Resistance to infection in cowpea by strains of cucumber mosaic virus (CMV) involves a local, hypersensitive response (HR) and a localization of infection. These responses can be separated by mutation at two sites (nucleotides 1978 and 2007, in codons 631 and 641) in the CMV 2a polymerase gene. Changes to both sites of a restricted strain allow systemic infection without an HR and increase the accumulation of both the 2a protein and viral RNA in protoplasts, while changing position 1978 alone results in a systemic infection, a systemic HR, and an increase in viral RNA accumulation in protoplasts. It is suggested that the inhibition response observed in protoplasts, where an HR does not occur, leads to localization of infection in whole plants and that different plant genes are involved in eliciting the HR and the localization response.

Infection of maize by the Fny strain of cucumber mosaic virus (CMV) and resistance against infection by the M strain of CMV were mapped to the coat protein gene on RNA 3 of CMV, using biologically active cDNA clones of Fny-CMV RNAs 1, 2, and 3 and RNAs 2 and 3 of M-CMV, as well as chimeras constructed between cDNA clones of M-CMV and Fny-CMV RNA 3. Changes in the coat protein gene of M-CMV RNA 3 at both positions 129 (Leu to Pro) and 162 (Thr to Ala) were required to overcome the resistance against M-CMV in maize. Resistance to M-CMV in maize was correlated with an inability to detect virus accumulation in the inoculated leaves. Since the coat protein of CMV is involved in virus movement, but not virus replication, the data suggest that the resistance in maize to M-CMV is due to the inability of the M-CMV coat protein to promote the cell-to-cell movement of CMV in maize.

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