Infection with Strains of Citrus Tristeza Virus Does Not Exclude Superinfection by Other Strains of the Virus

ABSTRACT Superinfection exclusion or homologous interference, a phenomenon in which a primary viral infection prevents a secondary infection with the same or closely related virus, has been observed commonly for viruses in various systems, including viruses of bacteria, plants, and animals. With plant viruses, homologous interference initially was used as a test of virus relatedness to define whether two virus isolates were “strains” of the same virus or represented different viruses, and subsequently purposeful infection with a mild isolate was implemented as a protective measure against isolates of the virus causing severe disease. In this study we examined superinfection exclusion of Citrus tristeza virus (CTV), a positive-sense RNA closterovirus. Thirteen naturally occurring isolates of CTV representing five different virus strains and a set of isolates originated from virus constructs engineered based on an infectious cDNA clone of T36 isolate of CTV, including hybrids containing sequences from different isolates, were examined for their ability to prevent superinfection by another isolate of the virus. We show that superinfection exclusion occurred only between isolates of the same strain and not between isolates of different strains. When isolates of the same strain were used for sequential plant inoculation, the primary infection provided complete exclusion of the challenge isolate, whereas isolates from heterologous strains appeared to have no effect on replication, movement or systemic infection by the challenge virus. Surprisingly, substitution of extended cognate sequences from isolates of the T68 or T30 strains into T36 did not confer the ability of resulting hybrid viruses to exclude superinfection by those donor strains. Overall, these results do not appear to be explained by mechanisms proposed previously for other viruses. Moreover, these observations bring an understanding of some previously unexplained fundamental features of CTV biology and, most importantly, build a foundation for the strategy of selecting mild isolates that would efficiently exclude severe virus isolates as a practical means to control CTV diseases.

Download Full-text

Genetic Diversity and Phylogenetic Analysis of Citrus tristeza virus Isolates from Turkey

Advances in Virology ◽

10.1155/2019/7163747 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 1

Author(s):

Gözde Erkiş-Güngör ◽

Bayram Çevik

Keyword(s):

Phylogenetic Analysis ◽

Citrus Tristeza Virus ◽

Molecular Characteristics ◽

Cloning And Sequencing ◽

Phylogenetic Groups ◽

The 1960S ◽

Tristeza Virus ◽

Virus Isolates ◽

Stem Pitting ◽

Citrus Tristeza

The presence of Citrus tristeza virus (CTV) in Turkey has been known since the 1960s and the virus was detected in all citrus growing regions of the country. Even though serological and biological characteristics of CTV have been studied since the 1980s, molecular characteristics of CTV isolates have not been studied to date in Turkey. In this study, molecular characteristics of 15 CTV isolates collected from different citrus growing regions of Turkey were determined by amplification, cloning, and sequencing of their major coat protein (CP) genes. The sequence analysis showed that the CP genes were highly conserved among Turkish isolates. However, isolates from different regions showed more genetic variation than isolates from the same region. Turkish isolates were clustered into three phylogenetic groups showing no association with geographical origins, host, or symptoms induced in indicator plants. Phylogenetic analysis of Turkish isolates with isolates from different citrus growing regions of the world including well-characterized type isolates of previously established strain specific groups revealed that some Turkish isolates were closely related to severe quick decline or stem pitting isolates. The results demonstrated that although CTV isolates from Turkey are considered biologically mild, majority of them contain severe components potentially causing quick decline or stem pitting.

Download Full-text

Genetic Variability of Croatian Citrus tristeza virus Isolates

International Organization of Citrus Virologists Conference Proceedings (1957-2010) ◽

10.5070/c51498j3x5 ◽

2010 ◽

Vol 17 (17) ◽

Author(s):

S. Cerni ◽

G. Nolasco ◽

M. Krajacic ◽

D. Škoric

Keyword(s):

Genetic Variability ◽

Citrus Tristeza Virus ◽

Tristeza Virus ◽

Virus Isolates ◽

Citrus Tristeza

Download Full-text

Walking Together: Cross-Protection, Genome Conservation, and the Replication Machinery of Citrus tristeza virus

Viruses ◽

10.3390/v12121353 ◽

2020 ◽

Vol 12 (12) ◽

pp. 1353

Author(s):

Svetlana Y. Folimonova ◽

Diann Achor ◽

Moshe Bar-Joseph

Keyword(s):

Citrus Tristeza Virus ◽

Fluorescent Protein ◽

Field Tests ◽

Fruit Trees ◽

Plant Viruses ◽

Cross Protection ◽

Virus Variant ◽

Tristeza Virus ◽

Direct Confirmation ◽

Citrus Tristeza

“Cross-protection”, a nearly 100 years-old virological term, is suggested to be changed to “close protection”. Evidence for the need of such change has accumulated over the past six decades from the laboratory experiments and field tests conducted by plant pathologists and plant virologists working with different plant viruses, and, in particular, from research on Citrus tristeza virus (CTV). A direct confirmation of such close protection came with the finding that “pre-immunization” of citrus plants with the variants of the T36 strain of CTV but not with variants of other virus strains was providing protection against a fluorescent protein-tagged T36-based recombinant virus variant. Under natural conditions close protection is functional and is closely associated both with the conservation of the CTV genome sequence and prevention of superinfection by closely similar isolates. It is suggested that the mechanism is primarily directed to prevent the danger of virus population collapse that could be expected to result through quasispecies divergence of large RNA genomes of the CTV variants continuously replicating within long-living and highly voluminous fruit trees. This review article provides an overview of the CTV cross-protection research, along with a discussion of the phenomenon in the context of the CTV biology and genetics.

Download Full-text

Citrus tristeza virus P33 Protein Is Required for Efficient Transmission by the Aphid Aphis (Toxoptera) citricidus (Kirkaldy)

Viruses ◽

10.3390/v12101131 ◽

2020 ◽

Vol 12 (10) ◽

pp. 1131

Author(s):

Turksen Shilts ◽

Choaa El-Mohtar ◽

William O. Dawson ◽

Nabil Killiny

Keyword(s):

Citrus Tristeza Virus ◽

Transmission Rate ◽

Control Strategies ◽

Virus Transmission ◽

Plant Viruses ◽

Transmission Mechanisms ◽

Infectious Clones ◽

Underlying Mechanisms ◽

Tristeza Virus ◽

Citrus Tristeza

Plant viruses are threatening many valuable crops, and Citrus tristeza virus (CTV) is considered one of the most economically important plant viruses. CTV has destroyed millions of citrus trees in many regions of the world. Consequently, understanding of the transmission mechanism of CTV by its main vector, the brown citrus aphid, Aphis (Toxoptera) citricidus (Kirkaldy), may lead to better control strategies for CTV. The objective of this study was to understand the CTV–vector relationship by exploring the influence of viral genetic diversity on virus transmission. We built several infectious clones with different 5′-proximal ends from different CTV strains and assessed their transmission by the brown citrus aphid. Replacement of the 5′- end of the T36 isolate with that of the T30 strain (poorly transmitted) did not increase the transmission rate of T36, whereas replacement with that of the T68-1 isolate (highly transmitted) increased the transmission rate of T36 from 1.5 to 23%. Finally, substitution of p33 gene of the T36 strain with that of T68 increased the transmission rate from 1.5% to 17.8%. Although the underlying mechanisms that regulate the CTV transmission process by aphids have been explored in many ways, the roles of specific viral proteins are still not explicit. Our findings will improve our understanding of the transmission mechanisms of CTV by its aphid vector and may lead to the development of control strategies that interfere with its transmission by vector.

Download Full-text