Abstract
Papaya ringspot virus (PRSV), a common potyvirus infecting papaya plants worldwide, can lead to either antagonism or synergism in mixed infections with Papaya mosaic virus (PapMV), a potexvirus. These two unrelated viruses produce antagonism or synergism depending on their order of infection in the plant. When PRSV is inoculated first or at the same time as PapMV, the viral interaction is synergistic. However, an antagonistic response is observed when PapMV is inoculated before PRSV. In the antagonistic condition, PRSV is deterred from the plant and its drastic effects are overcome. Here, we examine differences in gene expression by high-throughput RNA sequencing, focused on immune system pathways. We present the transcriptomic expression of single and mixed inoculations of PRSV and PapMV leading to synergism and antagonism. Upregulation of dominant and hormone-mediated resistance transcripts suggests that the innate immune system participates in synergism. In antagonism, in addition to innate immunity, upregulation of RNA interference-mediated resistance transcripts suggests that adaptive immunity is involved.
Highlights
Despite the acceptance of terms coined for the plant–fungal and plant–bacterial models, which were adapted for viruses, the immune system in plants as a response to viral infections still lacks a uniform general descriptive framework [1,2]
We previously reported that plants infected with Papaya mosaic virus (PapMV) showed systemic disease symptoms in less time, which were less severe than those infected with Papaya ringspot virus (PRSV), whose symptoms were evident at about 19 dpi [31]
PapMV infections resulted in mild mosaics, like those observed in the sequential infections, which led to viral antagonism (PapMV→PRSV), as reported before, with a damage value at 60 dpi (δ60 ) significantly greater than the PapMV single infection (PapMV→PRSV δ60 = 8 ± 0.5 and PapMV δ60 = 4 ± 0.0)
Summary
Despite the acceptance of terms coined for the plant–fungal and plant–bacterial models, which were adapted for viruses, the immune system in plants as a response to viral infections still lacks a uniform general descriptive framework [1,2]. PapMV infection was associated with a higher expression of two biochemical landmarks of the systemic acquired resistance (SAR): pathogenesis-related protein 1 (PR1), and reactive oxygen species (ROS) [31] Both responses, higher in antagonism than in synergism or PRSV infection, reflect immune activity in the plant. Since both single PRSV and PapMV infections can trigger components of the innate system (dominant and hormone-mediated resistance), we hypothesized that, during antagonism (PapMV→PRSV), PRSV is counteracted by the PapMV initial immune response through the onset of adaptive immunity (RNAi)
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