in Fig. 9.1. From the sequences of these DIs as well as DIs of other alphaviruses, specific functions for the elements found in these DIs have been proposed. Other approaches have then been used to confirm the hypotheses derived from such sequence studies. Thus, the 3′ end of the parental RNA, which is retained in all alphavirus DI RNAs, forms a promoter for the initiation of minus-strand RNA synthesis from the plus-strand genome. The 5′ end of the RNA is also preserved in many DI RNAs, such as those illustrated in Fig. 9.1. Surprisingly, however, it has been replaced by a cellular tRNA in some DI RNAs. The complement of this sequence is present at the 3′ end of the minus strand, where it forms a promoter for initiation of genomic RNA synthesis. The finding that the DI RNAs with the tRNA as the 5′ terminus have a selective advantage over the parental genome during RNA replication suggests that this promoter is a structural element recognized by the viral replicase. It also suggests that the element present in the genomic RNA is suboptimal, perhaps because the genomic RNA must be translated as well as replicated. Finally, repeated sequences from two regions of the genome are present in all alphavirus DI RNAs. It is thought that one sequence (shown as red patterned blocks in Fig. 9.1) is an enhancer element for RNA replication and the second (shown as yellow and green patterned blocks) is a packaging signal. Repetition of these elements may increase the efficiency of replication and packaging of the DI RNA.

FIGURE 9.1. Schematic representation of DIs (defective interfering particles) found after high multiplicity infection of Semliki Forest virus. The central block shows the genome of the nondefective virus, with vertical lines demarking the four nonstructural and five structural polypeptides. The blocks of sequence found in two different DIs are expanded fourfold below and above. Their location in the DI genome is illustrated with blocks of identical shading. Note that some blocks of unique sequence are repeated three times in DIa and one block is repeated four times in DIb.

Vesicular stomatitis virus (VSV) (Chapter 4) DI RNAs vary in size from a third to half the length of the virion RNA. Some DI RNAs are simply deleted RNA genomes, but others have rearrangements at the ends of the RNAs. Representative examples are illustrated in Fig. 9.2A. During replication of the RNA, the sequences at the ends must contain promoter elements for initiation of RNA synthesis. More genomic RNA (minus strand that is packaged in virions) is made than antigenomic RNA (which functions only as a template for genomic RNA synthesis) and therefore the promoter at the 3′ end of the antigenomic RNA is stronger than the promoter at the 3′ end of the genomic RNA. Thus, it is not surprising that some DI RNAs have the stronger promoter at the 3′ ends of both (+) and (−)RNA (as in Class II DIs), ensuring more rapid replication of the DI RNAs. The DI RNAs may have the luxury of doing this because they are not translated nor do they serve as templates for the synthesis of mRNAs.

FIGURE 9.2. Types of DIs generated from a rhabdovirus and a coronavirus. Upper panel: diagrammatic representation of the VSV genome and members of the four classes of DI particles. The leader and trailer are shown as patterned blocks. The genome is shown 3′ to 5′ for the minus strand (ochre underline). The parts of the DIs corresponding to the complement of the minus strand are underlined in green. A red triangle marks the internal deletion in the L gene, which is found in Class III and Class IV DIs. Lower panel: structures of naturally occurring DI RNAs of MHV (a murine coronavirus). DIssA, DI-a, etc. were isolated from MHV-infected cells. The bottom line shows a synthetic DI replicon called B36. Sequences in the DIs are color coded by their region of origin in the parental virus genome.

The well-studied alphavirus DI RNAs and the VSV DI RNAs are not translated. For many DI RNAs, however, translation is required for efficient DI RNA replication. The best studied examples of this are DIs of poliovirus and of coronaviruses (these viruses are described in Chapter 3). DI RNAs of poliovirus are uncommon and contain deletions in the structural protein region. It has been suggested that in this case it is the translation product that is required for efficient replication of the RNA (the replicase translated from the RNA may preferentially use as a template for replication the RNA from which it was translated). In contrast, for at least one well-studied DI of a coronavirus, translation of the RNA is required for efficient replication, but the translation product is not important. In this case, translation may stabilize the DI RNA, since there appears to be a cellular pathway to rid the cell of mRNAs that are not translatable. If so, it is uncertain how DI RNAs that are not translated avoid this pathway. Some representative naturally occurring DIs of mouse hepatitis virus, a murine coronavirus, are illustrated in Fig. 9.2B.

Because DI RNAs are replicated by the helper virus machinery and encapsidated by the capsid proteins of the helper virus, they interfere with the parental virus by diverting these resources to the production of DI particles rather than to the production of infectious virus particles. It was the first noted by von Magnus in the early 1950s that influenza virus, passed at high multiplicity for many passages, produced yields that cycled between high and low. This effect is illustrated schematically in Fig. 9.3A. We now know that this is due to the presence of DI particles. In early passages virus yields are high. When DIs arise, they depress the yield of virus. Because high multiplicities of infection are required to maintain DI replication, so that cells are infected with both the helper and the DI, low yields of virus lead to a reduction in DI replication in the next passage or two. Reduced DI replication leads to higher yields of virus. Thus, the yield of infectious virus continues to fluctuate.

FIGURE 9.3. Stylized illustration of the influence of defective interfering particles on viral evolution. (A) Short-term generation of DI particles during undiluted passage and the cyclical fluctuations in infectious virus yield and concentration of DIs. This effect was first described by von Magnus in 1946 during repeated passage of influenza virus at high multiplicity. (B) Role of DI particles in driving long-term evolution of viruses. The net result of hundreds of passages is that variant 2 and its DIs completely replace the original wild type or standard virus 1.

Adapted from Encyclopedia of Viruses, Figure 2 on p. 373.

In a laboratory setting, at least, DIs can drive the evolution of the wild-type virus. This is shown schematically in Fig. 9.3B. When virus is passed at high multiplicity for very many generations, mutants often arise that have altered promoters that are recognized by mutant replication proteins. Such mutants are resistant to the DIs that are in the population at the time, because the mutant replication proteins do not recognize the promoters in the DIs. The mutant virus rapidly takes over the population of virus because of its selective advantage. However, new DIs then arise that will interfere with the mutant virus, and the cycle repeats.

It is unclear whether DI particles serve a biological role in nature or whether they are artifacts of abortive recombination that appear in the laboratory because of the high multiplicities of infection that are often used. It has been argued that DIs may arise late in the infection of an animal by a virulent virus and lead to attenuation of symptoms by reducing the yield of infectious virulent virus. As described in earlier chapters, such attenuation could be important for the persistence of a virus in nature. Hepatitis delta virus, described later, is a satellite that replicates only in a cell infected by HBV. Thus, it is clear that it is possible to achieve the multiplicities required to maintain a defective virus in at least some circumstances. Reconstruction experiments in mice have shown that it is possible to attenuate the virulence of lymphocytic choriomeningitis virus by injecting DIs along with the virus. However, it is not clear that DIs will arise in an acute infection in time to ameliorate symptoms. Thus, it has not been possible to provide firm evidence that DIs actually modulate the virulence of their parents in nature, and the question remains open.

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Methods for Analysis of Golgi Complex Function

Lucy Pigati, ... Heike Fölsch, in Methods in Cell Biology, 2013

Summary

The use of replication defective viruses is a viable alternative to transient transfection methods. Among its many advantages is the flexibility of the system, its high infection rates, and low cost. Especially when working with hard-to-transfect cell lines, defective viruses allow for nearly 100% infectivity, which is crucial for biochemical experiments. Viruses are easily titrated giving the researcher great control over infection efficiencies and expression levels. The protocol outlined here provides a detailed guide through a variety of different infection conditions, which should allow the interested reader to readily adopt these methods to her or his laboratory.

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Infections in Systemic Autoimmune Diseases: Risk Factors and Management

Andrew Ustianowski, Karen Devine, in Handbook of Systemic Autoimmune Diseases, 2020

3 HDV coinfection

HDV is a defective virus (virusoid) that can replicate only in persons with HBV infection. HDV can be transmitted either via simultaneous infection with HBV (coinfection) or subsequent infection superimposed on CHB (superinfection). It is estimated that globally about 5%–10% of patients with CHB are coinfected with HDV with higher prevalence in injection drug using populations. High-prevalence areas include the Mediterranean basin, Middle East, Indian subcontinent, Japan, Taiwan, Greenland, the Horn of Africa, West Africa, the Amazon Basin, and certain areas of the Pacific.

It is well recognized that acute infection can be more severe (with increased rates of fulminant liver failure) [44] and that progression to liver fibrosis and cirrhosis is more rapid, in the setting of HDV coinfection than with HBV alone [45]. There are no known associations or correlates, above those known for HBV, with autoimmune diseases or treatments.

Hepatitis D is diagnosed by serology in the first instance, but then active infection is confirmed by detection of DNA in serum. The assessment of liver disease and other factors are the same thereafter as for HBV monoinfection.

The only recognized treatment for hepatitis D coinfection is currently interferon-alpha, though some of the newer agents being developed for HBV appear to have very good efficacy for HDV also.

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Hepatitis Viruses

Jennifer Louten, in Essential Human Virology, 2016

12.2.4 Hepatitis D Virus

HDV is a defective virus, meaning that it is unable to replicate on its own. Also known as "hepatitis delta virus," HDV requires infection of the same cell with HBV, which contributes the HBsAg that HDV uses for virion assembly. This can occur through coinfection, meaning that HDV and HBV are contracted at the same time, or by superinfection, in which a person with chronic HBV infection becomes newly infected with HDV as well. HDV is transmitted through contact with infectious blood or contaminated injection devices. The incubation period is 90 days when coinfection occurs, and 14–56 days after superinfection. HDV infection can be acute or chronic; if HBV is cleared from the host, which happens in the majority of cases, then HDV is unable to replicate.

The geographical prevalence of HDV is identical to that of HBV, since it requires HBV to create infectious virions. Worldwide, 15–20 million people are estimated to be infected with HDV, less than 10% of those with HBV. However, several studies have indicated that chronic coinfection with HBV and HDV leads to more severe liver disease than chronic HBV infection alone. The nucleoside analog reverse transcriptase inhibitors used to prevent HBV infection do not prevent HDV replication, although interferon-α treatment has been shown to have some efficacy in reducing HDV viral loads. Vaccination against HBV protects against HDV infection.

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Volume 2

Jacob A Hoffman, ... Rishi Arora, in Emerging Technologies for Heart Diseases, 2020

34.2.1 Viral gene vectors

Viral vectors are live, replication deficient viruses which have been genetically modified to allow the insertion of transgenes. Compared to non-viral plasmid insertion which must be directly injected into the tissue, viral vectors have the theoretical advantage of minimally invasive delivery via the blood stream.

Retroviral vectors were the first vectors used for gene therapy. They have been used in numerous FDA approved clinical studies in both phase I and II including glioma and severe combined immunodeficiency. These studies have raised safety concerns about the risks of retroviral therapy, but advances in retroviral vector technology hope to mitigate these risks [5]. These vectors can integrate and express transduced genes in the host DNA in a more stable manner [6]. The use of retroviral vectors in the myocardium, however, is limited. Retroviral vector technology requires active cellular reproduction to allow integration and expression of its transgene. This is problematic in terminally differentiated tissue like the myocardium. To overcome these obstacles, an area of active investigation is using lentiviral vectors in which the human immunodeficiency virus (HIV) machinery is used to transfer transgenes to post mitotic cells such as cardiac myocytes [7]. Lentiviral vectors are able to transfect intact nuclear membranes allowing transgene expression in terminally differentiated cells. A major advantage of lentiviral technology is what appear to be long term gene expression and multiple safeguards to protect against wild type reversion compared to other retroviral vectors [8]. In comparison to non-retroviral vectors, such as adenoviral vectors, lentivirus appears to have similar transfection efficiency when injected into the myocardium [7]. Additionally, lentiviral vectors have large packaging capacities, with transgenes cassettes of up to 10 kb having sufficiently high expression levels in vitro [9]. However, the safety and efficacy of lentiviral vectors have yet to be demonstrated in any clinical trial of cardiac gene therapy to date.

The adenovirus (AD) and adeno-associated viruses (AAV) are currently the most commonly used viral vectors for cardiac gene therapy. The wild type adenovirus is a double stranded DNA virus that is one cause of the common cold. AD vectors have the 35 kb viral genome removed to allow delivery of moderate sized genes. This makes AD vectors simple to produce and distribute and easy to transduce with relative efficiency [10]. However, the AD vector has limited gene expression (2–4 weeks) and can cause intense immunological host responses that may lead to short term morbidity and organ damage [11]. This has led to disappointing short-term results for the AD vector in clinical trials [12,13].

These limitations have led to the development of the adeno-associated virus (AAV) vector which share no relationship to the adenovirus and are a distinct class of virus. These vectors have multiple advantageous features including the capacity for long term gene expression. In some pre-clinical trials in skeletal muscle, AAV expression has persisted for prolonged periods of time, some for several years [14,15]. There are a number of main AAV capsid serotypes [1–9], each consisting of different capsid proteins. These serotypes possess varying tissue tropism, some of which are very specific. In particular, AAV serotypes 6 and 9 have been shown to have particularly high cardiac tropism [16]. Another aspect of AAV biology that makes it a strong candidate for cardiac gene transfer is the modularity of the viral capsid; by varying the makeup of viral capsid proteins, it is possible to generate new, chimeric AAVs with improved transfection efficiency and tropism [17,18]. An example of this is AAV2i8, a chimeric AAV created by swapping a homologous sequence from AAV 8 into the AAV2 vector, resulting in enhanced muscle tropism (cardiac and smooth) in addition to a decrease in hepatic transduction [17]. Further tissue specificity can be achieved with the use of atrial specific promoters to drive transgene expression only in the desired tissue [19].

The primary disadvantage of AAV vectors is a limited gene insert size which makes it difficult to transduce larger genes and complex ion channels. Another disadvantage is delayed expression of the gene likely due to the need to convert the single stranded viral genome to the double stranded host genome [20]. Furthermore, transduction efficiency is more limited in larger mammal studies compared to the initial studies in rodents [21].

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Axon Growth and Regeneration: Part 2

Alan R. Harvey, ... Jennifer Rodger, in International Review of Neurobiology, 2012

10 Viral Vector Delivery of Neurotrophic Factors

Viral vectors are modified, replication-deficient viruses in which the viral genome is replaced by a therapeutic gene, providing an in vivo method for long-term, targeted supply of a trophic factor to injured neurons, including RGCs (Hellström & Harvey, 2011). Initial studies used a modified adenovirus (AdV) to deliver neurotrophic factors for protective RGC therapy. AdV vectors have been trialed that encode CNTF (van Adel, Arnold, Phipps, Doering, & Ball, 2005; Weise et al., 2000), BDNF (Di Polo, Aigner, Dunn, Bray, & Aguayo, 1998; Isenmann, Klöcker, Gravel, & Bähr, 1998), or GDNF (Schmeer et al., 2002; Straten et al., 2002) under the control of the cytomegalovirus promoter. These vectors do not appear to transduce RGCs very efficiently, perhaps due to glial barriers, but Müller glia are consistently transduced. Transgene expression and secretion of associated proteins from retinal cells increased RGC survival in the short-term in all cases, but an effect on axonal regeneration into PN grafts was not seen (Weise et al., 2000). RGC transduction with AdV can be achieved by applying the vector to the ON stump (Kugler, Klöcker, Kermer, Isenmann, & Bähr, 1999).

In the past decade, numerous studies have shown that a vector based on the adeno-associated virus serotype 2 (AAV2) is particularly effective in transducing adult RGCs after intravitreal injection (e.g., Hellström et al., 2009). Neurotrophic factor genes that have been used with AAV vectors include BDNF (Hellström & Harvey, 2011; Leaver, Cui, Plant, et al., 2006; Pease et al., 2009; Schuettauf et al., 2004), bFGF (Sapieha, Peltier, Rendahl, Manning, & Di Polo, 2003; Schuettauf et al., 2004), GDNF (Wu et al., 2004), and CNTF (Leaver, Cui, Bernard & Harvey, 2006; Leaver, Cui, et al., 2006; Pease et al., 2009). In all cases, there was increased RGC survival and with AAV–bFGF some limited regrowth of RGC axons across an ON nerve crush was reported (Sapieha et al., 2003). AAV-mediated transduction of TrkB also increased the survival of injured RGCs, an effect enhanced by coadministration of rBDNF (Cheng, Sapieha, Kittlerova, Hauswirth, & Di Polo, 2002). Using AAV2–BDNF, we obtained a significant increase in RGC viability after ON crush, however there was no discernible impact on axonal regeneration, with few axons crossing the injury site (Leaver, Cui, et al., 2006). Thus, this factor, and most likely NT-4/5, whether delivered by direct injection of recombinant protein or by vector-mediated methods, is a potent RGC survival factor after ON injury but appears to induce local sprouting proximal to the injury site (e.g., Cui et al., 2003; Klöcker, Jung, Stuermer, & Bähr, 2001; Sawai et al., 1996) and is not effective in promoting long-distance axonal regeneration. In contrast, injection of AAV2 encoding a secretable form of CNTF increased RGC viability about fourfold, and in both rats and mice, RGC axons regenerated across the crush site for several millimeters within distal ON, in mice some reaching as far as the optic chiasm (Leaver, Cui, Bernard & Harvey, 2006; Leaver, Cui, et al., 2006).

The contrasting effects of BDNF and CNTF delivery on RGC axonal regeneration has recently been confirmed in studies in which we injected AAV2 vectors prior to grafting an autologous PN onto the cut ON in adult rats (Hellström & Harvey, 2011; Leaver, Cui, Bernard & Harvey, 2006). All of our AAV2 vectors are bi-cistronic, that is, the therapeutic transgene is linked via an internal ribosome reentry site to the green fluorescent protein (GFP) reporter gene. The GFP gene is downstream of the growth-promoting gene and is expressed only when the therapeutic gene is expressed, allowing direct visualization of the extent of RGC transduction in injected eyes. The PN grafts are generally about 1.5 cm long and are blind ended, sutured to fascia on the cranium. Prior to sacrifice, all PN grafts are injected at their distal end with fluorogold (FG) in order to retrogradely label all RGCs that have regenerated an axon through the graft. Immunostaining the retinal whole mounts with an antibody to β-III tubulin (Cui et al., 2003) allows quantification of total RGC survival, transduction efficiency and localization, and the proportion of surviving RGCs that regenerated an axon (FG positive). In most cases (but see later), to allow time for activation of transgene expression, the chosen AAV2 vector is injected into the vitreous 10–14 days before ON injury and surgery.

In PN-grafted rats, AAV–CNTF but not control AAV–GFP promoted excellent RGC survival, with on average, about 25,000 RGCs viable 7 weeks after ON–PN surgery (Leaver, Cui, Bernard & Harvey, 2006). Remarkably, close to 50% of these surviving RGCs were retrogradely labeled with FG and thus had successfully regrown an axon at least 1 cm within a PN graft. Even though the PN grafts are blind ended and not connected to central targets, these numbers remain remarkably similar 15 months after surgery (Hellström & Harvey, 2011). In contrast, a single ocular injection of AAV2–BDNF (4 μl; 1 × 1012 gc/ml) in adult rats also increased the viability of axotomized RGCs (on average, about 16,400 RGCs, 4 weeks postinjury), but the proportion of these surviving RGCs that regenerated an axon into a PN graft was only about 8% (Hellström & Harvey, 2011). Note here that after injection of either the CNTF or the BDNF AAV2 vector, there was an increase not only in GFP-labeled RGC numbers but also in total viable RGCs, consistent with the proposal that virally transduced cells release trophic factors that can provide paracrine support for neighboring nonmodified cells. This is an issue that will be revisited later when discussing the effects of neurotrophins on RGC dendritic architecture.

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Hepatology

ProfessorCrispian Scully CBE, MD, PhD, MDS, MRCS, FDSRCS, FDSRCPS, FFDRCSI, FDSRCSE, FRCPath, FMedSci, FHEA, FUCL, FBS, DSc, DChD, DMed (HC), Dr (hc), in Scully's Medical Problems in Dentistry (Seventh Edition), 2014

General aspects

HDV (or delta agent) is an incomplete virus carried within the HBV particle and will only replicate in the presence of HBsAg. Therefore, there is no HDV without HBV infection. HDV spreads parenterally, mainly by shared hypodermic needles. Risk groups are as for HBV (see Box 9.3). HDV has been transmitted to patients and staff in health-care facilities.

HDV is endemic, especially in the Mediterranean littoral and among intravenous drug abusers, and is found worldwide. It is not endemic in northern Europe or the USA, but some haemophiliacs and others have acquired the infection and the prevalence is rising.

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RHABDOVIRUSES (RHABDOVIRIDAE): Plant Rhabdoviruses

Andrew O. Jackson, ... Diane M. Lawrence, in Encyclopedia of Virology (Second Edition), 1999

Defective Interfering RNAs

Animal rhabdoviruses passaged at high multiplicities of infection commonly accumulate defective-interfering (DI) particles. These DIs are dependent on the wild-type virus for their replication, and their presence results in a substantial decrease in the titer of the helper virus. The RNA molecules associated with DIs are typically internally deleted forms of the wild-type viral genomic RNA that retain the complementary 3′ and 5′ terminal sequences.

Formation of plant rhabdovirus DIs has been observed with PYDV and SYNV. PYDV passaged at high multiplicities of infection developed DIs after 30 successive mechanical transfers. The slowly sedimenting particles appeared not to be infectious in local lesion assays, but their protein composition was similar to those of the parental virus. In addition, the presence of the DIs decreased the amount of PYDV that could be isolated from infected plants. In the case of SYNV DIs, calyx tissues of Nicotiana edwardsonii examined 5 months after inoculation were shown to contain a high proportion of particles approximately three quarters as long as those of wild-type SYNV. Purified short particles were not infectious when inoculated alone, but when coinoculated with wild-type virions, short particles predominated upon reisolation. RNA isolated from these short particles was approximately 25% shorter than RNA from complete virions. The DI RNAs were able to hybridize to SYNV cDNA probes, but additional information about their structure has not been reported. From these results, the appearance of plant rhabdovirus DIs appears to be an uncommon occurrence that contrasts with the high frequency of animal rhabdovirus DIs.

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