This study investigates why cloned geminiviruses fail to be transmitted by whiteflies despite being infectious. Researchers used African cassava mosaic virus (ACMV) isolates from Kenya and Nigeria to create pseudorecombinants by swapping genomic components DNA A and DNA B. Results showed that both components contained defects preventing whitefly transmission. Analysis revealed that DNA B mutations impaired virus acquisition by whiteflies, likely due to defective movement proteins preventing the virus from reaching appropriate plant tissues. DNA A mutations, particularly in the coat protein gene, prevented successful inoculation back into plants even when acquisition occurred. Notably, wild-type virus lost transmissibility after repeated mechanical passages through alternative plant hosts, while cloned virus maintained transmissibility, suggesting field isolates may be mixtures of transmissible and non-transmissible forms. The findings demonstrate that geminivirus movement proteins play a crucial role in insect transmission by determining correct virus localization in plant tissues, though they do not directly interact with vectors.

Key findings

• Both DNA A and DNA B components of cloned ACMV-K contain defects preventing whitefly transmission, neither pseudorecombinant alone restores transmissibility
• DNA B defects prevent virus acquisition by whiteflies through impaired movement proteins and incorrect tissue distribution
• DNA A defects, particularly in the coat protein, prevent virus inoculation back into plants despite successful acquisition
• Wild-type ACMV loses insect transmissibility after 20-25 mechanical passages through alternative hosts, while cloned virus maintains transmissibility
• Movement proteins are essential for determining correct virus location in plant tissues for whitefly acquisition, though they do not interact directly with the vector