Abstract

Although the wheat curl mite, Aceria tulipae, reared on wheat plants infected with brome mosaic virus (BMV) failed to transmit the virus to wheat plants, the virus was detected in high concentrations in these mites (“exposed mites”) by infectivity, specific serological reaction, and electron microscopy of mite extracts. Exposed mites maintained the virus in their bodies in an infective and morphologically unaffected state for at least 6 days when kept on virus-free wheat plants. Thin sections of exposed mites revealed infection of a large part of the alimentary system (midgut and a part of foregut) with the virus. BMV virions, in crystalline arrays, were packed in a large number of membrane bound, ball-like structures in the gut cells and uniformly filled the gut lumen. Cytopathic effects such as degeneration of microvilli, reduction in the number and size of mitochondria, and disintegration of the endoplasmic reticulum were noted in severely infected gut cells where almost all the cytoplasm was replaced by masses of virus. Virions were also found in the body cavity in different parts of the mite's body. No viruslike particles were found in salivary glands or nervous tissue, or in virusfree mites examined. When virusfree mites were allowed a 15–16 hr acquisition access period on BMV infected plants, held subsequently on healthy plants, and were examined immediately after and at different subsequent times, a clearly discernible increase in virus content of the midgut cells was observed. BMV infection in the gut cells by day 7 after the start of acquisition access showed an abundance of large, multilayered virus crystals and aggregates of unarranged virions embedded in the cytoplasm. Nurse cells lining the genital canal were also infected by the virus. Cylindrical- or spindle-shaped inclusion bodies composed of long, thin filaments occurred in the gut lumen of A. tulipae that had a 15–16 hr acquisition access to virus-infected plants. BMV appears to multiply locally in the gut tissue of the mites, indicating that transmissibility and specificity of a virus to an arthropod vector may not always be a function of virus multiplication in the arthropod. Possible reasons for inability of A. tulipae to transmit BMV are discussed.

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