Antagonism or synergism between papaya ringspot virus and papaya mosaic virus in Carica papaya is determined by their order of infection.

Antagonism between unrelated plant viruses has not been thoroughly described. Our studies show that two unrelated viruses, papaya ringspot virus (PRSV) and papaya mosaic virus (PapMV) produce different symptomatic outcomes during mixed infection depending on the inoculation order. Synergism occurs in plants infected first with PRSV or in plants infected simultaneously with PRSV and PapMV, and antagonism occurs in plants infected first with PapMV and later inoculated with PRSV. During antagonism, elevated pathogenesis-related (PR-1) gene expression and increased reactive oxygen species production indicated the establishment of a host defense resulting in the reduction in PRSV titers. Polyribosomal fractioning showed that PRSV affects translation of cellular eEF1α, PR-1, ß-tubulin, and PapMV RNAs in planta, suggesting that its infection could be related to an imbalance in the translation machinery. Our data suggest that primary PapMV infection activates a defense response against PRSV and establishes a protective relationship with the papaya host.

The absence of eukaryotic initiation factor eIF(iso)4E affects the systemic spread of a Tobacco etch virus isolate in Arabidopsis thaliana.

Translation initiation factor eIF4E exerts an important role during infection of viral species in the family Potyviridae. Particularly, a eIF(iso)4E family member is required for Arabidopsis thaliana susceptibility to Turnip mosaic virus, Lettuce mosaic virus, and Tobacco etch virus (TEV). In addition, a resistance mechanism named restriction of TEV movement (RTM) in A. thaliana controls the systemic spread of TEV in Col-0 ecotype. Here, we describe that TEV-TAMPS, a Mexican isolate, overcomes the RTM resistance mechanism reported for TEV-7DA infection of the Col-0 ecotype but depends on eIF(iso)4E for its systemic spread. To understand at which level eIF(iso)4E participates in A. thaliana TEV-TAMPS infection, the viral RNA replication and translation were measured. The absence or overexpression of eIF(iso)4E did not affect viral translation, and replication was still observed in the absence of eIF(iso)4E. However, the TEV-TAMPS systemic spread was completely abolished in the null mutant. The viral protein genome-linked (VPg) precursor NIa was found in coimmunoprecipitated complexes with both, eIF(iso)4E and eIF4E. However, the viral coat protein (CP) was only present in the eIF(iso)4E complexes. Since both the VPg and the CP proteins are needed for systemic spread, we propose a role of A. thaliana eIF(iso)4E in the movement of TEV-TAMPS within this host.