Papaya meleira virus (PMeV) is the causal agent of papaya sticky disease, which is characterized by a spontaneous exudation of fluid and aqueous latex from the papaya fruit and leaves. The latex oxidizes after atmospheric exposure, resulting in a sticky feature on the fruit from which the name of the disease originates. PMeV is an isometric virus particle with a double-stranded RNA (dsRNA) genome of approximately 12 Kb. Unusual for a plant virus, PMeV particles are localized on and linked to the polymers present in the latex. The ability of the PMeV to inhabit such a hostile environment demonstrates an intriguing interaction of the virus with the papaya. A hypersensitivity response is triggered against PMeV infection, and there is a reduction in the proteolytic activity of papaya latex during sticky disease. In papaya leaf tissues, stress responsive proteins, mostly calreticulin and proteasome-related proteins, are up regulated and proteins related to metabolism are down-regulated. Additionally, PMeV modifies the transcription of several miRNAs involved in the modulation of genes related to the ubiquitin-proteasome system. Until now, no PMeV resistant papaya genotype has been identified and roguing is the only viral control strategy available. However, a single inoculation of papaya plants with PMeV dsRNA delayed the progress of viral infection.

Among the most serious problems in papaya production are the viruses associated with papaya ringspot and papaya sticky disease (PSD). PSD concerns producers worldwide because its symptoms are extremely aggressive and appear only after flowering. As no resistant cultivar is available, several disease management strategies have been used in affected countries, such as the use of healthy seeds, exclusion of the pathogen, and roguing. In the 1990s, a dsRNA virus, papaya meleira virus (PMeV), was identified in Brazil as the causal agent of PSD. However, in 2016 a second virus, papaya meleira virus 2 (PMeV2), with an ssRNA genome, was also identified in PSD plants. Only PMeV is detected in asymptomatic plants, whereas all symptomatic plants contain both viral RNAs separately packaged in particles formed by the PMeV capsid protein. PSD also affects papaya plants in Mexico, Ecuador, and Australia. PMeV2-like viruses have been identified in the affected plants, but the partner virus(es) in these countries are still unknown. In Brazil, PMeV and PMeV2 reside in laticifers that promote spontaneous latex exudation, resulting in the affected papaya fruit’s sticky appearance. Genes modulated in plants affected by PSD include those involved in reactive oxygen species and salicylic acid signaling, proteasomal degradation, and photosynthesis, which are key plant defenses against PMeV complex infection. However, the complete activation of the defense response is impaired by the expression of negative effectors modulated by the virus. This review presents a summary of the current knowledge of the Carica papaya-PMeV complex interaction and management strategies.

Papaya sticky disease is caused by the association of a fusagra-like and an umbra-like virus, named papaya meleira virus (PMeV) and papaya meleira virus 2 (PMeV2), respectively. Both viral genomes are encapsidated in particles formed by the PMeV ORF1 product, which has the potential to encode a protein with 1563 amino acids (aa). However, the structural components of the viral capsid are unknown. To characterize the structural proteins of PMeV and PMeV2, virions were purified from Carica papaya latex. SDS-PAGE analysis of purified virus revealed two major proteins of ~40 kDa and ~55 kDa. Amino-terminal sequencing of the ~55 kDa protein and LC-MS/MS of purified virions indicated that this protein starts at aa 263 of the deduced ORF1 product as a result of either degradation or proteolytic processing. A yeast two-hybrid assay was used to identify Arabidopsis proteins interacting with two PMeV ORF1 product fragments (aa 321–670 and 961–1200). The 50S ribosomal protein L17 (AtRPL17) was identified as potentially associated with modulated translation-related proteins. In plant cells, AtRPL17 co-localized and interacted with the PMeV ORF1 fragments. These findings support the hypothesis that the interaction between PMeV/PMeV2 structural proteins and RPL17 is important for virus–host interactions.

Papaya sticky disease (PSD) is a severe disease that can destroy papaya trees. PSD is associated with a complex formed between a toti-like virus, Papaya meleira virus (PMeV), and an umbra-like virus—Papaya meleira virus 2 (PMeV2). PSD symptoms only appear after flowering, indicating that at the pre-flowering stage, there is a host stress response associated with tolerance to sticky disease symptoms. Transcriptomic and proteomic analyses of symptomatic plants revealed the modulation of protein turnover, suggesting the involvement of the ubiquitin/proteasome system (UPS) in this pathosystem. In parallel, the analysis of microRNAs modulated during the infection showed that microRNAs predicted to target UPS genes were specially altered. This study aimed to evaluate the importance of UPS for C. papaya–PMeV complex interaction by revisiting transcriptomic and proteomic datasets obtained from infected plants at different developmental phases. In the referred datasets, 1074 transcripts and 80 proteins were related to the UPS pathway. Among the 42 UPS-related genes responsive to PSD, 22 were detected at the transcript level and 21 at the protein level. In addition, the microRNAs predicted to target UPS-related genes were identified, especially those altered during papaya infection by PMeV complex. A total of 106 miRNAs assigned to 33 miRNA families and targeting 146 gene transcripts were found. Among them, 22 miRNAs were predicted to target four genes (U-box domain-containing protein, protein with BTB/POZ domains, 26S proteasome regulatory complex subunit PSMD10, and zinc finger C2H2 type domain) that were observed to be modulated at the transcript level at the pre-flowering stage and one gene (ubiquitin binding domain protein) modulated at the protein level at the post-flowering stage. Experimental evidence supports the idea that key miRNAs were especially relevant in controlling UPS during C. papaya response to the PMeV complex. The miRNA expression and the consequent reduction in transcripts levels could result in increased PMeV complex tolerance in C. papaya. The results presented here add to the knowledge on UPS involvement during virus infection in plants.