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An outbreak of a new disease occurred in cotton (Gossypium hirsutum) fields in northwest Argentina starting in the 2009-10 growing season and is still spreading steadily. The characteristic symptoms of the disease included slight leaf rolling and a bushy phenotype in the upper part of the plant. In this study, we determined the complete nucleotide sequences of two independent virus genomes isolated from cotton blue disease (CBD)-resistant and -susceptible cotton varieties. This virus genome comprised 5,866 nucleotides with an organization similar to that of the genus Polerovirus and was closely related to cotton leafroll dwarf virus, with protein identity ranging from 88 to 98%. The virus was subsequently transmitted to a CBD-resistant cotton variety using Aphis gossypii and symptoms were successfully reproduced. To study the persistence of the virus, we analyzed symptomatic plants from CBD-resistant varieties from different cotton-growing fields between 2013 and 2015 and showed the presence of the same virus strain. In addition, a constructed full-length infectious cDNA clone from the virus caused disease symptoms in systemic leaves of CBD-resistant cotton plants. Altogether, the new leafroll disease in CBD-resistant cotton plants is caused by an atypical cotton leafroll dwarf virus.

Cotton blue disease (CBD) is the most important disease present in cotton crops in South America and cotton leafroll dwarf virus (CLRDV) is the causal agent. The disease has been controlled by sowing cotton varieties resistant to CLRDV. However, in the 2009/10 growing season, an outbreak due to an atypical CLRDV isolate (CLRDV‐at) occurred in northwest Argentina. Although CLRDV and CLRDV‐at genomes are very closely related, the symptoms they produce in cotton plants are quite different. P0 is the most divergent protein between the isolates and in CLRDV is a silencing suppressor protein. This work characterized the silencing suppressor activity of the P0 protein encoded by CLRDV‐at (P0CL‐at) and evaluated its role in Cbd‐resistance break in cotton plants. It was demonstrated that P0CL‐at, despite having a mutation in the consensus of the F‐box‐like motif, was able to suppress local RNA silencing, but displayed lower activity than P0CL. P0CL and P0CL‐at showed no differences in the interaction with Gossypium hirsutum SKP1 orthologue (GSK1) and Nicotiana benthamiana SKP1 and both P0 proteins triggered destabilization of ARGONAUTE1. However, when the ability to enhance PVX symptoms was evaluated, P0CL‐at was shown to be a weaker pathogenicity factor than P0CL in N. benthamiana. Interestingly, trans‐expressed P0CL‐at enabled CLRDV to systemically infect CBD‐resistant plants, and a chimeric CLRDV‐P0CL‐at infectious clone succeeded in establishing infection in CBD‐resistant cotton varieties with symptoms resembling those produced by CLRDV‐at. These results strongly suggest that P0CL‐at is the avirulence (Avr) determinant involved in breaking cotton Cbd gene‐based resistance.

Poleroviruses are economically important plant viruses that infect cereal, vegetable, and fruit crops, and cause serious yield and quality losses worldwide. In this review we summarize the current knowledge of the function and regulation of polerovirus proteins and mention the methods employed by the different bodies of research that have produced these advances. Major biochemical and biological properties of these viral proteins are discussed in the order in which their open reading frames are organized in the genome.

Our data further implicate oxidative stress as a possible inducer of apoptosis in lungs from animals exposed to low concentrations of this urban environmental contaminant.

During early postnatal ontogeny in most mammals, the lung is structurally and functionally immature. In some species with relatively altricial lung morphology, there is evidence of a coupling between functional maturity of the pulmonary cellular immune system and alveolar maturation. Herein, we examine changes in alveolar macrophage (AM) number and function occurring during alveolarization in a more precocial species, the pig, to determine if heightened oxidative metabolism and phagocytic ability is similarly delayed until completion of lung morphogenesis. We assessed cell differential in lavage fluid and evaluated two main functional parameters of AM phagocytic response, the generation of reactive oxygen species (ROS), and particle internalization. AM functional maturation occurred mainly during the first postnatal week: the proportion of AMs, ROS generation, and phagocytosis all increased significantly. These results suggest maturational improvement of the impaired AM-based pulmonary immune system of the neonate piglet occurs during the postnatal period of rapid alveolarization.

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