Citrus psorosis virus (CPsV): Difference between revisions

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The virus is untraceable in isolated plant sap. However, young citrus leaves exhibiting severe symptoms homogenised in 0.05 M phosphate buffer, pH 7 or Tris buffer, pH 8, both of which contain 0.5% 2-mercaptoethanol, traces of infection can be retained for at least 2 hours at 25°C or 24-48 h at 4°C [3].
The virus is untraceable in isolated plant sap. However, young citrus leaves exhibiting severe symptoms homogenised in 0.05 M phosphate buffer, pH 7 or Tris buffer, pH 8, both of which contain 0.5% 2-mercaptoethanol, traces of infection can be retained for at least 2 hours at 25°C or 24-48 h at 4°C [3].


CPsV ‘A’ is denoted by bark-scaling, thinning of branches, older leaves with chlorotic blotches, or pustules. Ringspots of fruits. CPsV ‘B’ causes extensive bark-scaling and branch deterioration, with chlorotic blotches in leaves appearing earlier than normal. Fruits are inedible; infection is a decline in health leading to eventual death.  At a molecular level, infected plant cells exhibit large quantities of abnormal cholorplasts, mitochondria and misshaping and enlargement of nuclei/nucleolous[5]. Mitochondria in particular are bent and elongated[5]. Displacement of bodies in nucleous as well as inclusion bodies which possibly contain virus particles have been reported[5].  
CPsV ‘A’ is denoted by bark-scaling, thinning of branches, older leaves with chlorotic blotches, or pustules. Ringspots of fruits. CPsV ‘B’ causes extensive bark-scaling and branch deterioration, with chlorotic blotches in leaves appearing earlier than normal[4]. Fruits are inedible; infection is a decline in health leading to eventual death.  At a molecular level, infected plant cells exhibit large quantities of abnormal cholorplasts, mitochondria and misshaping and enlargement of nuclei/nucleolous[5]. Mitochondria in particular are bent and elongated[5]. Displacement of bodies in nucleous as well as inclusion bodies which possibly contain virus particles have been reported[5].  


Restoration of trees in CPsV infected areas is a rigorous process involving replanting and a bud certification program [4].
Restoration of trees in CPsV infected areas is a rigorous process involving replanting and a bud certification program [5].


==References==
==References==

Revision as of 15:26, 24 September 2012

A Viral Biorealm page on the family Citrus psorosis virus (CPsV)

Citrus sinensis, a common host of Citrus psorosis virus, exhibiting symptoms of bark and leaf deterioration. [1]

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Baltimore Classification


Group V: (-) sense single-stranded RNA viruses

Higher order categories


Family: Ophioviridae
Genus: Ophiovirus

Description and Significance


Citrus psorosis virus (CpsV) is considered to be the most infectious and problematic virus pathogen of citrus plants worldwide, mostly in citrus producing countries such as North, South American and the Mediterranean. CpsV is the oldest reported citrus virus, first reported symptoms in 1896 and known viral etiology in 1933. There are a variety of different strains and symptoms which vary from mild, type 'A,' to severe, type 'B.' Symptoms can be exhibited in leaves, fruit, bark, trunk and branches. Leaf infection displays chlorotic flecks, or a decrease in chlorophyll/healthy coloring, mottling and spots; fruit may show ring-like chlorotic areas[1]. Chlorosis decreases plant's efficiency to perform photosynthesis, or ability to produce carbohydrates necessary for energy, organism support and growth[1]. The most common symptom of psorosis is deterioration of bark, such as flaking or scaling on trunk and limbs. Early stages of this deterioration are marked by blisters or bubbles which grow and later result in patches.

Citrus plants which have been reported to exhibit this virus are grapefuit, mandarin, orange and tangerine, lemon, pomelo and lime. It is economically important in the production and distribution of citrus fruit.

Genome Structure


Three species of ssRNA have been detected in the Citrus psorosis virus (CpsV), each of which is contained in a capsid made up of the same proteins. The three genomic negative ssRNAs are 8184, 1644 and 1454 nucleotides in length. ORF 1 of RNA1, is located at 5’ end of the negative strand, and translates for a 280 kDa protein characteristic to that of RNA-dependent RNA polymerase. Separated from ORF1 by 109 nucleotides is ORF2 of RNA1, which encodes a 24 kDa protein which has no homologues in the database and performs unknown functions. Conversely, RNA2 has a single ORF encoding a novel protein of 54kDa which resembles a nuclear localization signal. In RNA2, specifically the 3’ terminal untranslated region, there is a known polydenylation signal. RNA3 has one ORF which encodes for its coat protein. The three RNAs have similar 3’ terminal regions, however, extremely differing 5’terminal regions. The particles are described as circular with a suggested “panhandle structure” which is formed by the base pairs of the terminal regions in each RNA strand; however, results vary throughout many studies of secondary structure predictions.

Virion Structure of CPsV virus


CPsV particles are characterized as spiral filaments belonging to the group of spiroviruses (SV). They are flexible and filamentous with kinks along the surface. The diameter measures about 3nm which occur in various configurations and have two known and early differentiated contour lengths of 690-760nm and the larger which is about 4 times as long. The filaments show a pattern of repeating units every 3nm along the particle length, which could possibly be coat protein molecules which form a doughnut like structure which RNA stands pass through. When in vitro, these structures which hold the RNA strands form complex linear as well as branched structures, about 9nm and half the length of the circular contour.

Reproductive Cycle of a ______virus in a Host Cell


Viral Ecology & Pathology


No confirmed transmission has been confirmed in CPsV, possible “natural” causes are reported to be the contributing factor[2]. Citrus plant areas have speculated that psorosis spreads through propagation of infected buds, soil, dodder, parasitic vines made of scales, and Olpidium-like fungus[2]. Tissue grafting has been confirmed to be one of the vectors of transmission[2].


The virus is untraceable in isolated plant sap. However, young citrus leaves exhibiting severe symptoms homogenised in 0.05 M phosphate buffer, pH 7 or Tris buffer, pH 8, both of which contain 0.5% 2-mercaptoethanol, traces of infection can be retained for at least 2 hours at 25°C or 24-48 h at 4°C [3].

CPsV ‘A’ is denoted by bark-scaling, thinning of branches, older leaves with chlorotic blotches, or pustules. Ringspots of fruits. CPsV ‘B’ causes extensive bark-scaling and branch deterioration, with chlorotic blotches in leaves appearing earlier than normal[4]. Fruits are inedible; infection is a decline in health leading to eventual death. At a molecular level, infected plant cells exhibit large quantities of abnormal cholorplasts, mitochondria and misshaping and enlargement of nuclei/nucleolous[5]. Mitochondria in particular are bent and elongated[5]. Displacement of bodies in nucleous as well as inclusion bodies which possibly contain virus particles have been reported[5].

Restoration of trees in CPsV infected areas is a rigorous process involving replanting and a bud certification program [5].

References

Example: Weir, Jerry P. " Genomic Organization and Evolution of the Human Herpesviruses." Virus Genes 16.1 (1998): 85-93.

Page authored for BIOL 375 Virology, September 2010